title: Establishment of Developmental Gene Silencing by Ordered Polycomb Complex Recruitment in Early Zebrafish Embryos

city: Salt Lake City

first: Graham

middle: James McGuire

last: Hickey

state: UT

address: 2000 Circle of Hope Drive

department: Oncological Sciences

institute: University of Utah


title: Establishment of Developmental Gene Silencing by Ordered Polycomb Complex Recruitment in Early Zebrafish Embryos [ATAC-seq]

status: Public on Jan 04 2022

country: USA

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Vertebrate embryos achieve developmental competency during zygotic genome activation (ZGA) by establishing chromatin states that silence yet poise developmental genes for subsequent lineage-specific activation. Here, we reveal how developmental gene poising is established de novo in preZGA zebrafish embryos. Poising is established at promoters and enhancers that initially contain open/permissive chromatin with ‘Placeholder’ nucleosomes (bearing H2A.Z, H3K4me1, and H3K27ac), and DNA hypomethylation. Silencing is initiated by the recruitment of Polycomb Repressive Complex 1 (PRC1), and H2Aub1 deposition by catalytic Rnf2 during preZGA and ZGA stages. During postZGA, H2Aub1 enables Aebp2-containing PRC2 recruitment and H3K27me3 deposition. Notably, preventing H2Aub1 (via Rnf2 inhibition) eliminates recruitment of Aebp2-PRC2 and H3K27me3, and elicits transcriptional upregulation of certain developmental genes during ZGA. However, upregulation is independent of H3K27me3 – establishing H2Aub1 as the critical silencing modification at ZGA. Taken together, we reveal the logic and mechanism for establishing poised/silent developmental genes in early vertebrate embryos.

overall_design: ATAC-seq in early Zebrafish embryos.

middle: J

first: Bradley

middle: R

last: Cairns


title: Effects of Buyang Huanwu Decoction on circRNA-miRNA-mRNA transcriptional network of rats with cerebral ischemia

city: Changsha

first: Bo-wei

last: CHEN

address: No. 95 Shaoshan Middle Road

country: China

institute: Hunan University of Chinese Medicine

summary: To reveal the effects of Buyang Huanwu Decoction on circRNA-miRNA-mRNA transcriptional network of rats with cerebral ischemia, explore its molecular mechanism for the treatment of cerebral ischemia.

overall_design: Three-condition experiment: control group, model group and Buyang Huanwu Decoction(BHD) group.The middle cerebral artery embolization method was used to replicate the cerebral ischemia model in all groups

last: Chen

first: Rong-mei

last: Tang

first: Jian

last: Yi

first: Bai-yan

last: Liu


title: Establishment of Developmental Gene Silencing by Ordered Polycomb Complex Recruitment in Early Zebrafish Embryos [ChIP-seq]

overall_design: ChIP-seq of histone marks/variant, Polycomb group proteins, and Jarid2 in early Zebrafish embryos.


title: Searching beyond the streetlight: neonicotinoid exposure alters the neurogenomic state of worker honey bees

city: Toronto

first: Amro

last: Zayed

state: Ontario

address: 4700 Keele Street

department: Biology

country: Canada

institute: York University

type: Expression profiling by high throughput sequencing

summary: Neonicotinoid insecticides have been implicated in honey bee declines, with many studies showing that sub-lethal exposure impacts bee behaviors such as foraging, learning and memory. Despite the large number of ecotoxicological studies carried out to date, most focus on a handful of worker phenotypes leading to a ‘streetlight effect’ where the a priori choice of phenotypes to measure may influence the results and conclusions arising from the studies. This bias can be overcome with the use of toxicological transcriptomics, where changes in gene expression can provide a more objective view of how pesticides alter animal physiology. Here, we used RNA sequencing to examine the changes in neurogenomic states of nurse and forager honey bees that were naturally exposed to neonicotinoids in the field and artificially exposed to neonicotinoid in a controlled experiment.

overall_design: Field Experiment - 5 Honey bee colonies located immeditely near neonicotinoid treated corn field and 5 honey bee colonies located at least 3km away from such field. One May 30th, 2014, right after corn plantation, 5 forager bees and 5 nurse bees were collected from each colony. They were immdetely frozen on dry ice and later, their brains were dissected. Apiary Expeirment - Ten colonies in a single apiary received artificial pollen for a 12-week period. Half of the colonies received a pollen patty spiked with clothianidin; the most commonly found NNI in the field study. The exposure started with 4.9ppb of clothianidin in week 1 and was lowered each week, until the dose reached 2.0ppb at week 5 and stayed the same until week 12 . Five nurses and five foragers were collected from each queen-right colony 30 days after the start of our experiment

first: Nadejda

last: Tsvetkov

first: Zayed

last: Amro


title: Multiomic analysis identifies CPT1A as a potential therapeutic target in platinum-refractory high grade serous ovarian cancer

city: Seattle

first: Amanda

last: Paulovich

state: WA

address: 1100 Fairview Ave. N.

institute: Fred Hutchinson Cancer Research Center

summary: Platinum-based chemotherapies are widely used anti-cancer drugs. Tumor resistance to platinum compounds is a major determinant of patient survival, including in high grade serous ovarian cancer (HGSOC). To understand mechanisms of platinum resistance and identify potential therapeutic targets in resistant HGSOC, we generated a comprehensive, reproducible data resource comprised of dynamic (+/-carboplatin) proteomic/posttranslational modification and RNASeq profiles from HGSOC intra-patient cell line pairs derived from 3 patients before and after acquiring platinum resistance. The molecular profiles revealed extensive responses to carboplatin and differential responses between sensitive and resistant cells. Higher oxidative phosphorylation and fatty acid oxidation (FAO) pathway expression were observed in the platinum-resistant cells, which was further validated in patient-derived xenograft (PDX) models. We show that both pharmacologic inhibition and CRISPR knockout of CPT1A, which represents a rate limiting step of FAO, sensitize HGSOC cells to platinum. Thus, FAO is a candidate therapeutic target to overcome platinum resistance.

overall_design: Cells from 3 HGSOC intra-patient cell line pairs (PEA1S/PEA2R, PEO1S/PEO4R, PEO14S/PEO23R) were treated with 80 mM carboplatin and harvested after 8 or 24 hours of treatment. A control sample was treated with vehicle and harvested at 24 hours. The experiment was repeated on three different days. RNAs were extracted for RNAseq.

first: Dongqing

last: Huang

first: Shrabanti

last: Chowdhury

first: Hong

last: Wang

first: Sara

last: Savage

first: Richard

middle: G

last: Ivey

first: Jacob

last: Kennedy

first: Jeffrey

last: Whiteaker

first: Chenwei

last: Lin

first: Xiaonan

last: Hou

first: Catherine

last: Huntoon

first: Uliana

last: Voytovich

first: Zahra

last: Shire

first: Qing

last: Yu

first: Steven

middle: P

last: Gygi

first: Andrew

middle: N

last: Hoofnagle

first: Zachary

middle: T

last: Herbert

first: Travis

middle: D

last: Lorentzen

first: Anna

last: Calinawan

first: Larry

middle: M

last: Karnitz

first: S

last: Weroha

first: Scott

middle: H

last: Kaufmann

first: Bing

last: Zhang

first: Pei

first: Michael

last: Birrer


title: A purine metabolic checkpoint that prevents autoimmunity and autoinflammation (T cell RNA Seq dataset)

city: Cambridge

first: Gavin

last: Sewell

state: Cambridgeshire

address: Puddicombe Way

department: Jeffrey Cheah Biomedical Centre, University of Cambridge

country: United Kingdom

institute: Cambridge Institute of Therapeutic Immunology and Infectious Disease

summary: In this study, we investigate how FAMIN activity in dendritic cells determines the release of mediators that affect priming, activation and gene transcription of CD8+ T cells.

overall_design: Supernatant from Famin-/- and Famin+/+ splenic CD11c+ dendritic cells were harvested following overnight incubation. CD8+ T cells were isolated from spleens and lymph nodes of OT-I;Rag–/– mice, stimulated with anti-CD3 and CD28 in the presence of supernatant obtained from Famin-/- or Famin+/+ dendritic cells for 24 hours.  Total RNA was extracted using the RNeasy Mini Kit (QIAGEN, 74104) in accordance with the manufacturer's instructions. Libraries were prepared using TruSeq stranded mRNA library prep kit (Illumina, 20020594). Sequencing of libraries was performed using an Illumina NextSeq 500 platform with NextSeq 500-Mid Output kit generating 2x150bp end reads. FastQ files were quality-checked and any residual adaptor sequences were removed using TrimGalore. Reads were then aligned to the reference genome Ensembl Mus_musculus.GRCm38 using STAR. Differential gene expression analysis was performed on read count files using edgeR.

first: Svetlana

last: Saveljeva

first: Arthur

last: Kaser


title: Gene expression change in the lingual nerve and the traumatic neuromas after the injured lingual nerve.

city: Wakayama

first: Takashi

last: Nakanishi

state: Wakayama

address: Kimiidera 811-1

department: Oral and Maxillofacial Surgery

country: Japan

institute: Wakayama Medical University

summary:
The lingual nerves are incidentally injured in many oral and maxillofacial surgical procedures, traumatic neuroma was observed at the proximal stump of the injured lingual nerve in patients with severe lingual nerve disturbance. Various genes including genes related to nerve regeneration are expressed in the rat and mouse traumatic neuroma, as regeneration mechanism works after lingual nerve injury. Few reported have showed the expressed genes in the traumatic neuroma of the human lingual nerve.
In this study, we compared the gene expression between pooled RNA sample from three traumatic neuromas removed in microneurosurgery in the lingual nerve and an RNA sample from the normal lingual nerve on the unaffected side of the removed tongue with cancer. The 2,357 genes increased more than twofold in the traumatic neuroma compared with the normal lingual nerve. Then, we analyzed the upregulated genes in DAVID and DAVID indicated that the 20 upregulated genes were associated with protein secretion to the extracellular space in the pathways. This study identified the 20 candidate genes at the nerve regeneration stage in the traumatic neuroma in the human lingual nerve.

overall_design: We removed the three traumatic neuromas in the microneurosurgery after the lingual nerve injury. We measured the expression of genes in Affymetrix GeneChip®, and we compared with a pooled RNA sample from three traumatic neuromas and an RNA sample from the normal lingual nerve on the unaffected side of the removed tongue with cancer. Total RNA was extracted from the traumatic neuroma removed lingual nerve and normal lingual nerve. An equal amount of RNA from 3 traumatic neuroma was pooled and used for microarray analysis.

first: T

first: Y

last: Yamamoto


title: Establishment of Developmental Gene Silencing by Ordered Polycomb Complex Recruitment in Early Zebrafish Embryos [RNA-seq]

first: Graham

last: Hickey

overall_design: RNA-seq in early Zebrafish embryos.

first: Bradley

last: Cairns


title: ChIP-Seq analysis of LCOR and mutated variants lacking the nuclear receptor binding domain or the HTH motif in MDA-MB-231 breast cancer cells

city: Barcelona

first: Cristina

middle: Lopez

last: Rodriguez

address: Carrer Dr. Aiguader, 88

country: Spain

institute: UPF

summary: LCOR is a tumor suppressor that induces differentiation of mammary stem cells and cancer stem cells. LCOR orchestrates and sensitizes cells to interferon in ER-negative breast cancer cells. LCOR can act as a co-repressor of activated nuclear receptors and also as a transcription factor by DNA direct binding through its HTH domain. These domains are the most conserved regions of LCOR across vertebrates, suggesting a conserved regulatory function. Here we performed ChiP-seq analysis of LCOR in MDA-MB-231 cells with ectopic expression of the LCOR wild-type, LCOR without the nuclear receptor binding domain (LSKAA) and LCOR with deleted DNA binding domain (HTH). This analysis allows to compare the genome wide distribution of LCOR depending on these specific protein domains

overall_design: Evaluation of LCOR direct gene regulation depending on specific protein conserved regulatory domains

first: Toni

last: Celià-Terrasa

first: Iván

last: Pérez-Núñez

first: Catalina

last: Rozalén


title: WGBS of control and DAC-treated CT26 cells.

status: Public on Jan 03 2022

city: Shanghai

first: Ganjun

last: Yu

state: Shanghai

address: 800 Xiangyin Road, Shanghai, China.

institute: National Key Laboratory of Medical Immunology & Institute of Immunology

type: Methylation profiling by high throughput sequencing

summary: PD-1 blockade has demonstrated impressive clinical outcomes in colorectal cancers that have high microsatellite instability. However, the therapeutic efficacy for patients with tumors with low microsatellite instability or stable microsatellites needs further improvement. Here, we have demonstrated that low-dose decitabine could increase the expression of immune-related genes such as major histocompatibility complex genes and cytokine-related genes as well as the number of lymphocytes at the tumor site in CT26 colorectal cancer-bearing mice. A more significant inhibition of tumor growth and a prolongation of survival were observed in the CT26 mouse model after treatment with a combination of PD-1 blockade and decitabine than in mice treated with decitabine or PD-1 blockade alone. The anti-tumor effect of the PD-1 blockade was enhanced by low-dose decitabine. The results of RNA sequencing and whole-genome bisulfite sequencing of decitabine-treated CT26 cells and tumor samples with microsatellite stability from the patient tumor-derived xenograft model have shown that many immune-related genes, including antigen processing and antigen-presenting genes, were upregulated, whereas the promoter demethylation was downregulated after decitabine exposure. Therefore, decitabine-based tumor microenvironment re-modulation could improve the effect of the PD-1 blockade. The application of decitabine in PD-1 blockade-based immunotherapy may elicit more potent immune responses, which can provide clinical benefits to the colorectal cancer patients with low microsatellite instability or stable microsatellites.

overall_design: CT26 cells were seeded at a density of 1 × 105 cells/ml in a six_x0002_well culture plate. After 24 h, the medium was replaced with complete medium containing 1 μM DAC every 24 h for 3 days.After the third DAC treatment, the medium was replaced with fresh complete medium without DAC, and the cells were cultured for an additional 24 h and then used for subsequent experiments.Control groups were treated synchronously under the same conditions except for the absence of DAC.


title: WGBS of control and DAC-treated tumor tissue from PDX model

overall_design: Fresh tumor samples from patients identified as MSS were selected for PDX model establishment. At 28 days post-inoculation, we administered DAC 20 μg to each mouse for 5 consecutive days by intraperitoneal injection. The control groups were given the same volumes of saline in the same manner. On the seventh day after the end of the drug treatment, the tumors were collected and conducted extraction of DNA and RNA.


title: Transcriptomic profiles of Candida albicans grown in the presence or absence of mucin glycans

first: Julie

last: Takagi

state: CA

address: 70 Massachusetts Ave, 56-230

institute: MIT

summary: We use high-throughput sequencing to profile the response of the opportunistic fungal pathogen Candida albicans to mucins and mucin-glycans from the mucosal niche. We find that C. albicans undergoes a genome-wide phenotypic shift in response to mucins and their attached glycans suppressing virulence-associated pathways.

overall_design: Examination of differential gene expression in C. albicans in response to mucin sugars

middle: S

first: Katharina

last: Ribbeck


title: scRNA-seq to examine the reaction of a subpopulation of ependymal cells, EpA cells, to spinal cord injury.

city: Solna

first: Moa

last: Stenudd

address: Berzelius väg 25

department: Cell and Molecular Biology

country: Sweden

institute: Karolinska Institutet

summary: We performed single cell RNA sequencing to examine the reaction of a subpopulation of ependymal cells, EpA cells, to spinal cord injury. The experiment contains cells from spinal cords of Troy-CreERT2 mice on a Rosa26-tdTomato background. The spinal cord samples come from uninjured and injured spinal cords (3 days after injury).

overall_design: Examination of transcriptional changes occurring in spinal cord EpA ependymal cells isolated from the mouse spinal cord subjected to dorsal funiculus incision injury. Injured (3 days after injury) and uninjured conditions were examined.

first: Stenudd

last: Moa

first: Llorens-Bobadilla

last: Enric

first: Zamboni

last: Margherita

first: Frisén

last: Jonas


title: Oestrogen promotes innate immune invasion of Candida albicans through inactivation of complement

city: Canterbury

first: Rebecca

middle: Anne

last: Hall

address: Giles Lane

department: School of Biosciences

institute: University of Kent

summary: Candida albicans is a commensal of the urogenital tract and the predominant cause of vulvovaginal candidiasis (VVC). Roughly, 70% of otherwise healthy women succumb to VVC at least once in their life time. Elevated oestrogen levels are associated with C. albicans colonisation of the vagina and symptomatic infection. However, little is known about how C. albicans adapts to oestrogen. Here, we investigate how adaptation of C. albicans to elevated concentrations of oestrogen on the C. albicans host-pathogen interaction. Growth of C. albicans in physiological relevant concentrations of oestrogen promoted fungal innate immune evasion through reduction of both macrophage and neutrophil phagocytosis. Oestrogen-induced innate immune evasion was mediated via inhibition of opsonophagocytosis through enhanced Gpd2 dependent acquisition of Factor H on the fungal cell surface. The zebrafish larval model of infection confirmed that in vivo oestrogen and Gpd2 promote pathogenicity. Understanding the impact of oestrogen on C. albicans host-pathogen interaction will help improve our knowledge on how oestrogen promotes VVC.

overall_design: Transcriptional response of C. albicans (SC5314) to YPD with or without 10 µM of oestrogen for 4h at 37c.

first: Pizga

last: Kumwenda

first: Fabien

last: Cottier

first: Ben

last: Keevan

first: Hannah

last: Gallagher

first: Lisa

last: Wood


title: DAC-treated tumor tissue from PDX model and DAC-treated CT26 cells.

summary: This SuperSeries is composed of the SubSeries listed below.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Refer to individual Series


title: RNA sequencing of control and DAC-treated CT26 cells.


title: Analysis of Wild Type and hepatocyte-specific CD36 knockout (CD36LKO) mice liver Transcriptomes under high fat diet (HFD)

city: Chongqing

first: Hong

last: Qin

address: Yuzhong District Medical College Road

institute: ChongQing Medical University

summary: We generated hepatocyte-specific CD36 knockout (CD36LKO) mice to study in vivo effects of CD36 on de novo lipogenesis (DNL) under high fat diet (HFD). Lipid deposition and DNL were analyzed in primary hepatocytes isolated from CD36LKO mice or HepG2 cells with CD36 overexpression. RNA-sequence, co-immunoprecipitation and proximity ligation assay were carried out to determine its role in regulating DNL.  Results: Hepatic CD36 expression was upregulated in NAFLD mice and patients, and CD36LKO mice exhibited attenuated HFD-induced hepatic steatosis and insulin resistance. We identified hepatocyte CD36 as a key regulator for DNL in the liver. Sterol regulatory element-binding protein 1 (SREBP1) and its downstream lipogenic enzymes such as FASN, ACCα and ACLY were significantly downregulated in the liver of HFD-fed CD36LKO mice, whereas overexpression CD36 stimulated insulin-mediated DNL and lipid droplet formation in vitro. Mechanistically, CD36 was activated by insulin and formed a complex with insulin induced gene-2 (INSIG2), that disrupts the interaction between SREBP cleavage-activating protein (SCAP) and INSIG2, thereby leading to the translocation of SREBP1 from ER to Golgi for processing. Furthermore, treatment with 25-hydroxycholesterol or betulin, molecules shown to enhance SCAP/INSIG interaction, reversed the effects of CD36 on SREBP1 cleavage.

overall_design: CD36 KO vs. WT

first: Han

last: Zeng

first: Ping

last: Yang

first: Yaxi

last: Chen


title: RNA sequencing of control and DAC-treated tumor tissue from PDX model

first: Ganjun

last: Yu


title: Hepatocyte RNA-seq analysis in liver-specific XBP1 knockout mice fed a high fat sugar diet

city: Chicago

first: Priyam

last: Patel

state: IL

address: 750 North Lake Shore Drive, Rubloff 11-146

department: Quantitative Data Science Core

institute: Northwestern University

summary: X-box binding protein 1 (XBP1) is a key component of the unfolded protein response (UPR) and plays important roles in the pathogenesis of nonalcoholic fatty liver diseases (NAFLD). Mice with liver-specific XBP1 deletion developed great liver injury and fibrosis in a dietary model of NAFLD. This project is to investigate hepatocyte-specific transcriptome profiling in XBP1-deficient mice fed a high fat sugar diet.

overall_design: Liver-specific Xbp1 deficient mice or flox controls were fed either regular chow or a high fat sugar (HFS) diet for up to 6 weeks. Hepatocytes were isolated at the conclusion of the experiments and RNA was extracted with Trizol. Samples in HFS diet cohorts (n=6) were pooled into three replicates.

first: Richard

last: Green

first: Xiaoying

last: Liu


title: Reversal of RNA toxicity in myotonic dystrophy via a decoy RNA-binding protein with high affinity for expanded CUG repeats [human]

city: PARIS

first: Denis

last: Furling

state: ILE-DE-FRANCE

address: 52 blv Vincent Auriol

country: France

institute: Centre de Recherche en Myologie

summary: Myotonic dystrophy type 1 (DM1) is an RNA-dominant disease whose pathogenesis stems from the functional loss of muscleblind-like RNA-binding proteins (RBPs), which causes the formation of alternative-splicing defects. The loss of functional muscleblind-like protein 1 (MBNL1) results from its nuclear sequestration by mutant transcripts containing pathogenic expanded CUG repeats (CUGexp). Here we show that an MBNL1∆ RBP engineered to act as a decoy for CUGexp reverses the toxicity of the mutant transcripts.

overall_design: In this study, MBNL1∆ treatment was assessed in differentiated  DM1 myoblasts and compared to untreated DM1  and  WT differentiated  myoblasts. The  overall transcriptome changes were analyzed by RNAseq.

first: Ludovic

last: Arandel

first: Maria

last: Kondili


title: Role of Macrophages in the Foreign Body Response to Poly(ethylene glycol) Hydrogels

city: Boulder

first: Stephanie

last: Bryant

state: CO

address: 3415 Colorado Ave

department: Chemical and Biological Engineering

institute: University of Colorado

summary: Macrophages are known to be the drivers of the Foreign Body Response (FBR) to implanted biomaterials. While each macrophage population may polarize into distinct phenotypes, the timescales of this process and their functional roles in the FBR are not known. The goal of this study was to investigate temporal changes in macrophage polarization over the course of the FBR to a PEG hydrogel implant.  RNA-seq methods were applied  to map temporal changes in the transcriptome of implant-associated monocytes, which represent newly arrived blood monocytes prior to their maturation into macrophages, and separately implant-associated macrophages, which represent both recruited and tissue resident macrophages. The transcriptomics analysis of implant-associated monocytes revealed that pro-inflammatory pathways were up-regulated early and continued to increase at day 14, but by day 28 began to subside. On the contrary, macrophages were initially in a pro-inflammatory state, but underwent a shift in their polarization state to an alternatively activated pro-fibrotic state by day 14, correlating with the emergence of the fibrous capsule. They retained this state through day 28, which correlated with the continued growth of the fibrous capsule around the hydrogel implant.

overall_design: RNA-seq was used to monitor the transcriptome of Cx3Cr1+Ly6Chi-monocytes and Cx3Cr1+Ly6Clo-macrophages during the FBR at day 2, 14, and 28 post-implantation. Three biological replicates with the exception of the controls (n=2 biological replicates for macrophages) were used.

first: Scott

last: Alper

first: Thomas

last: Danhorn

first: Brian

last: O'Connor

first: William

last: Janssen

first: Lea

last: Barthel

first: Brittany

last: Thompson

first: Jennifer

last: Knapp

first: Sophie

middle: L

last: Gibbings

first: Stacey

last: Thomas

first: Luke

last: Amer

first: Leila

last: Saleh


title: Reversal of RNA toxicity in myotonic dystrophy via a decoy RNA-binding protein with high affinity for expanded CUG repeats [mouse]

overall_design: In thIs study, Gastrocnemius muscles of WT mice were injected with either saline, AAV-GFP or AAV-GFP-MBNL1∆, and overall transcriptome changes were analyzed by RNAseq.


title: Reversal of RNA toxicity in myotonic dystrophy via a decoy RNA-binding protein with high affinity for expanded CUG repeats


title: Unusual nucleosome formation and transcriptome influence by the histone H3mm18 variant

city: Fukuoka

first: Yasuyuki

last: Ohkawa

address: 3-1-1 Maidashi

institute: Medical Institute of Bioregulation

summary: We determined the structure, characteristics, and functional significance of the H3mm18 nucleosome, and provide insights into understanding genome regulation.

overall_design: We performed CEL-Seq2 in C2C12 cells.

first: Seiya

last: Hirai

first: Atsuko

last: Miyawaki-Kuwakado

first: Kosuke

last: Tomimatsu

first: Yoshimasa

last: Takizawa

first: Tetsuro

last: Komatsu

first: Yasuko

last: Takeda

first: Lumi

last: Negishi

first: Tomoya

last: Kujirai

first: Masako

last: Koyama

first: Hitoshi

last: Kurumizaka


title: Expression data of RAW264.7 cells cultured in conditioned medium of SCR or JMJD6-KO PymT-41C cells

city: MILANO

first: BIANCA

last: CIONI

state: MI

address: Via Antonio Amadeo 42

department: Research

country: Italy

institute: IRCCS Istituto Nazionale Tumori

summary: In our study we showed that JMJD6 expression in tumor cells can regulate macrophage differentiation in vitro through ANXA-1 secretion. For this experiment we cultured RAW264.7 cells cultured in conditioned medium of SCR or JMJD6-KO breast cancer PymT-41C cells for 24hrs and we then submitted the RAW264.7 cells for ClariomD assay

overall_design: In this dataset, we include the expression data from RAW264.7 cells cultured in normal medium (RAW NM), medium of SCR PyMT-41C cells (RAW CM SCR), medium of SCR PyMT-41C cells with addition of the ANXA-1 receptor blockade, CSH (RAW CM SC+CSHR) and, medium of JMJD6-KO PyMT-41C cells (RAW CM KO).

first: Bianca

last: Cioni

first: Daniele

last: Lecis

first: Francesca

last: Menichetti

first: Tiziana

last: Langella

first: Claudia

last: Chiodoni

first: Matteo

last: Milani

first: Loris

last: de Cecco

first: Laura

last: Botti

first: Mario

last: Colombo


title: Axiom PMDAr.6 SNP array for human skeletal muscle samples

city: Durham

first: Christopher

middle: G.

last: Vann

state: NC

address: 300 N. Duke St

department: Molecular Physiology Institute

institute: Duke University School of Medicine

summary: The current study examined the association between genotype and resistance training-induced changes in dual energy x-ray absorptiometry (DXA) derived lean soft-tissue mass (LSTM) and skeletal muscle fiber cross-sectional area (fCSA).  Over 315,000 genetic polymorphisms were interrogated using DNA microarrays.  Genome-wide association studies (GWAS) were performed to identify novel targets to reveal associations with PRE- to POST-training change scores in mean LSTM and fCSA.  The first GWAS indicated no single nucleotide polymorphisms (SNP) associated with DXA derived LSTM.  The second GWAS indicated two SNPs associated with changes in mean fCSA.  While the first target identified (chr2:205936849 [GRCh38.p12]) was not annotated the second target identified (chr7:41971865 [GRCh38.p12]) was identified as an intron variant of the GLI Family Zinc Finger 3 (GLI3) gene.  Follow-up analyses indicated fCSA increases were greater in the T/C and C/C GLI3 genotypes than the T/T GLI3 genotype.

overall_design:
Axiom PMDAr.6 SNP arrays (Thermo Fisher Scientific) were performed in accordance with the manufacturer's specifications on cryopreserved vastus lateralis human skeletal muscle samples (n=110) donated prior to a 12-week resistance exercise intervention.
Genome-wide association studies (GWAS) were performed to identify novel targets associated with PRE- to POST- resistance exercise change scores in dual energy x-ray absortiometry (DXA) derived lean soft tissue mass and fiber cross-sectional area (fCSA).

first: C

middle: B

last: Mobley

first: Ivan

last: Vechetti Jr

first: Stuart

last: Phillips

first: Michael

last: Roberts


title: ChIP-AP - An Integrated ChIP-Seq Analysis Pipeline

city: Boston

first: Mahmoud

middle: Adel

last: Bassal

state: Massachusetts

address: 3 Blackfan Circle

department: Hematology and Oncology

institute: Beth Israel Deaconess Medical Center

summary: ChIP-Seq is a technique used to analyse protein-DNA interactions. The protein-DNA complex is pulled down using a protein antibody, after which sequencing and analysis of the bound DNA fragments is performed. A key bioinformatics analysis step is “peak” calling - identifying regions of enrichment. Benchmarking studies have consistently shown that no optimal peak caller exists. Peak callers have distinct selectivity and specificity characteristics which are often not additive and seldom completely overlap in many scenarios. In the absence of a universal peak caller, we rationalized one ought to utilize multiple peak-callers to 1) gauge peak confidence as determined through detection by multiple algorithms, and 2) more thoroughly survey the protein-bound landscape by capturing peaks not detected by individual peak callers owing to algorithmic limitations and biases. We therefore developed an integrated ChIP-Seq Analysis Pipeline (ChIP AP) which performs all analysis steps from raw fastq files to final result, and utilizes four commonly used peak callers to more thoroughly and comprehensively analyse datasets. Results are integrated and presented in a single file enabling users to apply selectivity and sensitivity thresholds to select the consensus peak set, the union peak set, or any sub-set in-between to more confidently and comprehensively explore the protein bound landscape. (https://github.com/JSuryatenggara/ChIP-AP).

overall_design: SALL4 ChIP-Seq performed, 2 biological replicates (2 technical replicates each), 1 control (2 technical replicates)

first: Jeremiah

last: Suryatenggara

first: Kol

last: Yong

first: Danielle

middle: E

last: Tenen

first: Daniel

middle: A


title: Transcriptomics of receptive endometrium in women with sonographic features of adenomyosis

city: Maribor

first: Erika

last: Prašnikar

address: Ljubljanska ulica 5

department: Department of Reproductive Medicine and Gynaecological Endocrinology

country: Slovenia

institute: University Medical Centre Maribor

summary:
Purpose: We compared endometrial transcriptome profiles during the window of implantation (WOI) between women with and without uterine adenomyosis.
Methods: We obtained endometrial biopsies luteinizing hormone (LH)-timed to the WOI from women with sonographic features of adenomyosis (n=10) and controls (n=10). Isolated RNA samples were subjected to RNA sequencing (RNA-seq) and endometrial receptivity classification with a molecular tool for menstrual cycle phase dating (beREADY®, CCHT). RNA-seq data were analysed in the setting of the result of accurate endometrial dating.
Results: Out of 20 endometrial samples, 2 were dated to the early receptive phase, 13 to the receptive phase and 5 to the late receptive phase. Comparison of the transcriptomics data from all 20 samples provided 909 DEGs (p<0.05; nonsignificant after adjusted p value) in the adenomyosis group but only 4 enriched pathways (Bonferroni p value < 0.05). The analysis of 13 samples only dated to the receptive phase provided suggestive 382 DEGs (p<0.05; nonsignificant after adjusted p value) in the adenomyosis group, leading to 33 enriched pathways (Bonferroni p value < 0.05). These included pathways were already associated with endometrial biology, such as “Expression of interferon (IFN)-induced genes” and “Response to IFN-alpha”.
Conclusion: Accurate endometrial dating and RNA-seq analysis resulted in the identification of altered response to IFN signalling as the most promising candidate of impaired uterine receptivity in adenomyosis.

overall_design: Transcriptome sequencing of endometrial samples LH-timed to the WOI (LH+7 – LH+9) between women with and without sonographic features of adenomyosis

first: Tanja

last: Kunej

last: Gorenjak

first: Uroš

last: Potočnik

first: Borut

last: Kovačič

first: Jure

last: Knez


title: Multiple CTCF sites contribute to stable enhancer-promoter interactions in the β-globin locus

city: Busan

first: AeRi

last: Kim

address: 2, Busandaehak-ro 63beon-gil, Geumjeong-gu

country: South Korea

institute: Pusan national university

summary: We propose that multiple CTCF sites on same motif orientation could cooperate with each other for stable enhancer-promoter interactions in the β-globin locus.

overall_design: H3K27ac, H3K27me3 ChIP-seq was performed in control (Con), C3- and C4-deleted (dC34) and C5-, C6- and C7-deleted (dC5-7) MEL/ch11 cells.


title: Next-generation sequencing  analyzes EPC-drived exosome miRNA content and alterations of mRNA expression in exosomes treated HUVEC

first: Hui

last: Hu

address: #600, Yishan Rd

department: Institute of Diagnostic and Interventional Radiology

institute: Shanghai Jiao Tong University Affiliated Sixth People's Hospital

type: Non-coding RNA profiling by high throughput sequencing

summary:
Purpose: To dissect the mechanisms of  EPC-drived exosome in promoting  endothelial cells reendothelialization, next-generation sequencing was used to determine exosome miRNA content and alterations in mRNA expression in HUVEC.
Methods: The miRNA of EPC-drived exosomes sequencing was carried out on the HiSeq 2500 Platform (NovelBio Corp. Laboratory, Shanghai). The data analysis was carried out with the QIAseq miRNA quantification platform using unique molecular index (UMI) counts according to the manufacturer’s instructions. The mRNA analysis of three independent samples of PBS or EPC exosomes treated HUVEC was performed using the the HiSeq 2500 Platform (NovelBio Corp. Laboratory, Shanghai) following the manufacturer’s instructions. qRT–PCR validation was performed using TaqMan and SYBR Green assays.
Results: The 20 most highly expressed microRNAs identified in EPC exosomes s are listed in Table 1. The genes predicted to be targeted by those microRNAs most highly expressed in EPC exosomes (top 20 microRNAs comprising ~75% of all reads, Table 1) are most significantly enriched in the functional category ‘blood vessel development’within the top 10 categories. Further, endothelial-specific miR-21-5P was the most highly expressed microRNA in EPC exosomes.
Conclusions:EPC exosomes promote vascular endothelial repair by delivering functional miR-21-5p.

overall_design: EPC-drived exosome miRNA  and alterations of mRNA expression in exosomes treated HUVEC analysis by deep sequencing

first: Jungong

last: Zhao


title: Lymphoma transcriptome analysis after X-ray or Proton beam irradiation

city: Cincinnati

first: Nathan

last: Salomonis

state: OH

address: 3333 Burnet Avenue

department: Biomedical Informatics

institute: Cincinnati Children's Hospital

summary: Proton (PT) therapy represents an alternative to conventional X-ray therapy, and its clinical application for cancer treatment is on the rise due to associated dose deposit advantages. However, our knowledge of biological responses to PT, in comparison to X-ray, remains in its infancy. Identification of PT specific molecular signals is an important opportunity for the discovery of biomarkers and synergistic drugs. We have profiled the transcriptome regulation of lymphoma cells exposed to clinical sources of PT and X-ray radiation, respectively. Subsequent analysis demonstrated both common and radiation-specific deregulation of gene expression. Gene set enrichment discovered pathways unique to PT \ that contribute to the unfolded protein response (UPR) and mitochondrial transport.

overall_design: Expression profiles of BL41 (Human) and J3D (mouse) cell lines untreated or 12hr after exposure to 5Gy X-ray (Linac) or 5Gy Proton beam (Beam scanning, middle SOBP) irradiation

first: Mathieu

last: Sertorio

first: Ali

last: Nowrouzi

first: Mahdi

last: Akbarpour

first: Kashish

last: Chetal

first: Stephan

last: Brons

first: Anthony

last: Mascia

first: Shelby

last: McCauley

first: Andreas

last: Köthe

first: Jürgen

last: Debus

first: John

last: Perentesis

first: Amir

last: Abdollahi

first: Yi

last: Zheng

first: Susanne

middle: I

last: Wells


title: Transcriptome from wildtype and Jmjd8-KO eWAT of mouse.

city: Berkeley

first: Dongjoo

last: You

state: California

address: 316 Morgan UC Berkeley

department: NST

institute: UC Berkeley

summary: Using high throughput sequencing we report gene expression changes in eWAT of wild-type and Jmjd8-KO mice.

overall_design: Examination of  gene expression changes in eWAT between WT and Jmjd8-KO mice. Total RNA was isolated from 3 mice that were used in each group per genotype.

first: Sona

last: Kang

first: Hee-Woong

last: Lim


title: Distinct microglial transcriptional responses during opioid exposure or neuropathic pain [mouse]

city: Palo Alto

first: Gregory

last: Scherrer

address: 1050 Arastradero Rd

department: Anesthesiology

institute: Stanford University

summary: In settings of heightened pain sensitivity, such as following peripheral nerve injury (PNI) or opioid-induced hyperalgesia (OIH), microglia take on an activated phenotype. Functional studies have suggested that microglia activated by PNI or chronic opioids then engage common mechanisms to facilitate pain. Here we conducted RNA sequencing of acutely isolated spinal cord microglia to comprehensively interrogate commonality between PNI and OIH. By combining our results with meta-analysis of published datasets, we identify transcriptional signatures of microglial reactivity that differ between PNI models over time, opioid exposure, or CNS pathology, despite similar histological outcomes. Collectively, these results reveal a discrepancy between histological markers of activation and transcriptional response, and provide a resource of pain-associated microglial transcriptomes that caution against a universal signature of microglia activation.

overall_design: RNA sequencing of actutely isolated spinal cord microglia following peripheral nerve injury or opioid treatment, or RNA-seq of cultured rat cortical microglia after morphine treatment or TLR agonist treatment

first: Elizabeth

last: Sypek


title: Distinct microglial transcriptional responses during opioid exposure or neuropathic pain [rat]

overall_design: RNA sequencing of cultured rat cortical microglia after morphine treatment or TLR2 or 4 agonism


title: Distinct microglial transcriptional responses during opioid exposure or neuropathic pain

sample_organism:
Mus musculus
Rattus norvegicus

platform_organism:
Mus musculus
Rattus norvegicus

overall_design: Refer to individual Series


title: GRO-seq in mouse Epiblast-primed, Primitive endoderm-primed, and differentiated endoderm cells

city: Ithaca

first: Leighton

middle: James

last: Core

state: NY

address: 417 Biotechnology Building

department: Moleular Biology and Genetics

institute: Cornell University

summary: The identification of changes in transcriptional regulation during priming and differentiation of embryonic stem (ES) cells towards the endoderm lineage. Specific populations of ES cells, either primed or committed to endoderm, were isolated and subjected to global nuclear run on sequencing (GRO-Seq). The hHex-Venus (HV) reporter ES cell line, HVJu5.1 (Canham et al., 2010) was used to isolate HV- and HV+ ES cells. Primed ES cells were identified based on the expression of the HV marker in addition to the cell surface marker of undifferentiated ES cells, SSEA-1, (the lower and upper 25% of SSEA-1+, HV expressing cells). When challenged to differentiate, HV- ES cells are primed towards an epiblast fate, while HV+ ES cells are primed towards primitive endoderm. However, these populations are considered primed, rather than committed, as they will readily interconvert when re-introduced into standard ES cell culture conditions. ES cells were grown in self-renewing conditions (GMEM, LIF, 10% FCS, plated on gelatin coated dishes). Endoderm was obtained by differentiating ES cells in medium without the cytokine LIF for 5 days. The HV+, SSEA-1- differentiated fraction was then sorted and represents an early stage in endoderm differentiation.

overall_design: Three subpopulations were sorted by flow cytometry from clone HVJu5.1 of the HV ES cell line as such: HV-,SSEA-1+; HV+SSEA-1+; HV+, SSEA-1-; where HV = Hex-Venus expression. Two biological replicates were collected per sample. Nuclei were isolated from each population and GRO-seq was carried out.

first: Sophie

last: Morgani

last: Lis

first: Josh

last: Brickman


title: Clostridium tetani biomarkers for culture condition

status: Public on Jan 02 2022

city: Bilthoven

first: Jeroen

last: Pennings

address: A. van Leeuwenhoeklaan 9

country: Netherlands

institute: Natl. Inst. Public Health & Environment

summary: We used RNA-seq to determine Clostridium tetani gene expression changes in response to culture conditions and time. Changes in response to time were more pronounced than those in response to culture conditions. The tetanus toxin gene is always highly expressed but does show expression changes between culture conditions. These results may become part of an approach to reduce animal testing during vaccine manufacturing.

overall_design: 39 samples, comprising 6 growth conditions and 5 time points, with some replicates.


title: A subpopulation of cancer cells with high SIRPG expression promotes immune escape of non-small cell lung carcinoma through crosstalk with Hippo signaling

city: chengdu

first: hong

last: wu

address: 55 renmin south road

institute: sichuan cancer hospital

summary: Cancer stem like cells (CSLCs) acquire enhanced immune checkpoint responses to evade immune cell killing and promote tumor progression. Here we show that signal regulatory protein gamma (SIRPG) determines a small population of lung adenocarcinoma (LUAD) cancer cells for both CSLCs properties and immune evasion. SIRPGhigh population displays CSLCs properties and transmits the immune escape signal through sustaining CD47 expression to both SIRPGhigh and SIRPGlow/- tumor cells. SIRPG bridges MST1 and PP2A to facilitate MST1 dephosphorylation, resulting in Hippo/YAP activation leading to cytokine release by CSLCs, which stimulates CD47 expression in LUAD cells and consequently inhibits tumor cell phagocytosis. SIRPG promotes tumor growth and metastasis in vivo through YAP signaling. Notably, SIRPG targeting with genetic SIRPG knockdown or a SIRPG neutralization antibody inhibits CSLC phenotypes and elicits phagocytosis that suppresses tumor growth in vivo. SIRPG is upregulated in human LUAD and its overexpression predicts poor survival outcome. Thus, SIRPGhigh cells serve as CSLCs and tumor immune checkpoint initiating cells propagating the immune escape signal to the whole cancer cell populations. Our study identifies Hippo/YAP signaling as the first mechanism by which SIRPG is engaged and reveals that targeting SIRPG represents an immune and CSLC targeting strategy for lung cancer therapy.

overall_design: Examination of 2 different histone modifications in A549 cells.

first: Chuan

last: Xu


title: ISG 15 is associated with cervical cancer development

city: Shanghai

first: Sibo

last: Zhu

state: China

address: songhulu 2005

institute: Fudan University

summary:
Cervical cancer (CC) is a complex disease. Many factors contribute to the tumourigenesis and progression of CC neoplasms. Here, we analysed transcriptomic differences and simulated tumour progression to explore the pathogenesis of CC.
RNA-seq was performed to analyse the transcriptomic differences among normal tissue (NC), paracarcinoma tissue (TP), and primary tumour tissue (TT). Pseudo-time analysis was performed to simulate tumour progression. RT-qPCR and immunohistochemistry were used to analyse the expression of ISG15. Cell proliferation, wound healing, and Transwell assays were used to verify the effect of ISG15 on HeLa cells.
The RT-qPCR and immunohistochemistry results indicated that ISG15 had significantly higher expression in TT. We observed an increasing trend of ISG15 expression from NC to TP to TT, which suggests that elevated expression of ISG15 was closely associated with malignant evolution in CC tissues. HeLa cell experiments showed that ISG15-siRNA inhibited cell proliferation and invasion.
Our study verifies that ISG15 is upregulated in and positively associated with the development of CC. ISG15 may act as an oncogene in the tumourigenesis of CC.

overall_design: The experiment was performed by comparative sequencing analysis using RNA-seq from TT, TP(2 cm≤TP≥0.5 cm from the tumour tissue), and NC(≥2 cm away from the tumour tissue) samples collected from 14 CC patients who underwent surgery at the People’s Hospital of Shanghai Pudong New District from January 2019 to June 2020. All patients had CC at stages IB1-IIA2 (based on the Criteria for Clinical Staging of Cervical Carcinoma 2018 Modified Version of the International Federation of Gynecology and Obstetrics [FIGO]) and underwent wide hysterectomy and lymphadenectomy in the pelvic cavity.

first: Pingping

last: Tao

first: Liyan

last: Sun

first: Yanmei

first: Binlie

last: Yang


title: Transcriptomic changes in FOXP3 deficient CD8+ T cells

city: Pamplona

first: Juan

middle: Jose

last: Lasarte

state: Navarra

address: Avda Pio XII, 55

department: Inmunología e Inmunoterapia

institute: Centro de Investigación Médica Aplicada

summary: Characterization of  the functional differences observed by the absence of FOXP3 in CD8+ T lymphocytes. Highly purified OT-1 Foxp3Scurfy and OT-1 Foxp3wt T cells from the corresponding BM chimeric mice were isolated and left unstimulated or stimulated with SIINFEKL peptide for 6h in culture medium. RNA was then isolated and sequenced for the analysis of differential expression of mRNA transcripts

overall_design: OT-1 Foxp3Scurfy and OT-1 Foxp3wt T cells were left unstimulated or stimulated with SIINFEKL peptide for 6h. mRNA was then purified and analyzed by RNA-sec

middle: J

first: Teresa

last: Lozano


title: Transcriptomic analysis of mouse tissue after MNP treatment

city: Kaifeng

first: Haigang

state: Henan province

address: dongjing Road

department: School of Life Sciences

institute: Henan University

summary: Mice were recepted the MNP treatment for 4 h with exposing to higher magnetic field

overall_design: Examination of transcriptome level in mouse brain tissue treated with magnetic force.

last: Wu


title: Single cell transcriptional analysis reveals the effects of mucosal vaccination on mouse lung CD4 T cell compartments

first: Robyn

last: Jong

address: 500E Li Ka Shing, 1951 Oxford St mc3370, UC Berkeley

department: Molecular and Cell Biology

institute: Stanley Lab, UC Berkeley

summary: We report the results of single cell RNA sequencing (scRNA-seq) analysis on CD4+ T cells sorted from the lungs of mice vaccinated with a TB vaccine and infected with M. tuberculosis. To gain a more detailed understanding of the characteristics of the CD4 T cell response during M. tuberculosis infection and after mucosal vaccination, we performed scRNA-seq on CD4 T cells sorted from naïve and i.n. H1/ML-RR-cGAMP vaccinated infected mouse lungs at the peak of the T cell response, 3 weeks post infection. Subsets of CD4 T cells were manually annotated based on signature expression of lineage-specific transcription factor, cytokine, and cell surface markers.

overall_design: Mouse lung CD4 T cells pooled from mock (PBS control) or mucosally vaccinated with H1/ML-RR-cGAMP vaccine (IN vacc) 3 weeks post M. tuberculosis infection, 3 mice pooled per sample.

first: Sarah

last: Stanley


title: Functional characterization of the clonal hematopoiesis and myeloproliferative neoplasm associated polymorphism rs621940 located downstream of GFI1B

city: Nijmegen

first: Joost

last: Martens

state: Nederland

address: Geert Grooteplein 28

department: RIMLS

institute: Radboud University

summary: Transcription factor GFI1B suppresses its own gene expression, and deregulated GFI1B expression contributes to myeloid neoplasms. The DNA polymorphism rs621940 located 8 kb downstream of GFI1B predisposes for clonal hematopoiesis and myeloproliferative neoplasms. Whether rs621940 affects GFI1B expression is unknown. We observed clear GFI1B binding around the rs621940 locus in megakaryoblast MEG-01 cells using ChIP-seq. Pull-downs using DNA-sequences with either rs621940-allele followed by protein identification using mass spectrometry detected 24 differentially bound proteins in MEG-01 cells, but GFI1B was not among these. Also, GFI1B auto-repression was not different between either rs621940-allele in transient gene reporter assays. Deletion of an 1.6 kb fragment encompassing rs621940 in K562 cells did not alter GFI1B expression nor GFI1B auto-repression. In primary peripheral blood mononuclear cells from healthy donors, absolute GFI1B expression did not differ consistently between the rs621940 alleles. Finally, GFI1B haplotyping using long range DNA sequencing detected 3’ non-coding polymorphisms on the same chromosome as the rs621940 polymorphism. Yet, targeted deep RNA sequencing did not detect consistent effects of  rs621940 on allelic GFI1B expression. These studies find no evidence that rs621940 affects GFI1B expression nor GFI1B auto-repression.

overall_design: ChIP-seq analysis of th GFI1B proteins in MEG01 cells was performed using illumina high-throughput sequencing

first: Rinske

last: van Oorschot

first: Saskia

last: Bergevoet

first: Aniek

middle: O

last: de Graaf

first: Evelyn

last: Tönnissen

first: Kornelia

last: Neveling

first: Pascal

middle: C

last: Jansen

first: Marijke

last: Baltissen

first: Michiel

last: Vermeulen

first: Amit

last: Mandoli

first: Joop

first: Bert

last: van der Reijden


title: Transcriptome analysis of CHSY3 knockdown NP cells

first: Chen

last: Xu

address: No, 800, Rd. Xiangyin

institute: The Second Military Medical University

summary: Intervertebral disc degeneration is the main cause of low back pain and the mechanism of which is far from fully revealed. Although multiple factors are related to the intervertebral disc degeneration, inflammation and matrix metabolism dysregulation are the two key factors that play an important role in degeneration. Here, we found that CHSY3 is highly related to the nucleus pulposus degeneration. We generated CHSY3 knockout mice using Crisper/Cas9 system, and the NP cells are studied in this experiment.

overall_design: MRNA profiles were done using primary culture cells of mouse intervertebral disc nucleus pulposus (NP) tissue.

first: Leixin

last: Wei

first: Wen

last: Yuan


title: Transcriptomic respponses in the gut in Daphnia magna across toxic chemicals that inhibit feeding and food limiting conditions

city: Barcelona

first: Bruno

last: Campos

address: jordi girona, 18, 18

department: Environmental Chemistry

institute: IDAEA-CSIC

summary: The aim of this study was to assess the  transcriptomic responses in guts dissected from Daphnia magna individuals  exposed to concentrations of  selected compounds that peroduced low and high inhibitory effects on feeding. Chemical treatments included  Cd, Cu, fluoranthene, l-cyalothrine and  the cyanotoxin anatoxin a.  Two additional treatments including low and no food (starving) were also included to better account for transcriptomic responses  related to food limitation. We tested the hypothesis that the studied chemicals should share similar molecular signalling pathways across low and high levels of feeding impairment.

overall_design: Daphnia magna was exposed to Cd, Cu, fluoranthene, cyalothrin and  anatoxin a at 2 feeding inhibition levels. 3 different food levels and controls were also added to the experiment. 5 replicates per treatment with 3 random samples used to hybridization. The extracted guts were RNA extracted and this material used for microarray hibridization

first: Benjamin

last: Pina

first: Carlos

last: Barata


status: Public on Jan 01 2022

city: Zhengzhou

first: Chong-zhen

last: QIN

address: No. 1 East Jianshe Road, Erqi District, Zhengzhou

institute: the First Affiliated Hospital of Zhengzhou University

summary:
Purposes: To investigate the biological function of tRF in breast cancer by tRF and tiRNA sequencing
Methods: Breast cancer tissue samples and matched non-tumor adjacent tissues were obtained from five patients. Small RNA sequencing was performed on Illumina NexSeq instrument
Results: If P ≤ 0.05, fold change ≥ 2 as the cut off, there were 3 up-regulated tRFs & tiRNAs and 13 down-regulated tRFs & tiRNAs.
Conclusions:There were 3 up-regulated tRFs & tiRNAs and 13 down-regulated tRFs & tiRNAs in breast cancer tissue samples and matching adjacent tissue samples

overall_design: tRF & tiRNA sequencing of breast cancer tissue samples and matched non-tumor adjacent tissues from five patients.

first: Chongzhen

last: Qin

first: Menglin

last: Wu


title: Affymetrix SNP array data for preeclampsia samples

last: Liu

address: No.501, Haike Road, Zhangjiang Hi-Tech Park, Pudong, Shanghai

institute: Shanghai Institute of Materia Medica

summary:
Preeclampsia is a heterogeneous and complex disease caused by multiple factors, including heredity and environment. However, the underlying mechanism remains elusive due to diverse races, geography, and other factors. Previous findings have revealed that there is a tendency for preeclampsia to run in families. To define genetic factors associated with preeclampsia, we performed a genome-wide analysis of preeclampsia samples from 10 preeclampsia cases and 10 healthy age- and gravidity-matched normotensive pregnant women.
We identified 27 aberrant copy number variations related to preeclampsia, including 22 deletions and 5 duplications. These differential copy number variant regions involved 27 differential genes, including SPATA6L, PPP2R3B, PREX2, IL1RAPL1, OR52N1, OR52N5, CHSY1, DPP6, KRTAP9-7, LPA, NTRK1, BTNL3, TBC1D3F, TBC1D3, LOC440434 , EYA2, APOBEC3A_B, APOBEC3A, APOBEC3B, FHIT, EXT1, PRR14, FBRS, LMF1, MALT1, BCAS1, and MIR4756. These findings suggest that these differential genes may be associated with the pathogenesis of preeclampsia and require further investigation.

overall_design: Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from peripheral blood samples. Copy number analysis of Affymetrix CytoScan HD Cytogenetics array was performed for 10 preeclampsia cases and 10 healthy age- and gravidity-matched normotensive pregnant women. The high-frequency copy number variation regions of ordinary individuals in the Database of Genomic Variants (http://dgv.tcag.ca/dgv/app/home) were used as references for copy number analysis.

first: Bing-Shun

last: Wang


title: Comparative transcriptional analysis of lung fibroblasts from young and aged mice identifies PIM1/NFATc1 axis as a driver of persistent fibrosis

city: Rochester

first: Mrunal

middle: Kishor

last: Dehankar

state: MN

address: 200 First St. SW

department: Computational genomics

institute: Mayo Clinic

summary: Idiopathic pulmonary fibrosis (IPF) is an aging-associated disease characterized by the accumulation of myofibroblasts leading to the progressive scarring of the lung. To identify transcriptional gene programs driving persistent fibrosis in aged lungs, we performed a comparative RNA-seq analysis of fibroblasts freshly isolated from young and aged mouse lungs 30 days post-bleomycin injury. We discovered that lung fibroblasts isolated from young animals at this time point post-injury were transcriptionally similar to those isolated from uninjured mice. In contrast, aged lung fibroblasts isolated at the same time point exhibited a sustained pro-fibrotic state characterized by the elevated expression of genes implicated in inflammation, extracellular matrix remodeling, and cell survival. We identified the protein kinase pro-viral integration site of Moloney murine leukemia virus 1 (PIM1) and its direct target Nuclear Factor of Activated T Cells-1 (NFATc1) as putative drivers of the sustained profibrotic gene signatures observed in aged lung fibroblasts post-injury. PIM1 and NFATc1 transcripts were highly enriched in a pathogenic fibroblast population recently discovered in IPF lungs, and their protein expression was detected in fibroblastic foci. Overexpression of PIM1 in normal human lung fibroblasts potentiated their fibrogenic activation and this effect was dependent on NFATc1. Pharmacological inhibition of PIM1 in IPF-derived lung fibroblasts attenuated their activation and sensitized them to apoptotic stimuli. Finally, inhibition of PIM1 strongly reduced the expression of ECM remodeling and pro-survival genes and blocked the secretion of collagen in IPF lung explants ex vivo. Targeting PIM1/NFATc1 axis in pathogenic lung fibroblasts may represent a therapeutic strategy to limit their activation and promote fibrosis resolution in IPF.

overall_design: Aged (18 months) Col1a1-GFP mice were given 1 dose of saline or bleomycin intratracheally. After 30 days, lungs from aged sham (n=4), aged bleo (n=5) were digested into single cell suspension and flow sorted for GFP+, CD45-, CD31-, and Epcam- cells. Cells were sorted directly into lysis buffer and used for RNA isolation and RNA sequencing.

first: Giovanni

last: Ligresti

first: Tho

middle: X

last: Pham


title: Systemic stem cell activation following amputation primes distant appendages for future regeneration events in axolotl

city: Cambridge

first: Jessica

last: Whited

state: MA

address: 7 Divintiy Street, Sherman Fairchild - Whited Lab

institute: Harvard University

summary: A remarkable diversity in regenerative competency of extant species suggests an evolutionary influence, but few studies have identified potential selective pressures shaping this variation. Uncovering these selective pressures is critical to understanding the key molecular similarities, and differences, between regeneratorsand non-regenerators. Here we report that, in the highly-regenerative axolotl, an evolutionarily conserved body-wide stem cell activation response primes other limbs for faster regeneration, offering a selective advantage for this phenomenon. We further demonstrate the body-wide response requires peripheral nervous system input at these distant sites and is predicated on mTOR signaling. We definedgene expression changes within the signaling neural processes and nearby tissues, harboring responsive stem cells, leading to candidate genetic pathways central to this process. Functional experimentation confirmed a requirement for adrenergic signaling in amputation-induced activation of distant stem cells. Our study provides a direct link between body-wide cellular activation responses and regeneration, unifying previous reports from distant species of various natural regenerative abilities, such as planarians and mice, in a conceptual framework that centers the ability to convert the body-wide response to local tissue outgrowth as the key difference between regenerators and non-regenerators.

overall_design: 18 forelimb samples in total split into 2 cases: 4 denervated nerve vs 3 sham nerve, then 7 denervated surrounding tissue vs 4 sham surrounding tissue.  In all cases the denervated samples were compared to sham as a baseline.  The samples were aligned to an index of a Transcriptome (Bryant et al., Cell Reports, 2017.)

first: Duygu

last: Payzin-Dogru

first: Sarah

last: Wilson

first: Steven

last: Blair


title: Oligosarcomas, IDH-mutant are distinct and aggressive [SNP]

city: Heidelberg

first: David

last: Reuss

department: Neuropathology

country: Germany

institute: University Hospital Heidelberg

summary: Oligodendrogliomas are defined by IDH-mutations and codeletions of chromosomal arms 1p and 19q. In the past, case reports and small studies described gliomas with sarcomatous features arising from oligodendrogliomas, so called oligosarcomas. Here, we report a series of 23 IDH-mutant oligosarcomas forming a distinct methylation class. The tumors were recurrences from prior oligodendrogliomas or developed de novo. Precursor tumors of 11 oligosarcomas were histologically and molecularly indistinguishable from conventional oligodendrogliomas. Oligosarcoma tumor cells were embedded in a dens network of reticulin fibers, frequently showing p53 accumulation, positivity for SMA, and gain of H3K27 trimethylation (H3K27me3) as compared to primary lesions. In 5 oligosarcomas no 1p/19q codeletion was detectable, although it was present in the primary lesions. Oligosarcomas harbored an increased chromosomal copy number variation load with frequent CDKN2A/B deletions. Proteomic profiling demonstrated oligosarcomas to be highly distinct from conventional grade 3 oligodendrogliomas with consistent evidence for a smooth muscle differentiation. Expression of several tumor suppressors was reduced with NF1 being lost frequently. In contrast, oncogenic YAP1 was aberrantly overexpressed in oligosarcomas. Panel sequencing revealed mutations in NF1 and TP53 along with IDH1/2 and TERT promoter mutations. Survival of patients was significantly poorer for oligosarcomas than for grade 3 oligodendrogliomas and comparable to that of grade 4 IDH-mutant astrocytomas. These results establish oligosarcoma as a distinct type of IDH-mutant glioma differing from conventional oligodendrogliomas on the histologic, epigenetic, proteomic, molecular and clinical level. Diagnosis can be based on the characteristic DNA methylation profile or the combined evidence of sarcomatous histology, IDH-mutation and an oligodendroglioma-typical molecular alteration as TERT promoter mutation and/or 1p/19q codeletion.

overall_design: SNP samples

first: Dennis

last: Friedel


title: Ailanthone Inhibits Proliferation, Migration and Invasion of Osteosarcoma Cells by Downregulating the Serine Biosynthetic Pathway

first: Jianjun

last: Zhang

address: 600 Yishan R.

institute: Shanghai Jiao Tong University Affiliated Sixth People’s Hospital

summary: Osteosarcoma (OS) is a life-threatening disease affecting mainly children and adolescents, it is urgently needed to find novel anticancer agents against it. In the present study, we demonstrated that Ailanthone (AIL), a major component of the Chinese medicine Ailanthus altissima, significantly suppressed cell growth, inhibited cell migration and invasion, induced cell cycle arrest instead of apoptosis in OS cells. Mechanistically, combined transcriptomics, proteomics and metabolomics analyses revealed that AIL induced widespread changes in metabolic programs in OS cells, while the serine biosynthetic pathway was the most significantly affected pathway. The results were verified by reverse test. Metabolic reprogramming is an essential hallmark of malignancy including OS. Our findings suggest that AIL holds a great potential to be an OS treatment strategy through mediating metabolic reprogramming.

overall_design: To identify the altered pathways in human OS cell line Saos-2 after treatment with AIL

first: Xin

first: Haiyan

last: Hu


title: The Role of Leishmania GP63 in Modulation of Innate Inflammatory Response to Leishmania major Infection

city: MONTREAL

last: Langlais

state: QC

address: 740 Ave Dr Penfield, rm 4203, McGill Genome Centre

department: Human Genetics

institute: McGill University

summary: Leishmaniasis is a disease caused by the protozoan parasite Leishmania known to affect millions of individuals worldwide. In recent years, we have established the critical role played by Leishmania zinc-metalloprotease GP63 in the modulation of host macrophage signaling and functions, favouring its survival and progression within its host. Leishmania major lacking GP63 was reported to cause limited infection in mice, however it is still unclear how GP63 may influence the innate inflammatory response and parasite survival in an in vivo context. Therefore, we were interested in analyzing the early innate inflammatory events upon Leishmania inoculation within mice and establish whether Leishmania GP63 influences this initial inflammatory response. Experimentally, L. major WT, L. major GP63 KO or L. major GP63 rescue were intraperitoneally inoculated in mice and inflammatory cells recruited were characterized microscopically and by flow cytometry (number and cell type), and their infection determined. Pro-inflammatory markers such as cytokines, chemokines and extracellular vesicles (EVs, e.g. exosomes) were monitored and proteomic analysis was performed on exosome contents. Data obtained from this study suggest that Leishmania GP63 does not significantly influence the pathogen-induced inflammatory cell recruitment, but rather their activation status and effector function. Concordantly, internalization of promastigotes during early infection could be influenced by GP63 as less L. major KO amastigotes were found within host cells and appear to maintain in host cells over time. Collectively this study provides a clear analysis of innate inflammatory events occurring during L. major infection and further establish the prominent role of the virulence factor GP63 to provide favorable conditions for host cell infection.

overall_design: Murine peritoneal exudates from C57BL/6 mice injected i.p. with either PBS as control, or Leishmania major (WT, GP63 KO or rescued for GP63)

first: Martin

last: Olivier

first: Aretha

last: Chan

first: Jose-Mauricio

last: Ayala


title: Genome-wide maps of chromatin state in bone marrow cells

city: Muenster

first: Xiaoqing

last: Xie

address: Albert-Schweitzer-Campus 1

department: Department of Medicine A

institute: Hematology, Oncology and Pneumology

summary: GFI1 is a transcription factor and was implicated in the development of MDS. Reduced expression of GFI1 or presence of the GFI1-36N variant leads to epigenetic changes. Using GFI1-36S, -36N -KD, NUP98-HOXD13-tg mice and curcumin (a natural histone acetyltransferase inhibitor (HATi)), we now demonstrate that expansion of GFI1-36N or –KD, NUP98-HODXD13 leukemic cells can be delayed. Curcumin treatment significantly reduced AML progression in GFI1-36N or -KD mice and prolonged AML-free survival. Of note, curcumin treatment had no effect in GFI1-36S, NUP98-HODXD13 expressing mice. On a molecular level, curcumin treatment negatively affected open chromatin structure in the GFI1-36N or -KD haematopoietic cells but not GFI1-36S cells. Taken together, our study thus identified a therapeutic role for curcumin treatment in the treatment of AML patients (homo or heterozygous for GFI1-36N or reduced GFI1 expression) and possibly improved therapy outcome.

overall_design: Examination of different mice mode histone odifcation changes in bone marrow cells.

first: Daria

last: Frank

first: Pradeep

middle: K

last: Patnana

first: Judith

last: Schutte

first: Yahya

last: Al-Matary

first: Lanying

last: Wei

last: Dugas

first: Julian

last: Varghese

first: Subbaiah

last: Nimmagadda

first: Cyrus

last: khandanpour


title: Attempts for deriving extended pluripotent stem cells from common marmoset embryonic stem cells

city: Shinjuku

first: Sho

last: Yoshimatsu

state: Tokyo

address: 35 Shinanomachi

department: Physiology

institute: Keio University School of Medicine

summary: Extended pluripotent stem cells (EPSCs) derived from mice and humans showed an enhanced potential for chimeric formation. By exploiting transcriptomic techniques, we assessed the differences in gene expression profile between extended EPSCs derived from mice and humans, and those newly derived from the common marmoset (marmoset; Callithrix jacchus). Although the marmoset EPSC-like cells displayed a unique colony morphology distinct from murine and human EPSCs, they displayed a pluripotent state akin to embryonic stem cells (ESCs), as confirmed by gene expression and immunocytochemical analyses of pluripotency markers and three-germ-layer differentiation assay. Importantly, the marmoset EPSC-like cells showed interspecies chimeric contribution to mouse embryos, such as E6.5 blastocysts in vitro and E8.5 epiblasts in vivo in mouse development. Also, we discovered that the perturbation of gene expression of the marmoset EPSC-like cells from the original ESCs resembled that of human EPSCs. Thus, we established the efficacy of the method for the derivation of marmoset EPSCs

overall_design: RNA seq of marmoset EPSC-like cells

first: Mayutaka

last: Nakajima

first: Hideyuki

last: Okano


title: Oligosarcomas, IDH-mutant are distinct and aggressive [Methylation]

first: David

last: Reuss

type: Methylation profiling by genome tiling array

overall_design: DNA methlyation profiles of 226 brain tumor samples using Illumina HumanMethylation450 BeadChips or Illumina HumanMethylation850 BeadChips and genotyping of 12 samples (6 Oligodendroglioma, 6  Oligosarcoma) using Illumina HumanCytoSNP-12v2-1_L1.

first: Dennis

last: Friedel


title: circRNA expression in human myometrium during labor

city: Guangzhou

first: Kaiyuan

last: Ji

address: No.9 Jinsui Road, Guangzhou, China

department: Guangzhou Women and Children’s Medical Center

institute: Guangzhou Medical University

summary: The maintenance of coordinated powerful episodic contractions of the uterus is the crucial factor for normal labor. The uterine contractility is gradually enhanced with the progression of labor, which is related to the gene expression of myometrium, competing endogenous RNA (ceRNA) can also regulate the gene expression. To better understand the role of ceRNA network in labor, transcriptome sequencing was performed on the myometrium of 17 parturients at different labor duration. Furthermore, an correlated analysis was performed to identify mRNA, long non-coding RNA (lncRNA), circular RNA (circRNA), and microRNA (miRNA) which correlated with their expression levels and labor duration. Then, targeting relationships between mRNAs, lncRNAs, circRNAs and miRNAs were predicted, and the ceRNA regulatory network was established.This analysis identified 934 RNAs positively correlated with labor duration (859 mRNAs, 28 lncRNAs, 45 circRNAs, and 2 miRNAs) and 153 RNAs negatively correlated with labor duration (122 mRNAs, 28 lncRNAs, and 3 miRNAs).

overall_design: Examination of human myometrium in labor and not in labor

first: Lina

last: Chen

first: Huishu

last: Liu

first: Yihong

last: Luo


title: Deficient Pink1 Retrograde Mitochondrial-Nrf2 Signaling Induces EMT That Is Mitigated By A Mitochondria-tropic ROS Reducing Dendrimer

first: Sunan

last: Huang

state: Guangdong

address: NO.723, Xingke Road

institute: South China Botanical Garden

summary: Age-related macular degeneration (AMD), the leading cause of blindness among the elderly, is without effective treatment for early, dry disease. Retinal pigment epithelial (RPE) cell degeneration is a cardinal feature of dry AMD.  Given the reliance of photoreceptors on the RPE for maintaining health and vision, rejuvenating dysfunctional RPE is a logical treatment strategy. Here, the interplay between two cytoprotective pathways, Pink1 mediated mitophagy and the Nrf2 stress-response, was studied in human AMD tissue samples, RPE cells, and relevant mouse models. Pink1 immunolabeling was decreased in the RPE of early AMD eyes. The RPE from Pink1-/- mice and Pink1 deficient cultured human RPE cells displayed impaired mitophagy, decreased aerobic respiration, and increased mitochondrial reactive oxygen species (ROS) generation, and coincidently, developed morphological, molecular, and functional features of epithelial-mesenchymal transition (EMT). This change was triggered by novel retrograde mitochondrial to nuclear signaling that was initiated by mitochondrial ROS, which activated Nrf2 to induce TXNRD1, PI3K/AKT, and canonical EMT transcription factors Zeb1 and Snail. Nrf2 signaling was pivotal since its deficiency prevented EMT and increased cell death. A dendrimer containing N-acetyl cysteine that is tropic for the RPE and contains the mitochondrial targeting ligand Triphenyl phosphinium abrogates EMT in human RPE cells in vitro and in Pink1-/- mice. This study describes a novel interdependency of mitophagy and the Nrf2 antioxidant response in determining cell fate and introduces an RPE and mitochondrial specific ROS reducing dendrimer that can rescue RPE cells in EMT, a change recognized in early AMD.

overall_design: ARPE19 cells treated with four groups of siRNAs (scrambled, Nrf2, Pink1, or Nrf2-Pink1) using three biological replicates. Each biological replicate has two technical replicates.

first: Sayantan

last: Datta

first: Jiang

last: Qian

first: Debasish

last: Sinha

first: James

middle: T

last: Handa


title: A tumor suppression role for EZH2 in Diffuse Intrinsic Pontine Glioma pathogenesis

city: New York

first: Oren

last: Becher

address: 1468 Madison Ave 4th Fl,

department: Pediatric Hematology-Oncology

institute: Mount Sinai

summary: Pediatric high-grade gliomas, specifically diffuse intrinsic pontine gliomas (DIPG), account for 20% of clinical cases but have a 100% fatality rate. A majority of DIPG cases are characterized by the signature H3K27M mutation that is predicted to oppose EZH2, the methyltransferase enzyme of the Polycomb Repressor Complex 2 (PRC2). However, a clear understanding of EZH2’s role in DIPG is lacking. In this study, by incorporating Ezh2 loss and gain of function into our DIPG mouse models we demonstrate its tumor suppressor function. Genetic ablation of Ezh2 increased cell proliferation and tumor grade while expression of an Ezh2 gain of function mutation significantly reduced tumor incidence, increased tumor latency. Transcriptomic analysis revealed that EZH2 deletion upregulates an inflammatory response with upregulation of immunoproteasome genes such as Psmb8, Psmb9, and Psmb10 while EZH2 deletion an enrichment of the oxidative phosphorylation/mitochondrial metabolic pathway namely the isocitrate dehydrogenase Idh1/2/3 genes. Pharmacological inhibition of EZH2 augmented neural progenitor cell proliferation, supporting the tumor suppressive role of EZH2. In vivo treatment of DIPG tumor bearing Ntv-a;p53fl/fl; abcb1a-/-; abcb1b-/-; abcg2-/- (ABC knockout, ABC KO) mice with EZH2 inhibitor, EPZ-6438 did not alter proliferation or significantly impact survival. Together our results suggest that EZH2 has a tumor suppressor function in DIPG and warrants caution in clinical translation of these inhibitors to treat patients with DIPG.

overall_design: DIPG tumors from Ezh2 loss and gain-of-function mice (at least n=3 in control and test groups) were compared for their differentially expressed mRNA profiles by bulk RNA-sequencing

first: Swati

last: Dhar

first: Samantha

last: Gadd

first: Priyam

last: Patel

first: Daniel

last: Brat


title: miRNA of human myometrium in labor


title: Oligosarcomas, IDH-mutant are distinct and aggressive

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: RNA Sequencing Facilitates Quantitative Analysis of shWBSCR22 and corresponding control Transcriptomes

city: Beijing

first: Hua

address: 100 Pingleyuan,  Chaoyang District

institute: Beijing university of technology

summary: The human WBSCR22 protein was identified as a methyltransferase for 18S rRNA m7G, which is involved in pre-rRNA processing and 40S ribosome subunit biogenesis. Recent studies have shown that WBSCR22 expression is upregulated in many cancers, however, the function of WBSCR22 in pancreatic cancer is still unknown. The goals of this part study are to compare transcriptome profiling of PANC-1-shWBSCR22 cells to control cells. By identifying differentially expressed genes (DEGs) and enrichment pathways, the mechanism of WBSCR22 in pancreatic cancer can be better studied.

overall_design: mRNA profiles of PANC-1 cells transfected with shCtrl and shWBSCR22.

first: Xinhui


title: Transcriptomic analyses of the anti-adipogenic and pro-osteoblastic effects of aspirin in rat bone mesenchymal stem cell

first: Xinpeng

address: 157 health care road, nangang district, Harbin

department: StomatologicalHospital

institute: Southern Medical University

summary: Theoretically, the differentiation of mesenchymal stem cells (MSCs) into either adipocytic or osteoblastic phenotype can be deemed as a seesaw, where induction of one lineage comes at the expense of the other. Previously, researchers, including our team, found that aspirin promoted osteoblast differentiation of bone mesenchymal stem cells (BMSCs) whereas inhibiting adipogenic differentiation. However, the precise mechanisms, that is, which pathways, what biological process or key genes involved during this process, had not been systematically studied. In the present study, we tend to analyze the whole transcriptome of the anti-adipogenic and promote-osteoblastic effects of aspirin in BMSCs. Our results showed that aspirin’s presence restored or further strengthened the expression of an important part of the gene population repressed during adipogenesis or increased during osteogenesis. Besides, classical pathways related to osteogenic differentiation (p53 signaling pathway, focal adhesion, osteoclast differentiation, PI3K-Akt signaling pathway, MAPK signaling pathway, and Wnt signaling pathway) and the fat metabolism were also disturbed during the promote-osteoblastic and anti-adipogenic effects of aspirin. Therefore, our whole-genome transcriptomic results shed new light and open the door to more specific “omics” studies. Our results allow a better understanding of the anti-adipogenic and promote-osteoblastic effects of aspirin and pave the way to aspirin clinical use for the prevention and treatment of diseases like tissue defect and osteoporosis.

overall_design: The whole-genome transcriptome of the anti-adipogenic and promote-osteoblastic effects of aspirin in rat bone mesenchymal stem cells

first: Yuanbo

last: Zhan


title: USP9X stabilizes EWS-FLI1 to promote cancer cell growth in Ewing’s sarcoma

city: Dallas

first: Ralf

last: Kittler

state: Texas

address: 5323 Harry Hines Blvd

institute: University of Texas Southwestern Medical Center

summary: Ewing’s sarcoma (EWS) is a cancer of the bones or soft tissues in children and adolescents. EWS-FLI1 is a transcriptional factor and the key driver of EWS. To characterize the changes of downstream transcriptional profiles of EWS-FLI1 in A673 cells upon knockdown of EWS-FLI1 and deubiquitinase USP9X, RNA-seq was performed in A673 cells transfected with EWS-FLI1 esiRNA, USP9X esiRNA or GFP esiRNA as control. The data indicates that USP9X regulates transcriptional profiles of EWS through mediating EWS-FLI1.

overall_design: Transcriptional profile of A673 cells upon USP9X knockdown and EWS-FLI1 knockdown.

first: Shan

last: Wang

first: Rahul

last: Kollipara


title: Expression data from Healty Control and XP-A melanocytes

city: Kobe

first: Chihiro

last: Takemori

address: Kusunoki-cho 7-5-1

institute: Kobe University

summary:
Xeroderma Pigmentosum (XP) is a DNA repair disorder characterized by photosensitivity, resulting in occurrence of freckle-like pigmented maculae and depigmented maculae on sun-exposed areas. XP complementation group A (XP-A) is the most frequent type in Japan, and patients with XP-A present most severe cutaneous and neurological symptoms due to nucleotide excision repair deficiency. Here, we established induced pluripotent stem cells (iPSCs) derived from XP-A patients and successfully differentiated into melanocytes.
To elucidate the pathophysiology of XP, we comprehensively analyzed the difference in gene expression between XP-A-iMCs and healthy-control-iPSC-derived melanocytes (HC-iMCs) 4 hours and 12 hours after irradiation with 30 J/m2 or 150 J/m2 of UV-B using microarray analysis.

overall_design: HC-iMCs, XP-A-iMCs and NHEM were irradiated with low dose (30 J/m2) or high dose (150 J/m2) of UV-B, followed by incubation for 4 hours or 12 hours. Total RNA was extracted from UV-B irradiated and pre-irradiated samples.

first: Michiyo

last: Koyanagi-Aoi

first: Takeshi

last: Fukumoto

first: Makoto

last: Kunisada

first: Chieko

last: Hosaka

first: Seiji

last: Takeuchi

first: Akiharu

last: Kubo

first: Takashi

last: Aoi

first: Chikako

last: Nishigori


title: RNA Sequencing Facilitates Quantitative Analysis of shL3MBTL2 ,CGA-OE and corresponding control Transcriptomes

last: Huang

summary: L3MBTL2 is a crucial component of ncPRC1.6 and has been implicated in transcriptional repression and chromatin compaction. However, the repression mechanism of L3MBTL2 and its biological functions are largely undefined. CGA encodes the alpha subunit of glycoprotein hormones, however, we showed that CGA plays an individual tumor suppressor role in PDAC. The goals of this part study are to compare transcriptome profiling of PANC-1-shL3MBTL2 cells or PANC-1-CGA-OE cells to their corresponding control cells. By identifying differentially expressed genes (DEGs) and enrichment pathways, the mechanism of L3MBTL2 and CGA in pancreatic cancer can be better studied.

overall_design: mRNA profiles of PANC-1 cells transfected with shCtrl, shL3MBTL2, vector or CGA-OE.

last: Liu


title: Chromatin alterations during the epididymal maturation of mouse sperm refine the paternally inherited epigenome

city: College Station

first: MICHAEL

middle: C.

last: GOLDING

address: 4466 TAMU

institute: Texas A&M UNiversity

summary: Established dogma holds that all facets of chromatin organization and histone posttranslational modification are complete before sperm exits the testes. Using proteomic analysis to contrast immature spermatozoa and mature sperm from the epididymis, we find progressive changes in multiple histone posttranslational modifications, including H3K4me1, H3K27ac H3K79me2, H3K64ac, H3K122ac, H4K16ac, H3K9me2, and H4K20me3. In contrast, levels of H3K4me3 and H3K27me3 remained constant. Using chromatin immunoprecipitation coupled with deep sequencing, we find that changes in H3K27ac and H3K9me2 involve sharpening broad diffuse regions into narrow peaks, centered on promoters and distal enhancers driving embryonic development (H3K27ac) or tissue-specific genes sequestered in lamina-associated domains (H3K9me2). Maturing sperm contain the histone deacetylase enzymes HDAC1 and HDAC3, suggesting the NuRD complex may drive these changes. These data extend our understanding of germline programming and reveal that, in addition to trafficking noncoding RNAs, alterations to histone structure are a core feature of epididymal maturation.

overall_design: Examination of 2 different histone modifications in post-testicular murine spermatozoa during epididymal maturation

first: Michael

last: Golding

first: Yudhishtar

last: Bedi


title: Altered H3K27 trimethylation contributes to flowering time variations in polyploid Arabidopsis thaliana ecotypes

city: Gatersleben, Stadt Seeland, Germany

first: Hua

last: Jiang

address: Corrensstraße 3

institute: Leibniz Institute of Plant Genetics and Crop Plant Research (IPK) Gatersleben

summary: Polyploidy is a widespread phenomenon in flowering plant species. Polyploid plants frequently exhibit considerable transcriptomic alterations after whole-genome duplication (WGD). It is known that the transcriptomic response to tetraploidization is ecotype-dependent in Arabidopsis. Nevertheless, the biological significance and the underlying mechanism are unknown. Here, we showed that 4x Col-0 and 4x Ler presented different flowering times, with a delayed flowering time in 4x Col-0 but not in 4x Ler. We found that the expression of FLOWERING LOCUS C (FLC), the major repressor of flowering, was significantly increased in 4x Col-0 but subtle change in 4x Ler. Moreover, the level of a repressive epigenetic mark, trimethylation of histone H3 at lysine 27 (H3K27me3), was significantly decreased in 4x Col-0 but not in 4x Ler, potentially leading to different transcription levels of FLC and flowering time in 4x Col-0 and 4x Ler. Apart from the FLC locus, hundreds of genes showed differentially H3K27me3 alterations in 4x Col-0 and 4x Ler. Comparably, LIKE HETEROCHROMATIN PROTEIN 1 (LHP1) and transcription factors required for H3K27me3 deposition presented differential transcriptional changes between 4x Col and Ler, potentially account for differential H3K27me3 alterations in 4x Col-0 and Ler. Last, we found that the natural 4x Arabidopsis ecotype Wa-1 presented early flowering time, associated with low expression and high H3K27me3 of FLC. Taken together, our results showed a role of H3K27me3 alterations in response to genome duplication in Arabidopsis autopolyploids and that flowering time variation potentially functions in autopolyploid speciation.

overall_design: We compared the transcriptomes and genome profiles of H3K27me3 for diploid and tetraploid Col-0 and Ler

first: Jinping

last: Cheng

first: Guiqian

last: Zhang

first: Linhao

last: Xu

first: Chang


title: Lysophosphatidylcholine acyltransferase 1 controls the mitochondrial reactive oxygen species generation and survival of the retinal photoreceptor cells

city: Shinjuku-ku

first: Katsuyuki

last: Nagata

address: 1-21-1 Toyama

institute: National Center for Global Health and Medicine


title: Lysophosphatidylcholine acyltransferase 1 controls the mitochondrial reactive oxygen species generation and survival of the retinal photoreceptor cells [2w Retina]

summary: Due to the high energy demands and characteristic morphology, retinal photoreceptor cells require the specialized lipid metabolism for survival and functions. In this study, we focus on the roles of saturated fatty acids and their metabolism in these processes. Frame-shift mutation of lysophosphatidylcholine acyltransferase 1 (Lpcat1), which introduces saturated fatty acid into lysophosphatidylcholine to produce disaturated phosphatidylcholine (PC), has been reported as a causative for spontaneous retinal degeneration in mice (rd11 mice). However, the molecular basis of retinal degeneration caused by Lpcat1 mutation remains unclear. Here, we report that Lpcat1 deficiency induces light-independent and photoreceptor-specific apoptosis in mice. Lipidomic analyses of retina and isolated photoreceptor outer segment (OS) suggested that loss of Lpcat1 affects not only disaturated PC production, but also the proper cellular fatty acid flux presumably through altering saturated fatty acyl-CoA availabilities. Furthermore, we demonstrated that Lpcat1 deletion increased mitochondrial reactive oxygen species (ROS) levels in photoreceptor cells, but not in other retinal cells, without affecting the OS structure and trafficking of OS localized proteins. These results suggested that LPCAT1-dependent production of disaturated PC is critical for metabolic adaptation during photoreceptor maturation. Our findings highlight the therapeutic potential of saturated fatty acid metabolism in photoreceptor cell degeneration-related retinal diseases.

overall_design: Gene expression in retinal tissue was measured in 2-week-old Lpcat1 WT and KO mice.

first: Daisuke

last: Hishikawa


title: RNA -sequencing of high grade glioma (HGG) mouse cells encoding for H3.3-G34R vs H3.3-WT histones, derived from a Sleeping beauty based-genetically engineered mouse model

city: Ann Arbor

first: Margaret

last: Hartlage

address: 1150 W Medical Center Dr.

department: Neurosurgery

institute: University of Michigan

summary: RNA-sequencing of H3.3-G34R and H3.3-WT HGG cells was performed to uncover transcriptomic differences related to the presence of H3.3-G34R mutation in a pediatric high grade glioma model, using a Sleeping beauty derived genetically engenieered mouse model.

overall_design: We assessed the transcriptome of H3.3-WT and H3.3-G34R cells from a HGG mouse model using buld RNA-sequencing. We used five biological replicates for each group.

first: Santiago

last: Haase

first: Maria

last: Castro


title: Single cell transcriptomic analysis of spinal Dmrt3 neurons in zebrafish and mouse identifies distinct subtypes and reveal novel subpopulations within the dI6 domain

city: Uppsala

first: Henrik

last: Boije

address: Uppsala University, Dept. Of Neuroscience, Box 593, BMC

institute: Uppsala University

summary: The spinal locomotor network is frequently used for studies into how neuronal circuits are formed and how cellular activity shape behavioral patterns. A population of dI6 interneurons, marked by the Doublesex and mab-3 related transcription factor 3 (Dmrt3), has been shown to participate in the coordination of locomotion and gaits in horses, mice and zebrafish. Analyses of Dmrt3 neurons based on morphology,  functionality and the expression of transcription factors have identified different subtypes. Here we analyzed the transcriptomes of individual cells belonging to the Dmrt3 lineage from zebrafish and mice to unravel the molecular code that underlies their subfunctionalization. Indeed, clustering of Dmrt3 neurons based on their  gene expression verified known subtypes and revealed novel populations expressing unique markers. Differences in birth order, differential expression of axon guidance genes, neurotransmitters and their receptors, as well as genes affecting electrophysiological properties, were identified as factors underlying functional diversity. In addition, the comparison between fish and mice populations offers insights into the evolutionary driven subspecialization concomitant with the emergence of limbed locomotion.

sample_organism:
Danio rerio
Mus musculus

platform_organism:
Danio rerio
Mus musculus

overall_design: Transgenic animals were used to specifically label Dmrt3 expressing neurons during development  in zebrafish and in mouse. Two 384 well plates were collected with dmrt3 neurons for smart-seq2 sequencing, one for each species. Extra genes related to the transgenic lines were added to the species GTF files to allow inclusion of these genes in the analysis.

first: Jon

last: Jakobsson

first: Ana

last: Iglesias Gonzales

first: Jennifer

last: Vieillard

first: Malin

last: Lagerström

first: Klas

last: Kullander


title: Next Generation Sequencing of Ad-Ctrl sh and Ad-Tox4 sh treated mouse livers

first: Liheng

last: Wang

address: 1150 Saint Nicholas Avenue, Room 234

department: Department of Medicine

institute: Columbia University Medical Center

summary:
To interrogate the genome-wide target genes of TOX4, we performed RNA-seq from livers of 16-hr fasted animals (10-wk-old C57BL/6J male mice) following TOX4 KD.
The RNA-sequencing was performed by Columbia Genome Center. Poly-A pull-down was used to enrich mRNA from total liver RNA and library construction with Illumina TruSeq. Libraries were sequenced using Illumina NovaSeq 6000. Kallisto pipeline was used to quantify transcript abundance (Bray et al., 2016).

overall_design: Liver mRNA profiles from Ad-Ctrl sh and Ad-Tox4 sh treated mouse livers with 16-hr fast. Mice were sacced at Day 10 post adenovirus injection.

first: Domenico

last: Accili


title: RNA-sequencing of high grade glioma (HGG) human cells encoding for H3.3-G34R vs H3.3-WT histones, derived from  a patient harboring pHGG and stably tranfected with 3X-FLAG-tagged wild type H3.3 or a 3X-FLAG-tagged H3.3 harboring the G34R mutation

summary: RNA-sequencing of H3.3-G34R and H3.3-WT HGG cells was performed to uncover transcriptomic differences related to the presence of H3.3-G34R mutation, using human cells obtained from a patient harboring pHGG and stably tranfected with  3X-FLAG-tagged wild type H3.3 or a 3X-FLAG-tagged H3.3 harboring the G34R mutation.

overall_design: We assessed the transcriptome of H3.3-WT and H3.3-G34R cells from human cells obtained from a patient harboring a hemispheric pHGG. SJ-GBM2 cells were stably transfected with constructs to express a 3X-FLAG-tagged wild type H3.3 (generating the SJ-GBM2-H3.3-Wt cells) or a 3X-FLAG-tagged H3.3 harboring the G34R mutation (generating the SJ-GBM2-H3.3-G34R cells).  We used five biological replicates for each group.


title: microRNA expression data from human platelets infected by EBV in vitro

city: Kunming

first: Jing

last: Sun

state: Yunnan

address: NO. 935,JIAO LIN ROAD

institute: Institute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College

summary: Viruses can directly interact with platelets and modulate their function. Viral impact on platelet activation, and platelet-mediated modulations of innate and adaptive immune responses. Human herpesvirus 4, also known as Epstein–Barr virus (EBV) interaction with platelets occurs via complement receptor 2 (CR2), but the exact mechanism of action with platelets is still poorly understood. Epstein–Barr virus (EBV), is extremely efficient at establishing a persistent life-long infection in human B cells. In the present study,  GeneChips were performed in human platelets from three normal donors infected with the EBV-containing supernatant of the B95.8 marmoset cell line in vitro.

overall_design: Three negtive control samples and three EBV infected samples.

first: Yunzhang

last: Hu


title: Gene expression data from human platelets infected by EBV in vitro


title: Impact of cytostatic compounds on gene expression

city: Stanford

first: Jason

last: Rodencal

state: CA

address: 327 Campus Drive, Room 420

institute: Stanford University

summary: The cytostatic compounds palbociclib (CDK4/6 inhibitor, 2 uM) and pimasertib (MEK inhibitor, 0.5 uM) were added to the growth media of HT-1080 fibrosarcoma cells for 48 hours. Then, RNA was collected from the samples and sequenced.

overall_design: Two replicates of samples treated with DMSO, palbociclib (pal), or pimasertib (pim) were collected.

first: Scott

last: Dixon


title: Transcriptomic analysis of Serratia marcescens PLR treated Arabidopsis.

city: qingdao

first: ZIPENG

last: YU

address: No.72 Binhai Road,

institute: shandong university

summary: The main purpose of this work is to clarify the effect of bacterial PLR on lateral root development in Arabidopsis, especially focusing on the fluctuation of auxin signaling in plants, so as to explain that PLR promotes lateral root development by promoting auxin signaling in plants.

overall_design: We isolated total RNA from the 7-day-old Col-0 seedlings with or without Serratia marcescens PLR treatment.

first: Zipeng

last: Yu

first: ZhaoJun

last: Ding


title: RBM20 mutations result in cardiac remodelling and pathogenesis in mice

city: Madison

first: Hasan

last: Khatib

state: Wisconsin

address: 1675 Observatory Dr.

department: Animal and Dairy Sciences

institute: University of Wisconsin-Madison

summary: Genetic studies show that mutations in a gene named as RNA binding motif 20 (RBM20) are associated with dilated cardiomyopathy (DCM). We selected two mutations (S637A and S639G) located in arginine/serine-rich (RS) domain of RNA binding motif 20 (RBM20) and generated two knock-in mouse models (Rbm20S637A and Rbm20S639G) respectively. The heterozygous (HT) and homozygous (HM) in both mouse lines displayed DCM phenotype with enlarged left ventricular (LV) chamber, thinner ventricular walls and reduced ejection fraction. We also observed higher mortality rate in both HM mice, ~50% in Rbm20S639G and ~34% in Rbm20S637A at an early age (<100days). Differentially expressed and spliced genes from RNA-seq data were involved in arrhythmia, cardiomyopathy, and sudden death based on Human Phenotype Ontology enrichment analysis (FDR≤0.05) in both mouse lines. Immunofluorescent analysis in tissues and single cardiomyocytes respectively showed both mutations promote RBM20 nucleocytoplasmic trafficking and protein condensates, suggesting they are gain-of-function mutations, leading to high mortality rate at younger age. Together, we reported a new mechanism by which cardiac genetic mutations causes protein trafficking and RNA-protein aggregation in cardiac remodelling.

overall_design: Study the underlying mechanisms of two Rbm20 mutations in cardiac remodeling in mice.

first: Wei

last: Guo

first: Chunyan

first: Camila

middle: U

last: Braz

first: Yanghai

last: Zhang


title: Single cell RNA sequencing of primary murine hepatic stellate cells from healthy versus CCl4-treated mice.

city: Rochester

first: Mrunal

last: Dehankar

address: 200 First St. SW

institute: Mayo Clinic

summary: The goal of this project is to study hepatic stellate cell sub-populations in liver fibrosis and more specifically find a sub-population which responds to stiffness. Single cells were isolated from healthy versus CCl4-treated mice utilizing accudenz gradient method and were sequenced using 10X genomics technology.

overall_design: Hepatic stellate cell sub-populations in healthy versus fibrotic livers

first: Enis

last: Kostallari

first: Vijay

last: Shah

first: Ying

last: Li