title: Peptide YY: a Paneth cell antimicrobial peptide that maintains Candida gut commensalism.

first: Eugene

last: Chang

address: 900 E 57th St

department: Medicine

institute: University of Chicago

summary: The mammalian gut secretes a family of multifunctional peptides that affect appetite, intestinal secretions, and motility, while some regulate the microbiota. We report peptide YY (PYY1-36), but not endocrine PYY3-36, is an antimicrobial peptide (AMP) expressed by gut epithelial Paneth Cells (PC). PC-PYY has limited antibacterial activity, but shows selective activity against virulent hyphal, but not yeast forms, of Candida albicans. 5 PC-PYY is a cationic molecule that interacts with the anionic surfaces of fungal hyphae to cause membrane disruption  and transcriptional reprogramming to maintain the yeast phenotype of the fungus. PC-PYY is packaged into secretory granules and is secreted into and retained by surface mucus, which optimizes PC-PYY activity. Hence, PC-PYY acts as a selective antifungal AMP that contributes to the maintenance of gut fungal commensalism.

overall_design: In vitro cultures of C. albicans in yeast and hyphae forms were treated with a small peptide, PYY1-36 (30µM), or saline vehicle control and harvested for RNA after 4 h of treatment. (Yeast_ctrl=yeast+saline, Yeast_PYY=Yeast+PYY1-36, hyphae_ctrl=hyphae+saline, hyphae_PYY=hyphae + PYY1-36)

first: Joseph

last: Pierre

first: Brian

last: Peters

first: Diana

last: La Torre

first: Ashley

last: Sidebottom

first: Yun

last: Tao

first: Xiaorong

last: Zhu

first: Candace

last: Cham

first: Ling

last: Wang

first: Amal

last: Kambal

first: Katharine

last: Harris

first: Julian

last: Silva

first: Olga

last: Zaborina

first: John

last: Alverdy

first: Herbert

last: Herzog

first: Jessica

last: Witchley

first: Suzanne

last: Noble

first: Vanessa

last: Leone


title: Orthogonal metabolism of cellodextrin and xylodextrin is the keystone of synchronous utilization of cellulose and hemicellulose in Myceliophthora thermophila

status: Public on Feb 28 2024

city: Tianjin

first: Jingen

last: Li

address: Xiqi Dao 32, Tianjin Airport Economic Area

country: China

institute: Tianjin institute of industrial biotechnology,Chinses Academy of Sciences

type: Expression profiling by high throughput sequencing

summary: Plant biomass holds tremendous potential as a renewable feedstock in the production of biofuels and biochemicals. The effective co-utilization of the main components cellulose and hemicellulose in plant lignocellulose is critical to the economic viability of lignocellulosic biorefineries. Here, we found that the thermophilic cellulolytic fungi Myceliophthora thermophila can utilize cellulose and hemicellulose synchronously. To investigate the underlying molecular mechanisms, we firstly checked the soluble carbohydrate of the culture using plant biomass (corncob) as sole carbon source and revealed the presence of various oligosaccharides including cellodextrin and xylodextrin, both intracellularly and extracellularly in the cultures, in addition to glucose or xylose. Based on these, intracellular oligosaccharide metabolism was proposed and confirmed by identification of cellodextrin and xylodextrin metabolism pathway. Furthermore, sugar consumption assay showed that contrasting with synchronous utilization of mixed cello-/xylo-dextrin, the inhibition effect of glucose for the metabolism of xylose and cello-/xylo-dextrin exists in this fungus, suggesting Carbon Catabolite Repression (CCR) is largely avoided at the form of oligosaccharides. Transporter MtCDT-2 showing preference to xylobiose and the tolerance of cellobiose inhibition also helps to bypass metabolic inhibition. Finally, the expression of cellulase and hemicellulase genes, were found orthogonal induction by cellobiose/Avicel and xylobiose/xylan, which conferred the ability of the strain to synchronously utilize cellulose and hemicellulose. Taken together, the orthogonal oligosaccharide catabolic pathway in this fungus establishes the molecular basis for the synchronous utilization of cellulose and hemicellulose, which sheds new light on understanding the plant biomass degradation by fungi and provides alternative paradigm for development of lignocellulose biorefinery such as consolidated bioprocessing in the future.

overall_design: mRNA profiles of Myceliophthora thermophila cells exposed to Xylan, AX(mixed Avicel and Xylan), G2(cellobiose), X2(xylobiose), G2X2 (mixed cellobiose and xylobiose), and GX (mixed glucose and xylose).


title: Myeloid PDLIM2 repression as a common causal mechanism of lung disease pathogenesis and susceptibility to infection

status: Public on Feb 29 2024

city: Los Angeles

first: Fremont

last: Gao

state: California

address: 2011 Zonal Ave, HMR 903

country: USA

institute: USC

summary: Selective deletion of PDLIM2 in myeloid cells rendered mice more vulnerable to lung injury and mortality after LPS intratracheal instillation, which was associated with the exacerbated activation of pro-inflammation signaling pathways and the more diminished activation of anti-inflammation signaling pathways in the lung, and particularly, in lung macrophages and neutrophils.

overall_design: The experiments started with WT and Pdlim2 myeloid KO (mKO) mice of similar age. Each group was further divided into PBS and LPS-treated ones where treatment was administered through intratracheal injection. Lungs from these 4 groups of mice were dissected 48hr post treatment and were then dissociated into single cell suspension. scRNAseq was done with the combination of 10x genomics single cell 5’ kit and customized sample multiplexing using TotalSeq CD45 tag antibody.

first: Feng

first: Xujie

last: Liu

first: Fan

last: Sun

first: Yadong

last: Xiao

first: Zhaoxia

last: Qu


title: Focal adhesion kinase-YAP signaling axis drives drug-tolerant persister cells and residual disease in NSCLC (scRNA-Seq)

city: San Francisco

first: Wei

last: Wu

state: CA

address: 600 16th street

department: Department of Medicine

institute: University of California, San Franciso

summary: Targeted therapy is effective in many tumor types including lung cancer, the leading cause of cancer mortality. Paradigm defining examples are targeted therapies directed against non-small cell lung cancer (NSCLC) subtypes with oncogenic alterations in EGFR, ALK and KRAS. The success of targeted therapy is limited by drug-tolerant persister cells (DTPs) which withstand and adapt to treatment and comprise the residual disease state that is typical during treatment with clinical targeted therapies. Here, we integrate studies in patient-derived and immunocompetent lung cancer models and clinical specimens obtained from patients on targeted therapy to uncover a focal adhesion kinase (FAK)-YAP signaling axis that promotes residual disease during oncogenic EGFR-, ALK-, and KRAS-targeted therapies. FAK-YAP signaling inhibition combined with the primary targeted therapy suppressed residual drug-tolerant cells and enhanced tumor responses. This study unveils a FAK-YAP signaling module that promotes residual disease in lung cancer and mechanism-based therapeutic strategies to improve tumor response.

overall_design: Single cell RNA sequencing in isogenic EGFR-mutant PC9-C2 cells treated with 0.1% DMSO (harvest time points: 0.5h, 2h, 8h, 24h, and 48h), or with 2 µM osimertinib (harvest time points: 0.5h, 2h, 8h, 24h, 48h, 72h, 96h, 6d, 9d); including barcode analysis on single cell level. Relates to  Supplemental Fig. 5 (b-i; j).

first: Franziska

last: Haderk

first: Yu-Ting

last: Chou

first: Lauren

last: Cech


title: Sex differences in the expression and function of hepatic very low-density lipoprotein receptor during protein deficiency in mice

status: Public on Feb 27 2024

city: Tama Ward

first: Jiuxiang

last: Cao

state: Kanagawa

address: 1 Chome-1-1 Higashimita

department: School of Agriculture

country: Japan

institute: Meiji University

summary: Very low-density lipoprotein (VLDL) receptor (VLDLR), a member of the low-density lipoprotein receptor family, is responsible for VLDL uptake in peripheral tissues. We reported that significant increase in hepatic VLDLR levels following protein restriction in male mice does not contribute to hepatic fat accumulation, indicating that VLDLR may have hitherto unknown functions. Here, we used RNA-sequencing analysis of liver samples to analysis the effects of protein restriction on hepatic VLDLR in male and female mice.

overall_design: Wild-type (WT) and Vldlr knockout (KO) mice were fed a control or low-protein diet containing 20% or 2% protein, respectively, for 20 days. Total RNA was extracted from frozen liver samples and quantified using spectrophotometry. RNA library preparation and RNA sequencing were performed by Novogene Co., LTD.

first: Asako

last: Takenaka


title: A circadian transcriptional sub-network and EARLY FLOWERING 3 control timing of senescence and grain nutrition in bread wheat

city: Melbourne

first: Christopher

middle: Robert

last: Buckley

state: VIC

address: School of BioSciences, Level 3, Building 184, The University of Melbourne

country: Australia

institute: University of Melbourne

summary: Bread wheat (Triticum aestivum cv. Mace) mature and senescent flag leaves were collected over a 48 h time course in continuous conditions to investigate changes in circadian clock regulation that occur during leaf senescence.

overall_design: Wheat seeds of the Australian cultivar Mace were sown in a single growth room in two staggered batches, 28 days apart. Leaves were sampled concurrently when ‘mature’ plants were at ear emergence (Zadok’s stage 51-59) and ‘senescent’ plants had evident chlorophyll degradation in flag leaves. At dawn (Zeitgeber Time 0; ZT0), the growth room was set to continuous light and temperature (20ºC) and whole flag leaves from the primary tiller of four plants were collected every 2 h from ZT45 to ZT91 (48 h). Samples were immediately flash frozen in liquid nitrogen and stored at -80°C. RNA from two individual leaf samples was equally pooled to provide two replicates for sequencing.

middle: R

first: Michael

middle: J

last: Haydon


title: Hepatic Transcriptomic Responses to Ethinylestradiol in Embryonic Japanese Quail and Double-crested Cormorant

city: Ste-Anne-de-Bellevue

first: Yeon-Seon

last: Jeon

state: Quebec

address: 21111 Lakeshore

department: Natural Resource Sciences

country: Canada

institute: McGill University

summary: Species difference in susceptibility to toxicants is a critical issue in ecotoxicology. Transcriptomics is being proposed as a strategy to improve toxicity testing for regulatory risk assessment; however, different responses among species have not been extensively explored using this approach. In the present study, we identified dysregulated genes and pathways in Japanese quail (JQ) and double-crested cormorant (DCCO) embryos following exposure to ethinylestradiol (EE2). The objectives were to evaluate unique and overlapping transcriptomic responses to estrogenic exposure in the two species, and to determine whether these responses correspond to previously reported sensitivity difference at the organismal level. Exposures were conducted according to an avian egg injection protocol that we have proposed for standardization. EE2 was dissolved in dimethyl sulfoxide and injected into the air cell of eggs prior to incubation at nominal concentrations of 0, 3.33, and 33.3 µg/g egg weight. After 9-days (JQ) or 16-days (DCCO) of incubation (representing mid-incubation stage), liver tissues were collected from 5 embryos per treatment group for RNA-sequencing. Data were processed and analyzed using EcoOmicsAnalyst (www.ecoomicsanalyst.ca) and ExpressAnalyst (www.expressanalyst.ca). Following exposure to EE2, JQ and DCCO had 238 and 1987 differentially expressed genes, respectively, having 78 of them in common. The results of this study will contribute to a better understanding of the estrogenic effects of contaminants in birds, the expansion of taxonomic coverage in chemical risk assessment from model to non-model species, and the evaluation of transcriptomics and early-life stage tests as alternative toxicity testing methods. This study was conducted as a part of a large-scale Genome Canada-funded project, EcoToxChip project (www.ecotoxchip.ca).

overall_design: Liver mRNA profiles of embryonic day 9 Japanese quail and embryonic day 16 double-crested cormorant following single exposure to either solvent or ethinylestradiol solution

first: Jonathan

last: Sangiovanni

first: Emily

last: Boulanger

first: Doug

last: Crump

first: Niladri

last: Basu

first: Jeff

last: Xia

first: Markus

last: Hecker

first: Jessica

last: Head


title: RNA-seq analysis of match paired papillary and reticular skin fibroblasts cultivated as pro-angiogenic cell sheets

city: Saint-Viance

first: Adèle

last: Mauroux

address: ZAC de la Nau

country: France

institute: SILAB

summary: The aim of our study was to determin if papillary and reticular fibroblasts cell sheets expressed distinct genes involved in angiogenesis regulation and extracellular matrix. Thanks to our RNAseq analyssis, we demonstrated that papillary and reticular fibroblasts express specific signature of genes related to secreted angiogenic regulators and matrisome genes, suggesting that each subtype of fibroblasts differently regulate the formation of capillary via secreted factors and the microenvironment they generate. We confirmed this hypothesis with functional angiogenesis model in vitro. Overall, we show that papillary fibroblasts have a greater angiogenic potential and support the formation of dense branched vascular netword. On the other hand, reticular fibroblasts allow the formation of fewer vessel of larger diameter. This resultats are coherent with native skin vasculature and suggest that each fibroblasts subtypes play a role in regulating skin vascularisation.

overall_design: We used primary papillary and reticular fibroblasts from three distinct donors that we cultivated in pro-angiogenic that also stimulate matrix deposition. We generated experimental duplicates.

first: Florence

last: Ruggiero

first: Laurent

last: Muller


title: Control ChIP-seq from BLaER1 (ENCSR841CWN)

city: Stanford

first: ENCODE

last: DCC

address: 300 Pasteur Dr

institute: ENCODE DCC

type: Genome binding/occupancy profiling by high throughput sequencing

summary:
Control ChIP-Seq on BLaER1 cell line after 72 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR531CCR)

summary:
Input ChIP-seq in L3 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from K562 (ENCSR833ZKY)

summary:
ChIP-seq on human K562

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from ovary (ENCSR818VNL)

summary: For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from BLaER1 (ENCSR455AFK)

summary:
Control ChIP-Seq on untreated BLaER1 cell line.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from BLaER1 (ENCSR978XYH)

summary:
Control ChIP-Seq on BLaER1 cell line after 48 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from K562 (ENCSR501CEJ)


title: Mint-ChIP-seq from HCT116 (ENCSR821OKM)


title: Control ChIP-seq from BLaER1 (ENCSR958BKG)

summary:
Control ChIP-Seq on BLaER1 cell line after 9 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR530KWH)

summary:
ChIP-seq against eGFP-sptf-1 in L1 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from HCT116 (ENCSR790WQH)


title: Control ChIP-seq from A549 (ENCSR779AKU)

summary:
ChIP-seq on human A549

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from MCF-7 (ENCSR439GBR)

summary:
MCF7 immortalized cell line stably expressing C-terminal eGFP-TSC22D2 fusion protein.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from MCF-7 (ENCSR438BNB)

summary:
MCF7 immortalized cell line stably expressing C-terminal eGFP-ZNF331 fusion protein.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from Patski (ENCSR776VHJ)


title: Mint-ChIP-seq from Calu3 (ENCSR433FAZ)


title: Control ChIP-seq from BLaER1 (ENCSR452GUC)

summary:
Control ChIP-Seq on BLaER1 cell line after 120 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from K562 (ENCSR730EDP)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-ZNF75A fusion protein.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR633VXV)

summary:
Input ChIP-seq in L2 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR430JDM)

summary:
Input ChIP-seq in late embryonic worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR921BPO)

summary:
ChIP-seq against UNC-55 in LE worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from HCT116 (ENCSR633PSA)


title: Control ChIP-seq from SK-N-SH (ENCSR593IWN)

summary:
ChIP-seq on human SK-N-SH

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR422GZR)

summary:
ChIP-seq of transgenic worms expressing RPC-1-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from H9 (ENCSR725YWL)

summary:
H3K27me3 Mint-ChIP-seq on human H9.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from BLaER1 (ENCSR954ZQC)

summary:
Control ChIP-Seq on BLaER1 cell line after 24 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from brain (ENCSR603VTC)

summary: For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from BLaER1 (ENCSR399JUL)

summary:
Control ChIP-Seq on BLaER1 cell line after 3 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR581MER)

summary:
Input ChIP-seq in L1 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR893TGG)

summary:
Input control for ChIP-seq on transgenic flies expressing CG11902-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from K562 (ENCSR914PHJ)

summary:
ChIP-seq on human K562

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from BLaER1 (ENCSR871SEB)

summary:
Control ChIP-Seq on BLaER1 cell line after 12 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from BLaER1 (ENCSR566AUD)

summary:
Control ChIP-Seq on BLaER1 cell line after 6 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from brain (ENCSR385SSH)

summary:
H3K36me3 Mint-ChIP-seq on human H9 derived brain organoid

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR538KZZ)

summary:
Input ChIP-seq in LE worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from HCT116 (ENCSR562OQT)


title: Control ChIP-seq from BLaER1 (ENCSR845IKY)

summary:
Control ChIP-Seq on BLaER1 cell line after 36 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR276IVY)

summary:
This is the ChIP-seq control of transgenic worms expressing BLMP-1-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from BLaER1 (ENCSR255SDP)

summary:
Control ChIP-Seq on BLaER1 cell line after 18 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from BLaER1 (ENCSR354HOM)

summary:
Control ChIP-Seq on BLaER1 cell line after 168 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from K562 (ENCSR099EPT)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-ELF4 fusion protein.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR374VRB)

summary:
ChIP-seq against eGFP-nhr-12 in L3 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from GM23338 (ENCSR695NNR)

summary:
H3K27me3 Mint-ChIP-seq on human GM23338.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR259OSS)

summary:
Input ChIP-seq in L3 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR255HJY)


title: Control ChIP-seq from K562 (ENCSR093AOE)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-ZBTB26 fusion protein.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR095MXI)

summary:
This is the ChIP-seq control of transgenic worms expressing RPC-1-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR083MKO)

summary:
This is the ChIP-seq control of transgenic worms expressing POP-1-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from Patski (ENCSR343HAH)

summary: For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR346GYL)

summary:
Input ChIP-seq in L4 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR255EYF)

summary:
ChIP-seq against eGFP-unc-62 in L4 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR164BYW)

summary:
ChIP-seq against eGFP-hpl-2 in L1 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR086JMC)

summary:
Input ChIP-seq in YA worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR169GBD)

summary:
ChIP-seq against PRC-1 in YA worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from K562 (ENCSR226CLB)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-THRB fusion protein.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from natural killer cell (ENCSR036TAN)


title: Control ChIP-seq from HepG2 (ENCSR332CDN)

summary:
ChIP-seq on human HepG2

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from GM12878 (ENCSR161EAA)

summary:
GM12878 immortalized cell line stably expressing C-terminal eGFP-ZBTB11 fusion protein.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR131UVY)


title: Control ChIP-seq from K562 (ENCSR028MGN)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-HBP1 fusion protein.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR304RME)

summary:
ChIP-seq against eGFP-pha-4 in late embryonic worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR299IKN)

summary:
ChIP-seq against eGFP-alr-1 in L2 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Claudin-7 knockout by gene targeting

city: Columbia

first: YAN-HUA

last: Chen

state: SC

address: 631 Sumter Street

department: Chemistry and Biochemistry

institute: University of South Carolina

summary: To investigate the claudin-7 function in vivo, we generated a claudin-7 knockout mouse model by gene targeting through homologous recombination. In this study, we report that Cln7-/- pups show Na+, Cl-, and K+ wasting and chronic dehydration phenotypes. The dramatic increase of aldosterone synthase mRNA level suggests that these mice suffer from mishandling of NaCl and fluid in the distal nephrons. Deletion of claudin-7 invokes several compensatory changes, such as increased renin, serum-glucocorticoid-induced kinase 1 (SGK1), epithelial Na+ channel (ENaCα), Na+-Cl- cotransporter (NCC), as well as aquaporin (AQP) 2 mRNA levels, demonstrating the cross talks between paracellular and transcellular ion transport pathways.

overall_design: 8 mouse intestinal samples were analyzed with 4 wildtype (WT) and 4 claudin-7 knockout (KO). Both WT and KO contain 2 small and 2 large intestinal samples.

first: Yan-Hua

first: Tiaosi

last: Xing


title: Control ChIP-seq from whole organism (ENCSR008VTA)

summary:
Input control for ChIP-seq on transgenic flies expressing dl-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from SK-N-SH (ENCSR017UWW)

summary:
ChIP-seq on human SK-N-SH

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Vitiligo non-responding lesions to narrow band UVB have intriguing cellular and molecular abnormalities that may prevent epidermal repigmentation

city: Aurora

first: Stanca

last: Birlea

state: CO

department: Dermatology

institute: University of Colorado, Anschutz Medical Campus

summary: We have discovered that human vitiligo patients treated with narrow-band UVB (NBUVB) demonstrated localized resistance to repigmentation in skin sites characterized by distinct cellular and molecular pathways. We used the remaining slides from our immunostaining studies. 1.0 mm2 epidermal scrapes were collected from formalin fixed paraffin embedded (FFPE) transverse sections of biopsies from four paired responding and non-responding vitiligo lesions (8 samples total), following published work (Trejo et al., 2019; Yeakley). The material collected was subjected to whole transcriptome TempO-Seq assay. We used a novel method that combines epidermal scraping and TempO-Seq transcriptome analysis and found that the abnormal environment in non-responding was driven by dysregulated cAMP and WNT/β-catenin signaling pathways. Characterization of abnormal environment that prevents vitiligo repigmentation may open roads for discovery of new drugs that reverse depigmentation.

overall_design: Gene expression profiles of interfollicular epidermal samples isolated from biopsies of responding (repigmented) vitiligo lesions were compared to gene expression profiles of interfollicular epidermal samples isolated from paired biopsies of non-responding (depigmented) vitiligo lesions. Paired biopsies were collected from the same patients.

middle: A

first: Nathaniel

middle: B

last: Goldstein


title: Control ChIP-seq from whole organism (ENCSR122WYP)

summary:
Input ChIP-seq in L1 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR124QHO)

summary:
ChIP-seq against F45C12.2 in L4 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR021SOI)

summary:
ChIP-seq against eGFP-ces-1 in L3 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Transcriptome analyses of blue laser radiation treated E. coli K12 MG1655

city: Braunschweig

first: Mattes

last: Hintmann

address: Rebenring 56

department: Institut für Mikrobiologie

country: Germany

institute: TU Braunschweig

summary: E. coli K12 cells (in 9 g/L NaCl) were irradiated with blue laser ligth (448 nm) for 5 s (310 J/cm2) or 20 s (1240 J/cm2) both with an intensity of 62 W/cm2 and the transcriptome was compared to that of unirradiated cells

overall_design: Two-colour-experiment, irradiated vs. Unirradiated, triplicates for each condition (5 s and 20 s)

first: Rebekka

last: Biedendieck


title: TET1 catalytic activity is required for reprogrammign of imprinting control regions and the patterning of sperm-specific hypomethylated regions [RNA-seq: Female PGCs]

city: Philadelphia

first: Rexxi

middle: Diptya

last: Prasasya

state: PA

address: 3400 Civic Center Blvd

department: Cell and Developmental Biology

institute: University of Pennsylvania

summary: DNA methylation erasure is required for mammalian primordial germ cell reprogramming. TET enzymes iteratively oxidize 5-methylcytosine to generate 5-hydroxymethylcytosine (5hmC), 5-formylcytosine, and 5-carboxycytosine to facilitate active genome demethylation. Whether these bases are required to promote relication coupled dilution or active base excision repair during germline reprogramming remains unresolved due to the lack of genetic models that decouple TET1 activities. Here, we generated two mouse lines expressing catalytically inactive TET1 (Tet1-HxD) and TET1 that stalls at 5hmC (Tet1-V). This experiment was done to conduct transcriptiomic analysis of embryonic day (E)14.5 female primordial germ cells (PGCs) of WT, Tet1-HxD, Tet1-V, and Tet1-KO mice.

overall_design: RNAseq from E14.5 Female PGCs of wild type (WT), Tet1 catalytically dead mutant (HxD), Tet1 5hmC stalling mutant (V), and Tet1 KO mice that was sorted using Oct4-GFP reporter

first: R

middle: D

first: B

last: Caldwell

first: Z

last: Liu

first: S

last: Wu

last: Cincotta

first: J

last: Fowler

first: D

last: Laird

middle: M

last: Kohli

first: M

middle: S

last: Bartolomei


title: TET1 catalytic activity is required for reprogrammign of imprinting control regions and the patterning of sperm-specific hypomethylated regions [RNA-Seq]

summary: DNA methylation erasure is required for mammalian primordial germ cell reprogramming. TET enzymes iteratively oxidize 5-methylcytosine to generate 5-hyroxymethylcytosine (5hmC), 5-formylcytosine, and 5-carboxycytosine to facilitate active genome demethylation. Whether these bases are required to promote replication-coupled dilution or activate base excision repair during germline reprogramming remains unresolved due to the lack of genetic models that decouple TET1 activities. Here, we generated two mouse lines expressing catalytically inactive TET1 (Tet1-HxD) and TET1 that stalls at 5hmC (Tet1-V). This experiment was done to conduct genome wide DNA methylation profiling of catalytically inactive Tet1HxD/HxD sperm, 5hmC stalling Tet1V/V sperm, KO Tet1-/- sperm, and WT sperm. Sperm samples were collected from adult males (>10 week).

overall_design: RNAseq from E14.5 Male PGCs that was sorted using Oct4-GFP reporter


title: TF ChIP-seq from whole organism (ENCSR744BON)

summary:
ChIP-seq of transgenic worms expressing BLMP-1-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: F2833 scRNA-seq data for manuscript "Therapeutic vaccine containing a novel liposomal adjuvant shifts pathogenic Th17 cells into a Tr1-like phenotype"

city: Copenhagen

first: Katharina

last: Wørzner

address: Artillerivej 5

department: Infectious Disease Immunology

country: Denmark

institute: Statens Serum Institut

summary: Th17 cells can transdifferentiate into other T cell subsets in the context of infections or inflammatory conditions. In many autoimmune diseases, autoantigen-specific Th17 cells play a pivotal role in disease pathogenesis, however, there have been no attempts to target Th17 cell plasticity using vaccines. We aimed to change the phenotype of existing Th17 cells by a protein-in-adjuvant approach and found that antigen formulated in all-trans retinoic acid (ATRA)-containing cationic liposomes (CAF16) effectively inhibited existing Th17 responses. Strikingly, transcriptomic analysis of sorted Th17 cells from IL-17 fate reporter mice revealed a shift of antigen-specific Th17 cells to exTh17 cells, expressing functional markers associated with T cell regulation and tolerance. In addition, vaccination with myelin-specific (MOG) antigen in CAF16 reduced Th17 responses and alleviated disease in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS. This highlights CAF16 as a novel delivery system for ATRA with potential for changing the phenotype of existing Th17 cells in the context of immune mediated diseases.

overall_design: Cells from the spleen of IL-17A fate reporter mice immunized with either CAF01:H56 two times with two weeks in between (n = 10) or followed by four immunizations with CAF16:H56 were processed and stimulated with H56 (1 μg/ml) for 6 hours at 37 oC. Next, CD4+ T cells were isolated using the EasySep mouse CD4+ T cell isolation kit (STEMCELL Technologies Inc., Canada) according to the manufacturer’s recommendation. Live YFP+ cells were sorted using a BD FACSAria™ Cell Sorter (BD BioSciences). Cells were prepared for sequencing using the BD Rhapsody™ Immune Response Panel Mm (Cat.no: 633753, 397 genes, BD BioSciences) and the BD Rhapsody™ Scanner (BD BioSciences) according to the manufacture’s recommendations. Libraries were run on the NovaSeq 6000 with the NovaSeq 6000 SP reagent kit v1.5 (Illumina).

first: Julie

last: Zimmermann


title: F2702 bulk RNA-seq data for manuscript "Therapeutic vaccine containing a novel liposomal adjuvant shifts pathogenic Th17 cells into a Tr1-like phenotype"

overall_design: Cells from the spleen of IL-17A fate reporter mice were processed and CD4+ T cells were isolated using the EasySep mouse CD4+ T cell isolation kit (STEMCELL Technologies Inc., Canada) according to the manufacturer’s recommendation. YFP+ cells were sorted from pools of three mice vaccinated either with CAF01:H56 only or CAF01:H56 followed by CAF16:H56 using a BD FACSMelody™ Cell Sorter (BD BioSciences). Cells were sorted into 100 µl RNase free 1x PBS (Thermo Scientific) with 1 U/µl RNAse inhibitor (Thermo Scientific) and stored at -80 oC before RNA bulk sequencing (performed by CD Genomics (NY, USA)). RNA was extracted from the cell samples using RNeasy Micro Kit (Qiagen). RNA sample quality was assessed by High Sensitivity RNA Tapestation (Agilent Technologies Inc., California, USA) and quantified by Qubit 2.0 RNA HS assay (ThermoFisher, Massachusetts, USA). The SMART-Seq v4 ultra-low input kit was used to synthesize cDNA. Library construction was performed based on the manufacturer’s recommendation for Nextera XT kit. The final library quantity was measured by KAPA SYBR® FAST qPCR and library quality was evaluated by TapeStation D1000 ScreenTape (Agilent Technologies, CA, USA). Illumina® 8-nt dual-indices were used. Equimolar pooling of libraries was performed based on QC values and sequenced on an Illumina® NovaSeq S4 (Illumina, California, USA) with a read length configuration of 150 PE for 40 M PE reads per sample (20M in each direction).


title: Optimizing the experimental and computational methods for Infinium DNA methylation BeadChip on low input and single cells

city: Phialdelphia

first: Wanding

last: Zhou

state: Pennsylvania

address: 3501 Civic Center Blvd, Philadelphia, PA 19104, Colket Translational Research Building, 9300, Colket Translational Research Building

department: Pathology & Lab Medicine

institute: Children's Hospital of Philadelphia

type: Methylation profiling by genome tiling array

summary: In this study, the Infinium BeadChip DNA methylome profiling technology was optimized for suboptimal input DNA conditions, including ultra-low input down to single cells. We acquired knowledge on the boundaries and limits of the Infinium DNA methylation BeadChips with suboptimal input DNA. These findings offer comprehensive solutions to expand the application of this technology to cases with limited DNA.

overall_design: We tested multiple worflows using cell line (NIH3T3, B16-F0 and PGCs) DNA and evaluate performance at low input ranges

first: Sol Moe

last: Lee


title: Spatial Variability of Grape Berry Maturation Program at the Molecular Level

city: VR

first: Alessandra

last: Amato

address: strada le grazie 15

country: Italy

institute: University of Verona

summary: The application of sensors in viticulture is a fast and efficient method to monitor grapevine vegetative, yield, and quality parameters and determine spatial intra-vineyard variability. Molecular analysis at the gene expression level can further contribute to the understanding of the observed variability by elucidating how pathways contributing to different grape quality traits behave in zones diverging on any of these parameters. The intra-vineyard variability of a Cabernet Sauvignon vineyard was evaluated through a Normalized Difference Vegetation Index (NDVI) map calculated from a multispectral image and detailed ground-truthing (e.g., vegetative, yield, and berry ripening compositional parameters). The relationships between NDVI and ground measurements were explored by correlation analysis. Moreover, berries were investigated by microarray gene expression analysis performed at five time points from fruit set to full ripening. Comparison between the transcriptomes of samples taken from locations with the highest and lowest NDVI values identified 968 differentially expressed genes. Spatial variability maps of the expression level of key berry ripening genes showed consistent patterns aligned with the vineyard vigor map. These insights indicate that berries from different vigor zones present distinct molecular maturation programs and suggest that transcriptome analysis may be a valuable tool for the management of vineyard variability.

overall_design: The experiment was conducted in 2017 growing season in a commercial vineyard of approximately 12 hectares of Vitis vinifera cv. Cabernet Sauvignon (FPS clone 8 grafted onto 110R rootstock). The vineyard was planted in 1992 and located in the Alexander Valley American Viticultural Area of California (38°42'50N, 122°55'4W). The vines were trained as a bilateral cordon, established at 1.5 m above the ground, in a split canopy configuration, with the two cordons installed on two separate wires and pointing in opposite directions. Vine and row spacings were 1.8 and 3.35 m respectively. At each vineyard spot, four fully developed inflorescences (pre-bloom) per vine were labeled (therefore, a total of 36 clusters per spot). At each time point (from fruit set to full maturity), one berry per marked cluster was selected determining a sampling size of 36 berries per spot. Prior flash freezing in liquid nitrogen, the berries were weighed to calculate the spot average berry weight and represent berry growing profiles by vineyard spot. Eighteen frozen berries were ground in liquid nitrogen: 1 g of frozen powder was thawed to measure TSS over time, whereas the remaining material was stored and later used for gene expression analysis.

first: Ron

last: Shmuleviz

first: Pietro

last: Previtali

first: Elizabeth

last: Green

first: Luis

last: Sanchez

first: Maria

last: Alsina

first: Nick

last: Dokoozlian

first: Giovanni

last: Tornielli

first: Marianna

last: Fasoli


title: Foxp1 is required for renal intercalated cell differentiation and acid-base regulation

city: Camperdown

first: RENHUA

last: SONG

state: NSW

address: Charles Perkins Centre - D17, Level 4 West. The University of Sydney Johns Hopkins Drive

institute: Centenary Institute

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

overall_design: Refer to individual Series


title: Tumor lineage-specific immune response in brain metastatic disease: opportunities for targeted immunotherapy regimen?

city: Rotterdam

first: Shiva

last: Najjary

address: Dr. Molewaterplein 40

country: Netherlands

institute: Erasmus University Medical Center

summary: Metastases in the brain are the most severe and devastating complication of cancer. The incidence of brain metastasis is increasing. Therefore, the need of finding specific druggable targets for brain metastasis is demanding. The aim of this study was to compare the brain (immune) response to brain metastases of the most common tumor lineages, viz., lung adenocarcinoma and breast cancer. Targeted gene expression profiles of 11 brain metastasis of lung adenocarcinoma (BM-LUAD) were compared to 11 brain metastasis of breast cancer (BCBM) using NanoString nCounter PanCancer IO 360™ Panel. The most promising results were validated spatially using the novel GeoMx™ Digital Spatial Profiler (DSP) Technology. Additionally, Immune cell profiles and expression of drug targets were validated by multiplex immunohistochemistry. We found more active immune response in BM-LUAD as compared to BCBM. In the BM-LUAD, 138 genes were upregulated as compared to BCBM (adj. p ≤ 0.05). Conversely, in BCBM 28 genes were upregulated (adj. p ≤ 0.05). Additionally, genes related to CD45+ cells, T cells and cytotoxic T cells showed to be expressed higher in BM-LUAD compared to BCBM (adj. p = 0.01, adj. p = 0.023, adj. p = 0.023, respectively). The spatial quantification of the immune cells using the GeoMx DSP technique revealed the significantly higher quantification of CD14 and CD163 in tumor regions of BM-LUAD as compared to BCBM. Importantly, the immune checkpoint VISTA and IDO1 were identified as highly expressed in the BM-LUAD. Multiplex immunohistochemistry confirmed the finding and showed that VISTA is expressed  mainly in BM-LUAD tumor cells, CD3+ cells, and to less levels in some microglial cells in BM-LUAD. This is the first report on differences in the brain immune response between metastatic tumor of different lineages. We found a far more extensive infiltration of immune cells in BM-LUAD as compared to BCBM. In addition, we found higher expression of VISTA and IDO1 in BM-LUAD. Taken together, targeted immune therapy should be considered to treat patients with BM-LUAD.

overall_design:
RNA was extracted from FFPE samples of (LCBM n=11, BCBM n=11)

>>>Submitter states: RCC files will be available only upon request from the corresponding author<<<

first: Johan

last: Kros

first: Willem

last: de Koning

first: Disha

last: Vadgama

first: Karishma

last: Lila

first: Janina

last: Wolf

first: Dana

last: Mustafa


title: Effect of cAMP signaling activation during heart development in Pde2A deficient embryos.

city: Monterotondo

first: Manuela

last: Pellegrini

state: Rome

address: Via E Ramarini

institute: IBBC-CNR

summary: Background: Phosphodiesterases (PDEs) are the enzymes that hydrolyze cyclic nucleotides (cAMP and cGMP) playing a key role in the homeostasis of these two secondary messengers. PDE2A is a dual-specific PDE that breaks down both cAMP and cGMP and can be activated by cGMP. It appears peculiar that the Pde2A-deficient (Pde2A-/-) mouse model is embryonically lethal, likely due to a strongly reduced size of liver and to a severe anemia. In addition, the heart of Pde2A-/- embryos shows ventricular and atrial septum defects, hypertrabeculation, heart dilatation and non-compaction defect.   We recently highlighted a direct relationship between Pde2A impairment, consequent increase of cAMP and the onset of mouse congenital heart defects (CHDs), however the molecular mechanisms underlining the heart defects remain unknown. We found a significant modulation of more than 500 genes affecting biological processes involved in the immune system, cardiomyocyte development and contractility, angiogenesis, control of gene transcription and oxidative stress in hearts from Pde2A-/- embryos. Metoprolol and H89 administration were able to prevent heart dilatation and hypertabeculation in Pde2A-/- embryos. Metoprolol was also able to partially impede heart septum defect and oxidative stress at tissue and molecular levels. By using the antioxidant NAC partial rescue of cardiac defects was observed straightening the oxidative stress like one of the critical molecular mechanisms underpinning the CHDs associated to cAMP unbalance.

overall_design: Transcriptome analysis of Pde2A-/- embryonic heart was performed by RNA sequencing in 5 knockout and 6 wilde-type, the most altered genes were also analyzed by quantitative real time PCR

first: Silvia

last: Cardarelli

first: Martina

last: Biglietto

first: Valentina

last: Fustaino

first: Vladimir

last: Benes

first: Lucia

last: Monaco


title: Exploring the diversity and antibiogram of the soil around a tertiary care hospital and a university precinct in southern In-dia: A pilot study

city: Bundoora

first: Anya

last: Shindler

address: 1 Kingsbury Drive

institute: La Trobe University

summary: This study identified and compared the bacterial diversity and the antimicrobial resistance profile of clinically relevant isolates around a newly developed hospital and university precinct

overall_design: Soil samples were taken from eight plots next to a Hospital and University in India.  The samples underwent 16S sequecing and culturing for testing antibiotic resistance.

first: Shalini

last: Kunhikannan

first: Cassandra

last: Stanton

first: Jayson

last: Rose

first: Ashley

middle: E

last: Franks

first: Sumana

last: MN S

last: Kumar

first: Steve

last: Petrovski

first: Colleen

last: Thomas


title: TET1 catalytic activity is required for reprogrammign of imprinting control regions and the patterning of sperm-specific hypomethylated regions [CUT&RUN]

first: Rexxi

last: Prasasya

summary: DNA methylation erasure is required for mammalian primordial germ cell reprogramming. TET enzymes iteratively oxidize 5-methylcytosine to generate 5-hyroxymethylcytosine (5hmC), 5-formylcytosine, and 5-carboxycytosine to facilitate active genome demethylation. Whether these bases are required to promote replication-coupled dilution or activate base excision repair during germline reprogramming remains unresolved due to the lack of genetic models that decouple TET1 activities. Here, we generated two mouse lines expressing catalytically inactive TET1 (Tet1-HxD) and TET1 that stalls at 5hmC (Tet1-V). This experiment was done to conduct genome wide DNA methylation profiling of catalytically inactive Tet1HxD/HxD sperm, 5hmC stalling Tet1V/V sperm, KO Tet1-/- sperm, and WT sperm. Sperm samples were collected from adult males (>10 week). E17.5 WT prospermatogonia were collected using FACS of Oct4-GFP cells and CUT&RUN for H3K4me3 and IgG were done on 130,000 cells.

overall_design: 130,000 freshly sorted E17.5 Oct-GFP+ prospermatogonia cells were used for H3K4me and IgG CUT&RUN

first: R

first: B

last: Caldwell

first: Z

last: Liu

first: S

last: Wu

last: Cincotta

first: J

last: Fowler

first: D

last: Laird

last: Kohli

first: M

last: Bartolomei


title: Mint-ChIP-seq from Calu3 (ENCSR223QCG)

first: ENCODE

last: DCC

summary: For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: GE changes TTY23, AT22 & TAT12 vs S288C

city: Cuernavaca

first: Luis

last: Caspeta

state: Morelos

address: Av Universidad 2001

department: Ingeniería Celular y Biocatálisis

country: Mexico

institute: Instituto de Biotecnología - Universidad Nacional Autónoma de México

summary: The thermotolerant TTY23, acid tolerant AT22, and thermo-acid tolerant TAT12 yeast strains, generated by adaptive evolution experiments were grown at 30°C, pH 5.0 in the absence of acetic acid (optimal ancestral conditions). The mRNA of each strain was isolated and changes in expression were compared against the parental strain S288C.

overall_design:
The microarray YOMWG_15, constructed for the yeast strain S288C, following  the fabrication of GPL18099, but using oligo set for S. cerevisiae and  the protocols described here, was used in these experiments. This was elaborated by the DNA Microarrays Unit of the Institute of Cellular Physiology, in the National Autonomous University of Mexico The mRNA of each strain was isolated in the middle exponential phase of growth. Changes in gene expression were measured with microarrays using the SWAP method (Gomez-Mayen AP, Corral-Guille G, Riego‐Ruiz L (2019) Package ‘genArise’, retrieved from http:// bioco nduct or. org/ packa ges/ relea se/ bioc/html/genArise.html)
DNA microarrays unit of the National Laboratory of Technological Support to Genomic Sciences (contributor).

first: Lorena

last: Chávez

first: José

last: Santillan

first: Simón

last: Guzmán

first: Jorge

last: Ramírez


title: Dynamic landscape of enhancer-derived RNA during mouse early embryo development

city: Hangzhou

first: Hua

last: Yu

address: No.18 Shilongshan Road

institute: Westlake University

summary: Enhancer RNAs (eRNAs) play critical roles in diverse biological processes by mediating the activation of their target genes. However, the systematic landscape and potential regulations and functions of eRNAs during mammalian early embryo development remains elusive. Here, we present the comprehensive detection and characterization of eRNAs during mouse early embryo development. We demonstrated the spatiotemporal and allelic landscape of eRNA expression. We found the asymmetric activation of paternal-specific eRNAs during zygotic genome activation (ZGA). We identified TFs and their cooperation in regulating dynamic eRNA expression. eRNA are involved in multiple developmental signaling pathways through putatively regulating their target genes. Interestingly, we observed that the transcriptions of enhancers themselves are also widely modulated by eRNAs during mouse early embryo development. Critically, we de novo identified a novel eRNA transcribed from a super-enhancer region exclusively expressed at 2-cell stage of mouse early embryos and experimentally validated its key functional role in regulating ZGA and early embryo development.

overall_design: Examination of gene expression in control and SPENH0335 knocked-down mouse embryos of 2-cell stage.

first: Jing

last: Zhao


title: Transcriptional profiling of intestinal tissue from mice with and without Eif3h and Apc deficiency.

status: Public on Feb 26 2024

city: Glasgow

first: Kathryn

last: Gilroy

address: Switchback Road

country: United Kingdom

institute: Cancer Research UK Scotland Institute

summary: A profile of gene expression differences in mouse small intestine with and without short term induction of Apc and Eif3h deficiency.

overall_design: Expression data from intestine with and without Eif3h and Apc deficiency.

first: Nikola

last: Vlahov

first: Owen

last: Sansom


title: Screening of NFIL3 target genes (Affymetrix HTA 2.0 data set)

city: Xinxiang

first: Hai-Chuan

state: Henan

address: No. 601 Jinsui Avenue

institute: Xinxiang Medical University

summary:
To identify the target gene of NFIL3, we transfected K562 cells with siNFIL3 or siControl, respectively.
In order to better understand the function of NFIL3 gene, mRNA expression profiles were analyzed by using Affymetrix HTA2.0 Microarray in K562 cells transfected with siNFIL3 or siControl under hypoxia

overall_design: K562 cells were transfected with siNFIL3 or siControl under hypoxia, respectively. Next, mRNA expression profiles were analyzed by using Affymetrix HTA2.0 Microarray in K562 cells transfected with siNFIL3 or siControl under hypoxia.

first: Hai-chuan

first: Guo-min

last: Shen


title: Hepatocyte-specific mitogen-activated protein kinase phosphatase 1 (MKP1) in sexual dimorphism and susceptibility to alcohol induced liver injury

city: Louisville

first: Eric

middle: Christian

last: Rouchka

state: Kentucky

address: 522 East Gray Street

department: Biochemistry and Molecular Genetics

institute: University of Louisville

summary: To study the effects of a chronic, combined high fat and alcohol diet on liver gene expression patterns, a murine intragastric alcohol feeding system was developed. Gene expression profile comparisons from RNAseq data were completed for all experimental groups and their respective controls.

overall_design: Comparisons among two different groups, e.g.  high fat diet, and alcohol plus high fat diet fed during 8 weeks were evaluated and differential gene expression was determined.

first: Mary

middle: N

last: Walter

first: Diego

last: Montoya-Durango

first: Walter

last: Rodriguez

first: Yali

last: Wang

first: JingWen

last: Zhang

first: Julia

middle: H

last: Chariker

middle: C

first: Claudio

last: Maldonado

first: Anton

last: Bennett

first: Craig

last: McClain

first: Shirish

last: Barve

first: Leila

last: Gobejishvili


title: Dissecting the dynamic cellular transcriptional atlas of adult teleost testis development throughout the annual reproductive cycle

city: Qingdao

first: Chaofan

last: Jin

address: Yushan 5 road

institute: Ocean University of China

summary: The successful proliferation and differentiation of testicular cells are vital for the survival, continuity and preservation of species. However, a comprehensive molecular orchestration underlying the spermatogenic process in teleost testis development throughout the annual cycle remains elusive. In this study, the testicular cells derived from adult black rockfish at distinct stages—Regressed, Regenerating, and Differentiating were dissected via single cell transcriptome sequencing. A continuous developmental trajectory of spermatogenic cells, from spermatogonia to spermatids, was delineated, elucidating the molecular events involved in the spermatogonia development. Subsequently, the dynamic regulation of gene expressions associated with spermatogonia proliferation and differentiation was observed across spermatogonia subgroups and various developmental stages. A bioenergetic transition from glycolysis to mitochondrial respiration of spermatogonia during annual developmental cycle was demonstrated, and a deeper level of heterogeneity and molecular characteristics was revealed by re-clustering analysis. The developmental trajectory of Sertoli cells in annual reproductive cycle was examined, and the divergence of Leydig cells and macrophage were explored. Additionally, the interaction network between testicular micro-environment somatic cells and spermatogenic cell were established. Overall, our study provides detailed information on both germ and somatic cells within teleost testis during annual reproductive cycle, along with insights into the molecular regulation of spermatogonia dynamics, which lay the foundation for spermatogenesis regulation and germplasm preservation of endangered species.

overall_design: the testiticular cells were isolated from black rockfish testis at different stages, then scRNAseq was performed to dissect dynamic cellular transcriptional atlas of adult teleost testis development throughout the annual reproductive cycle


title: Quality evaluation of Enzymatic Methyl-seq library constructed using crude cell lysate

city: Yokohama

first: Yuki

last: Tanaka

address: 1-7-22 Suehiro-cho, Tsurumi-ku

department: Center for Integrative Medical Sciences

institute: RIKEN

type: Methylation profiling by high throughput sequencing

summary: Enzymatic Methyl-seq (EM-seq) is an enzyme-based method giving us reliable methylome data from small amounts of purified DNA. However, it is unclear whether EM-seq library can be constructed from crude cell lysate containing genomic DNA. We evaluated the quality of EM-seq libraries directly prepared from crude cell lysate.

overall_design:
We prepared the crude cell lysate containing genomic DNA from human induced pluripotent stem cells (iPSCs).
We then constructed the EM-seq libraries using crude cell lysate that contained genomic DNA of 10, 50, and 200 ng (crude-10ng, crude-50ng, and crude-200ng, respectively). We also constructed the libraries using purified genomic DNA of 10, 50, and 200 ng inputs (purified-10ng, purified-50ng, and purified-200ng, respectively).

first: Risa

last: Mizuguchi

first: Norio

last: Koseki

first: Harukazu

last: Suzuki

first: Takahiro


title: Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [snATAC-Seq]

city: West Hollywood

first: AGCT

last: Core

address: 8687 Melrose Ave, PDC B230

department: BMS

institute: Cedars Sinai Medical Center

summary: The steps governing healing with or without fibrosis within the same microenvironment are unclear. After acute kidney injury (AKI), the injured proximal tubular epithelial cells activate Sox9 for self-restoration. Using head-to-head comparison of injury- induced Sox9-lineages via spatiotemporal mapping, single-cell sequencing, and single-nuclei chromatin accessibility profiling, we identified a dynamic SOX9 switch. Lineages that regenerated epithelia silenced SOX9 and healed without fibrosis (SOX9on-off). In contrast, lineages that maintained Sox9 activity in attempt to regenerate, demarcated by SOX9-induced Cadherin 6 (SOX9on-on CDH6pos ) cell state, generated single-cell Wnt activity to provoke a fibroproliferative response in adjacent fibroblasts, driving AKI to chronic kidney disease. Transplanted human kidneys displayed similar SOX9/CDH6/WNT2B responses post-injury. Thus, we uncovered a mechanism linking fibrosis to sustained efforts to regenerate the injured tissue.

overall_design: single-nuclei ATACseq datasets of the day10 FACS-enriched Sox9-lineage cells from the acutely injured murine kidneys. Two biological replicates.

first: Shikhar

last: Aggarwal

first: Zhanxiang

first: David

last: Rincon Fernandez Pacheco

first: Anna

last: Rinaldi

first: Alex

last: Rajewski

first: Jasper

last: Callemeyn

first: Elisabet

last: Van Loon

first: Baptiste

last: Lamarthée

first: Ambart

last: Covarrubias

first: Jean

last: Hou

first: Michifumi

last: Yamashita

first: Haruhiko

last: Akiyama

first: S

last: Ananth Karumanchi

first: Clive

last: Svendsen

first: Paul

middle: W

last: Noble

first: Stanley

last: Jordan

first: Joshua

last: Breunig

first: Maarten

last: Naesens

first: Pietro

last: Cippà

first: Sanjeev

last: Kumar


title: Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [CUT&Run]

first: AGCT

last: Core

overall_design: Cut&Run datasets from Sox9, H3K4me3 and input samples generated from sorted/enriched Sox9-lineage cells in murine kidneys at 2 and 10 days post injury. Each group containing 4 biological replicates.

first: Shikhar

last: Aggarwal

first: Zhanxiang

last: Wang

first: David

last: Rincon Fernandez Pacheco

first: Anna

last: Rinaldi


title: Single-cell chromatin landscape of non-myocytes reveals AP-1 as a key transcriptional regulator contributing to highly cooperative networks among non-myocyte subtypes during zebrafish heart regeneration [ATAC-seq]

city: Chapel Hill

first: LI

last: QIAN

address: 111 Mason Farm Road, MBRB

department: Department of pathology

institute: UNC

summary: We applied single-cell Assay for Transposase Accessible Chromatin using sequencing (scATAC-seq) to determine the intrinsic genetic programs underlying nonCM subpopulation determination during zebrafish heart regeneration at a single cell level. A total of approximately 13,000 single non-CMs derived from zebrafish hearts isolated at different time points during heart regeneration were measured and defined into diverse cell populations, exploited for cell type-specific cis-regulatory elements and enriched motifs as control catalog of downstream cell-state-determining transcription factors.

overall_design: To assess the dynamics of chromatin lanscape of non-CMs during zebrafish heart regeneration, we collected the hearts from 7 days post amputation and lysis the nuclei to perform scATAC-seq.

first: Yanhan

last: Dong

first: Yuchen

last: Yang

first: Jiandong

last: Liu


title: Presence of a Neomycin selection cassette in the Amigo1 locus alters gene expression in the olfactory epithelium leading to region-specific defects in olfactory receptor neuron development

city: Montreal

first: Jean-François

last: Cloutier

address: 3801 University

department: Neurology and Neurosurgery

institute: The Neuro

summary: During development of the nervous system, neurons connect to one another in a precisely organized manner. Sensory systems provide a good example of this organization, whereby the composition of the outside world is represented in the brain by neuronal maps. Establishing correct patterns of neural circuitry is crucial, as inaccurate map formation can lead to severe disruptions in sensory processing. In rodents, olfactory stimuli modulate a wide variety of behaviours essential for survival. The formation of the olfactory glomerular map is dependent on molecular cues that guide olfactory receptor neuron axons to broad regions of the olfactory bulb and on cell adhesion molecules that promote axonal sorting into specific synaptic units in this structure. Here, we demonstrate that the cell adhesion molecule Amigo1 is expressed in a subpopulation of olfactory receptor neurons, and we investigate its role in the precise targeting of olfactory receptor neuron axons to the olfactory bulb using a genetic loss-of-function approach in mice. While ablation of Amigo1 did not lead to alterations in olfactory sensory neuron axonal targeting, our experiments revealed that the presence of a neomycin resistance selection cassette in the Amigo1 locus can lead to off-target effects that are not due to loss of Amigo1 expression, including unexpected altered gene expression in olfactory receptor neurons and reduced size of glomeruli in the ventral region of the olfactory bulb. Our results demonstrate that insertion of a neomycin selection cassette into the mouse genome can have specific deleterious effects on the development of the olfactory system and highlight the importance of removing antibiotic resistance cassettes from genetic loss-of-function mouse models when studying olfactory system development.

overall_design: Whole Olfactory Epithelium was dissected from postnatal day 7 mice from three different genotypes for a total of seven samples. One sample was from a wild-type mouse. 3 samples were from Amigo1-/- mice. 3 samples were from Amigo1neo/neo mice (these mice have an insertion of a neomycin cassette in the Amigo1 locus, replacing the Amigo1 coding region)

first: Reesha

last: Raja

first: Emilie

last: Dumontier

first: Alina

last: Phen


title: BCL6 is required for the thymic development of TCRαβ+CD8αα+ intraepithelial lymphocyte lineage

city: Beijing

first: Chen

address: Haidian District

department: Institute for Immunology and School of Medicine

institute: Tsinghua University

summary: TCRαβ+CD8αα+ intraepithelial lymphocytes (CD8αα+ αβ IELs), a specialized subset of T cells in the gut epithelium, develop from thymic agonist-selected IEL precursors (IELps). The molecular mechanisms underlying the selection and differentiation of this T cell type in the thymus are largely unknown. Here, we found that Bcl6 deficiency in αβ T cells resulted in nearly the absence of CD8αα+ αβ IELs. BCL6 was expressed by approximately 50% of CD8αα+ αβ IELs but the majority thymic PD1+ IELps post agonist selection; its deficiency blocked early IELp generation in the thymus. Moreover, BCL6 expression in IELps was induced by thymic TCR signaling in an ERK-dependent manner. As a result of Bcl6 deficiency, the precursors of IELps among CD4+CD8+ double positive (DP) thymocytes exhibited increased apoptosis during agonist selection, and impaired IELp differentiation and maturation. Taken together, our results elucidate BCL6 as a crucial transcription factor during the thymic development of CD8αα+ αβ IELs.

overall_design: For in vitro samle: sorted CD4+CD8+ DP thymocytes and in vitro cultured with plate-bound a-CD3(8μg/ml)+a-CD28(8μg/ml) for 24h, then sorted CD4-CD8- DN cells for in vitro bulk RNAseq. For in vivo sample: sorted CD4-CD8-CD5+TCRb+ thymocytes (agonist-p) from Bcl6-wt and Bcl6-cko mice for RNAseq

first: Qi

last: Xing

first: Xiaohong

last: Zhao


title: Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [RNA-Seq 2]

overall_design: RNAseq datasets from FACS-sorted (enriched) control uninjured Slc34a1 expressing proximal tubular epithelial cells (PTECs), cells that activate Sox9 at 48h after kidney ischemia reperfusion injury (IRI), and cells the express Sox9 at d14 after kidney IRI. Each group containing 3 biological replicates.

first: Alex

last: Rajewski

first: Jasper

last: Callemeyn

first: Elisabet

last: Van Loon

first: Baptiste

last: Lamarthée

first: Ambart

last: Covarrubias

first: Jean

last: Hou

first: Michifumi

last: Yamashita

first: Haruhiko

last: Akiyama

first: S

last: Ananth Karumanchi

first: Clive

last: Svendsen

first: Paul

last: Noble

first: Stanley

last: Jordan

first: Joshua

last: Breunig

first: Maarten

last: Naesens

first: Pietro

last: Cippà

first: Sanjeev


title: Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys

first: AGCT

last: Core

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

overall_design: Refer to individual Series


title: Spatial microniches of IL-2 synergize with IL-10 to drive lung migratory Th2 cells in response to inhaled allergen [scRNA-Seq]

city: Pittsburgh

first: Amanda

middle: Catherine

last: Poholek

address: 4401 Penn Ave., Rangos Research Center 8129

department: Pediatrics

institute: University of Pittsburgh

summary: The mechanisms that guide Th2 cell differentiation in barrier tissues are unclear but important for the development of allergic asthma. Using temporal, spatial and single cell transcriptomic tracking of house dust mite (HDM) specific T cells, we describe the molecular pathways driving allergen-specific Th2 cells. Early Blimp-1 expression occurs in a subset of CD4 T cells in the lymph node prior to lung migration driven by IL-10 from allergen-specific T cells, but was not required for GATA3 upregulation. Instead, IL-2 via STAT5 was required to directly repress Bcl6 and Bach2 to support GATA3 and Blimp-1 upregulation. Loss of Blimp-1 during priming in the lymph node ablated the formation of Th2 cells that migrate to the lung, indicating early Blimp-1 promotes the population of Th2 cells with migratory capability. Spatial microniches of IL-2 in the lymph node discriminate and support these earliest Blimp-1+ migratory Th2 cells, demonstrating that lymph node localization is a primary driver of differentiation. Our findings illuminate the molecular pathways for inhaled allergens to promote Th2 cells and identify an early requirement for IL-2 mediated spatial microniches and allergen-driven IL-10 from responding T cells that drive allergic asthma.

overall_design: 1DER CD45.1 Tg T cells were adoptively transferred to CD45.2 host, followed by intrasnasal immunization with 25ug of house dust mite daily for three days. On the fourth day, mediastinal lymph  nodes were harvested and dissociated for scRNAseq + CITEseq (Totalseq B0178 anti-mouse CD45.1)

first: Kun

last: He

first: Isha

last: Mehta


title: Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [RNA-Seq 1]

overall_design: RNAseq datasets from FACS-sorted (enriched) control cells that activate Axin2, a reporter of canonical Wnt pathway, "the Wnt responsive cells"; and the myofibroblast population early after kidney ischemia reperfusion injury (IRI) induced AKI. To this end, tamoxifen was administered at d2, and d4 to Axin2CreERT2/+:R26RtdT/+:Acta2-GFP animals, and at d6 dual positive (tdT positive and GFP positive) and tdT negative, GFP positive cells were enriched via FACS.  3 biological replicates.

first: Shikhar

last: Aggarwal

first: Zhanxiang

last: Wang

first: David

last: Rincon Fernandez Pacheco

first: Anna

last: Rinaldi

first: Alex

last: Rajewski

first: Jasper

last: Callemeyn

first: Elisabet

last: Van Loon

first: Baptiste

last: Kumar


title: Unraveling the Complex Relationship Between mRNA and Protein Abundance: A Machine Learning-Based Approach for Imputing Protein Levels from RNA-seq Data

city: Cleveland

first: Peng

last: Jiang

state: OH

address: 2121 Euclid Ave

institute: Cleveland State University

summary: The context-dependent correlation between mRNA and protein abundance has long been debated. RNA sequencing (RNA-seq), a high-throughput, commonly used method for analyzing transcriptional dynamics and identifying biomarkers, leaves questions about whether we can translate RNA-seq-identified gene signatures directly to protein changes. In this study, we utilized a set of 17 widely assessed immune and wound healing mediators in the context of canine Volumetric Muscle Loss (VML) to investigate the correlation of mRNA and protein abundance. Our data reveal an overall agreement between mRNA and protein levels on these 17 mediators when examining samples from the same experimental condition, such as the same wound biopsy. However, we observed a lack of correlation between mRNA and protein levels for individual genes under different conditions, underscoring the challenges in converting transcript level changes directly into corresponding protein level changes. As an initial attempt to address this discrepancy, we developed a machine-learning model to predict protein abundances from RNA-seq data, achieving high accuracy (Spearman's Rho: 0.78-0.99, imputed versus measured protein abundance; pooling all biopsies; 5-fold cross-validation). Our approach also effectively corrected multiple extreme outliers measured by antibody-based protein assays. Additionally, this model has the potential to detect post-translational modification events, as shown by accurately estimating activated transforming growth factor (TGF)-β1 levels. While preliminary, this study introduces a promising strategy for translating RNA-seq data into protein abundance and the associated biological relevance.

overall_design: The in vivo studies described herein have been approved by the s Institutional Animal Care and Use Committee at the University of Pittsburgh. A VML defect was created in the quadriceps muscles of ten female dogs. Tissue biopsy samples were collected at various intervals from day 1 to 42 following injury. The dogs were prepared for surgery by sedation, shaving of the surgical site, scrubbing with 70% ethyl alcohol, followed by a topical 10% povidone-iodine solution. and induction of surgical plane anesthesia with 2% thiopental sodium, intubation and maintenance with 1-3% isoflurane. A 10 cm long x 4 cm wide area was defined and an initial incision point at the greater trochanter that extended to the lateral epicondyle.  The subcutaneous tissue was bluntly dissected and the skin retracted to visualize the biceps femoris.  The underlying muscle tissue and fascia were surgically excised to a depth of 2-3 cm.  The depth of excision depended upon individual dog anatomy. This procedure results in the removal of between 50-70% of total muscle mass loss. The overlying skin was removed to leave an open wound that mimicked trauma-induced VML in the clinical setting.   The upper leg and wound site were covered with sterile dressings and all animals were administered antibiotic prophylaxis for the first 5 days post-surgery (cephalexin, 25 mg/kg) and analgesic every 8-12h for the first 5 days (buprenorphine, 0.002 mg/kg).  The overall health of each dog, including temperature, appetite, and activity levels, was monitored daily.  The dogs were fed a high-energy, high-protein diet (Advanced Protocol High-Density Canine Diet; PMI Nutrition LLC, Henderson, CO, USA) and provided unlimited access to water.

first: Archana

last: Prabahar

first: Ruben

last: Zamora

first: Derek

last: Barclay

first: Jinling

last: Yin

first: Mahesh

last: Ramamoorthy

first: Atefeh

last: Bagheri

first: Scott

last: Johnson

first: Stephen

last: Badylak

first: Yoram

last: Vodovotz


title: RNA sequencing data from wild type and Mst1/2 knockout esophageal epithelium

city: Shanghai

first: Yongchun

last: Zhang

state: Shanghai

address: 800 Dongchuan RD. Minhang District

department: School of Life Sciences and Biotechnology

institute: Shanghai Jiao Tong university

summary: Hippo signaling regulates the homeostasis of multiple organs. Mst1 and Mst2 (Mst1/2) are critical components of the Hippo signaling pathway. Here, we utilized RNA sequencing to determine the transcriptional change in the esophageal epithelium upon Mst1/2 deletion. The analysis of gene expression profiles allows us to understand the role of Mst1/2 in the regulation of various biological processes in the esophageal epithelium.

overall_design: Wild type (WT) and p63CreERT2;Mst1loxp/loxp;Mst2-/- (KO) mice were administered 3 doses of tamoxifen every 2 weeks. RNA was extracted from the esophageal epithelium after around 8 weeks and sequenced.

first: Yu

first: Haidi

last: Huang

first: Jiangying

last: Liu


title: Spatial microniches of IL-2 synergize with IL-10 to drive lung migratory Th2 cells in response to inhaled allergen

first: Amanda

last: Poholek


title: Efavirenz and Fexofenadine ameliorates the propagation of alpha-synuclein

city: Suwon-si

first: Sang Myun

last: Park

state: Gyeonggi-do

address: 164, Worldcup-ro, Yeongtong-gu

department: Pharmacology

country: South Korea

institute: Ajou University School of Medicine

summary: Current treatments for Parkinson's disease include drug therapy with L-DOPA and MAO-A inhibitors, as well as surgical methods like deep brain stimulation, which can delay disease progression but are not curative. Numerous clinical trials are underway for the development of new drugs, but no approved drugs exist yet.  In this study, a list of drugs that included efavirenz and fexofenadine was provided through deep learning. Using these drugs, it was found that they can alleviate the propagation of alpha-synuclein and reduce neuroinflammation in vitro models, in vivo mice, and C.elegans models. RNA-seq and IPA analyses revealed that efavirenz has an effect through the activation of CYP46A1 and the regulation of cholesterol metabolism. also, fexofenadine has an effect inflammation via regulating infiltrated peripheral immune cells. This study not only sheds light on the mechanism of propagation in Parkinson's disease but also suggests the potential use of efavirenz and fexofenadine as a potential treatment for Parkinson's disease through drug repurposing.

overall_design: To investigate the mechanisms of efavirenz, we performed an animal experiment in which we treated the striatum of M83 alpha-synuclein A53T Tg mice with 10 μg of alpha-synuclein PFF and administered efavirenz or fexofenadine for 4 weeks. Subsequently, we extracted RNA from the cortex and performed RNA-seq.

first: Jae-bong

last: Kim

first: Doyoon

first: SeungHo

first: HyunGoo

last: Woo

first: SangMyun


title: Alternative splicing of ALDOA determines tamoxifen resistance in breast cancer

city: yangzhou

last: Shiyi

state: Jiangsu

address: hanjiang district jiangyangzhonglu136, Hanjiang district, Jiangyangzhonglu 136

institute: yangzhou university

summary: Via analyzing the landscape of AS events in primary and relapse breast tumors from patients receiving tamoxifen-based therapy, it was revealed that exon skipping (ES) of exon 7.2 in 5’UTR of ALDOA pre-mRNA is associated with tamoxifen resistance. Therefore, RNA Sequencing is performed for MCF7-TAMR cells infected with ctr or ALDOA shRNAs to identify the molecular mechanism of ALDOA in mediating TAM resistance in breast cancer cells.

overall_design: We established MCF7-TAMR cell lines in which ALDOA was knockdowned by shRNA targeting ALDOA.

first: Shiyi

last: Yu

first: Haibo

last: Sun


title: Impact of exogenous IL-1ß stimulation on equine embryonic stem cell-derived tenocytes in three-dimensional culture

city: Hatfield

first: Ross

middle: Eric

last: Beaumont

state: Hertfordshire

address: Hawkshead Ln

department: Clinical science and services

institute: Royal Veterinary College

summary: Exogenous IL-1ß stimulation impacts tendon-associated and inflammatory gene expression in equine adult tenocytes but has no impact on embryonic stem cell (ESC)-derived tenocytes in two-dimensional culture. Whether these effects translate to the transcriptome-wide level in three-dimensional (3D) culture in unknown. Utilising RNA-Sequencing, we report that ESC-tenocytes have zero differentially expressed genes following two-weeks of IL-1ß stimulation with similar collagen gel contraction values between the control and IL-1ß conditions, respectively.

overall_design: We examined global gene expression profiles of three biological replicates of equine embryonic stem cell-derived tenocytes following two weeks of exogenous IL-1ß stimulation (1 nM) versus control. To examine if there were any differentially expressed genes between the two conditions, we utilised DESeq2 (LogFC >1 + padj<0.05) following Salmon alignment and tximport.

first: Beaumont

last: Ross

first: Smith

last: Emily

first: Guest

last: Debbie


title: High-fat and high-sucrose diet impairs female reproduction by altering ovarian transcriptomic and metabolic signatures

city: Jinan

first: Shan

last: Han

address: Wenhua West road

institute: Shandong University

summary: Excessive energy intake in modern society has led to an epidemic surge in metabolic diseases, such as obesity and type 2 diabetes. These disorders pose profound threats to women’s reproductive health. However, the precise impact and underlying pathogenesis of energy excess on female reproduction remain unclear. In this study, we established an obese and hyperglycemic female mouse model induced by a high-fat and high-sucrose (HFHS) diet, mimicking the modern lifestyle of overnutrition. These mice displayed marked reproductive dysfunction, including elevated serum testosterone levels, irregular estrous cycles, and impaired folliculogenesis. Analysis of the ovarian metabolome of the HFHS mice revealed a pronounced disturbance in amino acid metabolism. Transcriptomic profiling of these ovaries identified dysregulated genes involved in steroid hormone biosynthesis and glucolipid metabolism. Further multi-omic analysis unveils aberrations in ovarian arginine biosynthesis metabolism induced by HFHS diet. Notably, comparisons between HFHS mice and a cohort of women with polycystic ovary syndrome (PCOS) identified analogous reproductive and metabolic signatures. Therefore, our results provide direct in vivo evidence for the detrimental effects of overnutrition on female reproduction and offer insights into the metabolic underpinnings of PCOS.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for ovarians of HFHS mice and its NCD controls

first: Congcong

first: Yuqing


title: Transcriptomic analysis and fusion gene identification of Exos, MPs, MBRs

city: Bundoora

first: Wittaya

last: Suwakulsiri

state: Victoria

address: Plenty Road and, Kingsbury D

department: Biochemistry and Chemistry

institute: La Trobe University

summary: Previously, we reported that human primary (SW480) and metastatic (SW620) colorectal (CRC) cells secrete (shed) midbody remnants (MBRs), exosomes (Exos), and microparticles (MPs) are molecularly distinct at the protein level. To gain further biochemical insights into MBRs, Exos, and MPs and their emerging role in CRC, we performed, and report here for the first time, a comprehensive transcriptome and long noncoding RNA sequencing analysis and fusion gene identification of these three EV classes using the next-generation RNA sequencing technique. Differential transcript expression analysis revealed that MBRs have a distinct transcriptomic profile compared to Exos and MPs with a high enrichment of mitochondrial transcripts lncRNA/pseudogene transcripts that are predicted to bind to ribonucleoprotein complexes, spliceosome and RNA/stress granule proteins. A salient finding from this study is a high enrichment of several fusion genes in MBRs compared to Exos, MPs and cell lysates from their parental cells such as MSH2 (gene encoded DNA mismatch repair protein MSH2). This suggests potential EV-liquid biopsy targets for cancer detection. Importantly, the expression of cancer progression-related transcripts found in EV classes derived from SW480 (EGFR) and SW620 (MET and MACCA1) cell lines reflects their parental cell types. Our study is the first discovery of RNA and fusion gene compositions within MBRs (including Exos and MPs) that could have an impact on EV functionality in cancer progression and detection using EV-based RNA/ fusion gene candidates for cancer biomarkers

overall_design: To investigate transcriptomic profiles of Exos, MPs, MBRs

first: Richard

last: Simpson


title: Repeated Immunization with ATRA-containing Liposomal Adjuvant Transdifferentiates Th17 Cells to a Tr1-like Phenotype

city: Copenhagen

first: Katharina

last: Wørzner

address: Artillerivej 5

institute: Statens Serum Institut


title: Gene expression analysis of  the cochlea of Opa1 KO mice

city: Lyon

first: Frédéric

last: Flamant

state: France

address: 46 allée d'Italie

department: IGFL

institute: ENSL

summary: RNA was extracted from dissected cochlea at post-natal day 15, from either Opa1+/- mice of their wild-type littermates.

overall_design: 4 WT samples, 4 heterozygote samples.

first: Corentin

last: Alfortit

first: Frederic

first: Jing

last: Wang

first: Romain

last: Guyot


title: Chromatin Chromatin remodeling protein CHD4 regulates axon guidance of spiral ganglion neurons in developing inner ear

city: Piscataway

first: Kelvin

middle: Y.

last: Kwan

state: NJ

address: 604 Allison Rd.

department: Cell Biology & Neuroscience

institute: Rutgers University

summary: The chromodomain helicase binding protein 4 (CHD4) is an ATP-dependent chromatin remodeler—De-novo pathogenic variants of CHD4 cause Sifrim-Hitz-Weiss syndrome (SIHIWES). Patients with SIHIWES show delayed development, intellectual disability, facial dysmorphism, and hearing loss. Many cochlear cell types, including spiral ganglion neurons (SGNs), express CHD4. SGNs are the primary afferent neurons that convey sound information from the cochlea, but the function of CHD4 in SGNs is unknown. We employed the Neurog1(Ngn1) CreERT2 Chd4 conditional knockout animals to delete Chd4 in SGNs. SGNs are classified as type I and type II neurons. SGNs lacking CHD4 showed abnormal fasciculation of type I neurons along with improper pathfinding of type II fibers. CHD4 binding to chromatin from immortalized multipotent otic progenitor-derived neurons was used to identify candidate target genes in SGNs. Gene ontology analysis of CHD4 target genes revealed cellular processes involved in axon guidance, axonal fasciculation, and ephrin receptor signaling pathway. We validated increased Epha4 transcripts in SGNs from Chd4 conditional knockout cochleae. The results suggest that CHD4 attenuates the transcription of axon guidance genes to form the stereotypic pattern of SGN peripheral projections. The results implicate how epigenetic changes affect circuit wiring by modulating axon guidance molecule expression and provide insights into neurodevelopmental diseases.

overall_design: CUT&Tag for CHD4, H3K4me3, p300 and IgG control from proliferating iMOPs (immortablized mutipotent otic progenitors) and iMOP-derived neurons.

first: Kim

last: Jihyun

first: Martinez

last: Edward

first: Qiu

last: Jingyun

first: Ni

last: Julie

first: Kwan

last: Kelvin Y.


title: TF ChIP-seq from whole organism (ENCSR791QVO)

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

institute: ENCODE DCC

summary:
ChIP-seq against eGFP-eor-1 in L3 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Senolytic treatment alleviates doxorubicin-induced chemobrain

city: Gainesville

first: Thomas

last: Foster

state: FL

address: 1149 S Newell Dr.

department: Neuroscience

institute: University of Florida

summary: Doxorubicin (Dox) is a widely used treatment for cancer, which can result in chemotherapy induced cognitive impairments (chemobrain). Chemobrain is associated with inflammation and oxidative stress similar to aging. As such, Dox treatment has also been used as a model of aging. However, it is unclear if Dox induces brain changes similar to that observed during aging, since Dox does not readily enter the brain. Rather, the mechanism for chemobrain likely involves induction of peripheral cellular senescence and the release ofsenescence-associated secretory phenotype (SASP) factors, which enter the brain to disrupt cognition. We examined the effect of Dox on peripheral and brain markers of aging and cognition. In addition, we employed the senolytic, ABT-263, which also has limited access to the brain. While Dox treatment influenced several measures linked to aging, including peripheral inflammation, morphological measure of microglial activation, cognition, and synaptic function,the effects of Dox treatment on brain (i.e. dentate gyrus) gene expression did not approximate aging to the same degree as other measures.Regardless, ABT-263 prevent or limited most of the Dox induced effects, including brain gene expression. The resultsemphasize a link between cognitive decline and the release of SASP factors from peripheral senescent cells and indicate thatdifferences between aging and Dox treatment on brain gene expression are important in considering Dox treatment as a model of aging.

overall_design: Transcriptional profiles were analyzed in the DG sub-region of hippocampus from rats belonging to various groups: Young (Total n = 26); Vehicle (n = 10),  DOX (n = 8), DOX + ABT-263 (n = 8) treated rats.

first: Vivekananda

last: Budamagunta

first: Ashok

last: Kumar

first: Asha

last: Rani

first: Linda

last: Bean

first: Sahana

last: Sindhu

first: Yang

last: Yang

first: Daohong

last: Zhou


title: Global PUS1 mRNA targets detection by STAMP

city: Guangzhou

first: Yan-Xia

last: Hu

state: Guangdong

address: 600 Tianhe Road, Tianhe District

institute: The Third Affiliated Hospital, Sun Yat-sen University

summary: Recently, several studies revealed that pseudourine exists on mRNA. However, identification of ψ sites for specific PUS remains a certain ambiguity. PUS1, an important pseudouridine synthase, plays a critical role in cell growth and tumorigenesis of HCC. Here, we utilized an IP-free approach, Surveying Targets by APOBEC-Mediated Profiling (STAMP) and analyzed C-to-U editing sites to realize PUS1-bound mRNAs. And then, we identified the potential mRNA pseudouridylation targets of PUS1 by intersecting editing sites’ host genes with these that known to pseudouridylated.

overall_design: To delineate the landscape of mRNA targets of PUS1, we utilized an IP-free approach, STAMP, wherein APOBEC1 was fused to PUS1 and facilitated C-to-U editing of PUS1-bound mRNAs. Subsequently, we performed RNA-seq to analyze the whole transcriptome, followed by detection of C-to-U editing. The editing sites only emerged in PUS1-APOBEC1 overexpressed Hep3B cells were considered for further analysis. Since pseudouridylated mRNAs have been extensively identified by high-throughput sequencing methods, to further reduce false-positive, we intersected editing sites’ host genes with these that known to pseudouridylated using StarBase V2.0 (https://starbase.sysu.edu.cn/starbase2/).

first: Li-Ting

last: Diao

first: Ya-Rui

last: Hou

first: Zhen-Dong

last: Xiao


title: Neoadjuvant and adjuvant pembrolizumab for advanced high-grade serous carcinoma (NeoPembrOV): A randomized phase II GINECO clinical trial

first: Olivia

last: Le Saux

address: 28 rue Laennec

institute: Cancer Research Center of Lyon

summary: PD-1/PD-L1 blockade did not show survival benefit in high grade ovarian carcinomas. By using paired samples from the NeoPembrOv randomized phase II trial and by combining RNA-seq and multiplexed immunofluorescence stainings, we explored the impact of NeoAdjuvant ChemoTherapy (NACT) ± Pembrolizumab (P) on the tumor environment and identified parameters correlating to response. 1) The combination therapy resulted in a significant increase of intraepithelial CD8+PD-1+ T cells that correlated to clinical benefit. 2) High CD8B/FOXP3 and high CD8B/ENTPD1 ratios were significantly associated with response to NACT+P, while KDR and VEGFR2 expression were associated with resistance. 3) Combining endothelial and monocyte signatures and the CD8B/FOXP3 ratio predicted response to NACT+P with an AUC of 0.93 (95% CI 0.84–1.00). These results indicate that targeting regulatory T cells and endothelial cells, especially VEGFR2+ endothelial cells, could overcome ovarian cancer immune resistance.

overall_design: We explored the impact of NeoAdjuvant ChemoTherapy (NACT) ± Pembrolizumab (P) on the tumor environment.

first: Maude

last: Ardin

first: Justine

last: Berthet

first: Sarah

last: Barrin

first: Morgane

last: Bourhis

first: Yasmine

last: Lounici

first: Isabelle

last: Treilleux

first: Pierre-Alexandre

last: Just

first: Guillaume

last: Bataillon

first: Aude-Marie

last: Savoye

first: Marie-Ange

last: Mouret-Reynier

first: Elodie

last: Coquan

first: Olfa

last: Derbel

first: Louis

last: Jeay

first: Suliman

last: Bouizaguen

first: Intidhar

last: Labidi-Galy

first: Séverine

last: Tabone-Eglinger

first: Eric

last: Tartour

last: Galy-Fauroux

first: Marc-Henri

last: Stern

first: Magali

last: Terme

first: Christophe

last: Caux

first: Bertrand

last: Dubois

last: Ray-Coquard