title: ATAC-seq from forebrain (ENCSR810HQR)

summary:
ATAC-seq on embryonic e14.5 mouse forebrain

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: ATAC-seq from GM18868 (ENCSR580JBA)

status: Public on Apr 22 2021

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

country: USA

institute: ENCODE DCC

type: Genome binding/occupancy profiling by high throughput sequencing

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: ATAC-seq from RWPE2 (ENCSR080SNF)

summary:
ATAC-seq on human cell line RWPE-2

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: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR579DBA)


title: ATAC-seq from hindbrain (ENCSR312LQX)

summary:
ATAC-seq on postnatal p0 mouse hindbrain

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: DNase-seq from activated T-cell (ENCSR810CTB)


title: ATAC-seq from K562 (ENCSR582NPJ)

summary:
ATAC-seq on human cell line 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: ATAC-seq from intestine (ENCSR079GOY)

summary:
ATAC-seq on postnatal p0 mouse intestine

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: DNase-seq from activated T-cell (ENCSR312INU)


title: ATAC-seq from K562 (ENCSR803QIE)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR324SGE)


title: ATAC-seq from GM19397 (ENCSR839IAD)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR801VSK)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR566HLQ)


title: ATAC-seq from forebrain (ENCSR310MLB)

summary:
ATAC-seq on postnatal p0 mouse forebrain

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: ATAC-seq from GM18873 (ENCSR304ZDQ)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR075MQZ)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR799MAX)


title: ATAC-seq from K562 (ENCSR304UWR)


title: ATAC-seq from spleen (ENCSR078EBD)

summary:
ATAC-seq on human spleen

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: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR799MVH)


title: ATAC-seq from forebrain (ENCSR559FAJ)

summary:
ATAC-seq on embryonic e12.5 mouse forebrain

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: DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR565RQI)


title: DNase-seq from liver (ENCSR561FZE)


title: DNase-seq from heart left ventricle (ENCSR070CMW)


title: DNase-seq from suppressor macrophage (ENCSR069ICJ)


title: ATAC-seq from cerebellum (ENCSR554JQP)

summary:
mouse cerebellum

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: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR553WJB)


title: ATAC-seq from HG03097 (ENCSR608KJD)


title: ATAC-seq from HG03175 (ENCSR305XRF)


title: ATAC-seq from hindbrain (ENCSR798FDL)

summary:
ATAC-seq on embryonic e14.5 mouse hindbrain

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: ATAC-seq from K562 (ENCSR303NUP)


title: ATAC-seq from heart (ENCSR068YGC)

summary:
ATAC-seq on embryonic e14.5 mouse heart

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: DNase-seq from NAMALWA (ENCSR301OGM)


title: ATAC-seq from HG03280 (ENCSR554WGQ)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR323LVJ)


title: ATAC-seq from K562 (ENCSR793YFK)


title: ATAC-seq from K562 (ENCSR068MIW)


title: ATAC-seq from limb (ENCSR551WBK)

summary:
ATAC-seq on embryonic e12.5 mouse limb

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: ATAC-seq from megakaryocyte-erythroid progenitor cell (ENCSR064IHX)

summary:
PSU mouse MEP 50,000 cells ATAC-seq

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: ATAC-seq from erythroblast (ENCSR793RAV)

summary:
PSU mouse Erythroblast 50,000 cells ATAC-seq

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: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR548KXH)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR551LAH)


title: DNase-seq from MCF 10A (ENCSR789VGQ)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR541ZOU)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR543WNA)


title: ATAC-seq from K562 (ENCSR548GGF)


title: ATAC-seq from HG03196 (ENCSR063UNG)


title: ATAC-seq from liver (ENCSR302LIV)

summary:
ATAC-seq on embryonic e12.5 mouse liver

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: ATAC-seq from heart (ENCSR552ABC)

summary:
ATAC-seq on embryonic e13.5 mouse heart

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: DNase-seq from activated CD8-positive, alpha-beta T cell (ENCSR294YEJ)


title: ATAC-seq from K562 (ENCSR296YAS)


title: DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR060TTR)


title: DNase-seq from liver (ENCSR789AYI)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR050VTC)


title: DNase-seq from CD8-positive naive resting alpha-beta T cell (ENCSR044JIR)


title: ATAC-seq from HG03066 (ENCSR040PBN)


title: ATAC-seq from omental fat pad (ENCSR788TRR)

summary:
ATAC-seq on human adipose tissue of omentum

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: DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR534OJE)

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: DNase-seq from activated T-cell (ENCSR038POV)


title: ATAC-seq from HG02973 (ENCSR038WVV)


title: ATAC-seq from HG03342 (ENCSR528YDD)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR531UVE)


title: ATAC-seq from subcutaneous adipose tissue (ENCSR540BML)

summary:
ATAC-seq on human adipose tissue

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: ATAC-seq from liver (ENCSR032HKE)

summary:
ATAC-seq on embryonic e14.5 mouse liver

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: ATAC-seq from K562 (ENCSR524ZSN)

summary:
ATAC-seq on human cell line 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: ATAC-seq from liver (ENCSR785NEL)

summary:
ATAC-seq on embryonic e11.5 mouse liver

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: ATAC-seq from HG02798 (ENCSR524CPZ)


title: ATAC-seq from HG03354 (ENCSR025MEO)


title: ATAC-seq from embryonic facial prominence (ENCSR031HDN)

summary:
ATAC-seq on embryonic e12.5 mouse embryonic facial prominence

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: DNase-seq from hindbrain (ENCSR289BTM)


title: DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR294DND)


title: DNase-seq from embryonic facial prominence (ENCSR775YJL)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR287GYT)


title: ATAC-seq from body of pancreas (ENCSR515CDW)

summary:
ATAC-seq on human body of pancreas

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: ATAC-seq from GM21381 (ENCSR512YXO)


title: ATAC-seq from neural tube (ENCSR282YTE)

summary:
ATAC-seq on embryonic e11.5 mouse neural tube

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: ATAC-seq from K562 (ENCSR281LEY)


title: DNase-seq from midbrain (ENCSR773SAG)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR019MZH)


title: ATAC-seq from GM19023 (ENCSR512FHU)


title: ATAC-seq from K562 (ENCSR522ALT)


title: ATAC-seq from GM21390 (ENCSR024WOD)


title: DNase-seq from activated CD8-positive, alpha-beta T cell (ENCSR776BTO)


title: ATAC-seq from K562 (ENCSR509MYW)


title: ATAC-seq from HG03558 (ENCSR278JWM)


title: ATAC-seq from K562 (ENCSR800RAH)


title: ATAC-seq from GM21786 (ENCSR275LCF)


title: ATAC-seq from GM21367 (ENCSR509JPT)


title: ATAC-seq from kidney (ENCSR023QZX)

summary:
ATAC-seq on embryonic e15.5 mouse kidney

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: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR284GAG)


title: DNase-seq from activated CD4-positive, alpha-beta memory T cell (ENCSR021YFW)


title: ATAC-seq from body of pancreas (ENCSR773USD)


title: DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR284VNJ)


title: DNase-seq from activated T-cell (ENCSR771JQH)


title: DNase-seq from CD4-positive naive resting alpha-beta T cell (ENCSR778DWG)


title: ATAC-seq from K562 (ENCSR021GTX)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR768AWY)


title: ATAC-seq from K562 (ENCSR508LLL)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR273USD)


title: ATAC-seq from K562 (ENCSR503EZG)


title: DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR502GWQ)


title: ATAC-seq from G1E (ENCSR280ZDP)

summary:
PSU mouse G1E 50,000 cells ATAC-seq

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: ATAC-seq from Peyer's patch (ENCSR017RQC)

summary:
ATAC-seq on human Peyer's patch

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: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR765ZML)


title: ATAC-seq from K562 (ENCSR017LGQ)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR015FZF)


title: ATAC-seq from forebrain (ENCSR273UFV)

summary:
ATAC-seq on embryonic e11.5 mouse forebrain

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: DNase-seq from forebrain (ENCSR014SFF)


title: DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR274XTS)


title: ATAC-seq from transverse colon (ENCSR761TKU)

summary:
ATAC-seq on human transverse colon

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: DNase-seq from activated T-cell (ENCSR273GCF)


title: ATAC-seq from GM18520 (ENCSR762YFD)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR493IQY)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR266NDC)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR494IWJ)


title: DNase-seq from cortex (ENCSR263XCT)


title: ATAC-seq from GM18867 (ENCSR492FJO)


title: ATAC-seq from K562 (ENCSR761CBY)


title: ATAC-seq from hindbrain (ENCSR012YAB)

summary:
ATAC-seq on embryonic e11.5 mouse hindbrain

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: ATAC-seq from ovary (ENCSR490MSG)

summary:
ATAC-seq on human ovary

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: ATAC-seq from embryonic facial prominence (ENCSR261ICG)

summary:
ATAC-seq on embryonic e15.5 mouse embryonic facial prominence

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: ATAC-seq from HG03064 (ENCSR487SOP)


title: DNase-seq from suppressor macrophage (ENCSR011VJK)


title: ATAC-seq from gastroesophageal sphincter (ENCSR260ZIV)

summary:
ATAC-seq on human esophagogastric junction

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: DNase-seq from forebrain (ENCSR756SPS)

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: ATAC-seq from megakaryocyte (ENCSR498DQA)

summary:
PSU mouse Megakaryocyte 50,000 cells ATAC-seq

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: DNase-seq from MCF 10A (ENCSR752EPH)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR010TMX)


title: ATAC-seq from K562 (ENCSR259HTB)


title: ATAC-seq from HG03571 (ENCSR000RBT)


title: DNase-seq from transverse colon (ENCSR760QZM)


title: ATAC-seq from stomach (ENCSR486XAS)

summary:
ATAC-seq on embryonic e15.5 mouse stomach

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: ATAC-seq from kidney (ENCSR758IRM)

summary:
ATAC-seq on embryonic e14.5 mouse kidney

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: DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR474HQW)


title: DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR471RHG)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR470QCE)


title: DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR749YCR)


title: ATAC-seq from HG03060 (ENCSR470ZNM)


title: DNase-seq from SK-N-DZ (ENCSR000FJL)


title: DNase-seq from kidney tubule cell (ENCSR257CIZ)


title: DNase-seq from heart (ENCSR749ILN)


title: DNase-seq from NCI-H460 (ENCSR000FJH)


title: ATAC-seq from K562 (ENCSR741QNS)

summary:
ATAC-seq on human cell line 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: ATAC-seq from K562 (ENCSR745KUZ)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR740DJQ)


title: DNase-seq from activated CD4 positive, naive alpha-beta T cell (ENCSR478SWA)


title: ATAC-seq from GM18907 (ENCSR487QSB)


title: ATAC-seq from liver (ENCSR255XTC)

summary:
ATAC-seq on embryonic e16.5 mouse liver

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: ATAC-seq from GM18858 (ENCSR011NJP)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR486FMF)


title: ATAC-seq from midbrain (ENCSR468GUI)

summary:
ATAC-seq on embryonic e15.5 mouse midbrain

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: ATAC-seq from K562 (ENCSR737HKX)


title: DNase-seq from K562 (ENCSR000EOT)

summary:
UW human K562 DNase-seq P5 wild type

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: ATAC-seq from granulocyte monocyte progenitor cell (ENCSR257PGU)

summary:
PSU mouse GMP 50,000 cells ATAC-seq

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: DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR735MJZ)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR467LJT)


title: ATAC-seq from K562 (ENCSR005BVE)


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR734VFU)


title: ATAC-seq from GM18511 (ENCSR253QLW)


title: DNase-seq from activated T-cell (ENCSR466SUZ)


title: DNase-seq from vagina (ENCSR733YNW)


title: Gene expression of E2f7/8/Rb1 triple mutant liver tumors

city: Utrecht

first: Bart

last: Westendorp

address: Uppsalalaan 8

department: Molecular Health Sciences

country: Netherlands

institute: Utrecht University

type: Expression profiling by high throughput sequencing

summary: E2F-transcription factors activate many genes involved in cell cycle progression, DNA repair, and apoptosis. Hence, E2F-dependent transcription must be tightly regulated to prevent tumorigenesis, and therefore metazoan cells possess multiple E2F regulation mechanism. The best-known is the Retinoblastoma protein (RB), which is mutated in many cancers. Atypical E2Fs (E2F7 and -8) can repress E2F-target gene expression independently of RB and are rarely mutated in cancer. Therefore, they may act as emergency brakes in RB-mutated cells to suppress tumor growth. Currently it is unknown if and how RB and atypical E2Fs functionally interact in vivo. Here, we demonstrate that mice with liver-specific combinatorial deletion of Rb and E2f7/8 have reduced life spans compared to E2f7/8 or Rb deletion alone. This was associated with increased proliferation and enhanced malignant progression of liver tumors. Hence, atypical repressor E2Fs and RB cooperatively act as tumor suppressors in hepatocytes. We propose that the complex interactions between atypical E2Fs and RB on maintenance of genetic stability underlie this context-dependency.

overall_design: RNA-sequencing data of four Alb-Cre-E2f7 E2f8 Rb1 conditional triple knockout liver tumors, four Alb-Cre-E2f7 E2f8 conditional double knockout liver tumors, and four age-matched wild-type mice.

first: B


title: SNAT - Single cell RNA sequencing of mouse cells sorted from sciatic nerves at postnatal day 1 (P1) and P60

city: Zurich

first: Ge

last: Tan

address: Winterthurerstrasse 190

department: Functional Genomics Center Zurich

country: Switzerland

institute: University of Zurich

summary: Sciatic nerves from P1 and from P60 mice were dissociated, and the resulting cell suspension was sorted with FACS. All cells positive for beta-actin dsred (including Schwann cells also expressing eYFP due to P0Cre-mediated recombination) were collected for RNA sequencing with 10X Genomics.

overall_design: Cells were acutely extracted from P1 and from P60 mouse sciatic nerves derived from beta actin-dsred transgenic animals. The dsred fluorescence allows the selection of dsred positive nerve cells from dsred negative debris in the suspension. Of note, Schwann cells in these experiments additionally express eYFP due to P0cre-mediated recombination. The sorted cells were further processed for library preparation using 10X Genomics. At each age, three independent Chromiun runs were performed, each run loaded with cells derived from independent biological samples. Each biological sample derives from an original cell suspension containing pooled cells extracted from male and female mice in a 1:1 ratio.

first: Daniel

last: Gerber

first: Jorge

middle: A

last: Pereira

first: Joanne

first: Slavica

last: Dimitrieva

first: Emilio

last: Yángüez

first: Ueli

last: Suter


title: SNAT - RNA sequencing of murine developing peripheral nerves

summary: RNA sequencing of peripheral nerve lysates covering various developmental stages in mice (E13.5, E17.5, P1, P5, P14, P24, P60)

overall_design: Sciatic nerves were extracted at various developmental stages: E17.5, P1, P5, P14, P24 and P60. The perineurium and overlaying layers were stripped as much as possible from these sciatic nerves prior to RNA extraction. Furthermore, peripheral nerves distal to the DRG were pooled from embryos at E13.5. Each time point consists of 4 independent biological samples. 2 of these samples derive from male animals, and  2 other samples derive from female animals.


title: SNAT - Single cell RNA sequencing of mouse sorted Schwann cells at postnatal day 5 (P5)

summary: Single cell RNA sequencing of sorted mouse Schwann cells expressing eYFP due to P0Cre-mediated recombination.

overall_design: Schwann cells were acutely extracted from P5 mouse pups which, besides of beta-actin dsred, also express eYFP upon P0cre-mediated recombination. The eYFP fluorescence allows the selection of eYFP positive Schwann cells from eYFP negative debris and non-Schwann cells in the nerve.  384-well plates were used to collect one cell per well, and these individual Schwann cells were further processed for library preparation using the SmartSeq2 chemistry. Two of these plates were sequenced at P5, each plate with cells derived from independent biological samples. The cells sorted into each plate derive from an original cell suspension containing pooled cells extracted from male and female mice in a 1:1 ratio.


title: Combination of urine exosomal mRNAs and lncRNAs as novel diagnostic biomarkers for bladder cancer

status: Public on Apr 20 2021

city: Beijing

first: Haiming

last: Huang

address: No. 8, Xishiku St., Xicheng Dist.

country: China

institute: Peking University First Hospital

summary: Total RNAs were subjected to RNA isolation and RNA-seq analyses were generated by deep sequencing using Illumina sequencing platform. We performed RNA sequencing on three matched muscle-invasive bladder cancer (MIBC) tissues with superficial tumor regions and deep infiltrating tumor regions in order to assess its potential as biomarkers. Quantitative real-time PCR were used to validate the expression pattern of mRNAs and lncRNAs in urine exosomes. Bioinformatic tools including Gene ontology, and KEGG pathway analysis were utilized.

overall_design: Sequence was performed on three matched superficial and deep infiltrating tumor regions of MIBC.

first: haiming

first: haixia

last: Li

first: jiayin

last: Hou

first: jialin

last: Du

first: bo

last: Jin

first: lu

last: Pang


status: Public on Apr 21 2021

city: New York

first: Sophie

middle: M

last: Morgani

state: NY

address: Rockefeller Research Labs, 430 E 67th St

department: Development Program

institute: Sloan Kettering Institute, MSKCC

overall_design: RNA-sequencing of Rreb1+/+ and Rreb1-/- embryonic day 7.5 mouse embryos. Mouse embryos were collected at embryonic day 7.5 from intercrosses between Rreb1+/- mice. Samples of the parietal endoderm were taken during dissection for genotyping. Embryos were immediately frozen in Trizol and RNA was extracted for sequencing once genotype was determined. Five embryos were selected from each genotype (Rreb1+/+ and Rreb1-/-) RNA-sequenced performed. se embryos were collected from Rreb1+/- intercrosses

first: Anna

middle: K

last: Hadjantonakis


title: Transgenerational effect of mutants in the RNA-directed DNA methylation pathway on the triploid block

city: Uppsala

first: Juan

middle: C

last: Santos-González

state: Uppsala

address: Almas Allé 5

department: Department of Plant Biology and Forest Genetics

country: Sweden

institute: SLU

type: Methylation profiling by high throughput sequencing

summary: Hybridizations of plants that differ in number of chromosome sets (ploidy) frequently causes endosperm failure and seed arrest, a phenomenon referred to as triploid block. Unreduced diploid gametes generated by the omission of second division1 (osd1) mutant induce the triploid block, similar as tetraploid (4x) plants. We recently found that mutations in NRPD1, encoding the largest subunit of the plant-specific RNA Polymerase IV (Pol IV), can suppress the triploid block. Pol IV generates small RNAs required to guide de novo methylation in the RNA-directed DNA methylation (RdDM) pathway. Strikingly however, mutations in other components of the RdDM pathway like RDR2 and NRPE1 fail to suppress the triploid block when inherited in the osd1 background, but have a suppressive effect as 4x mutants. In this study, we aimed at understanding the cause for this discrepancy. We found that the ability of mutants in the RdDM pathway to suppress the triploid block depends on their degree of inbreeding. While nrpd1 is able to suppress in the first homozygous generation, mutants in RDR2, NRPE1, and DRM2 require at least one additional round of inbreeding to exert a suppressive effect.  Our data thus reveal that loss of RdDM function differs in its effect in early and late generations and that Pol IV acts at an early stage of triploid block establishment.

overall_design: 6 genome-wide cytosine methylation libraries and 6 ChIP sequencing libraries. 6 genome-wide cytosine methylation libraries were generated from Arabidopsis leaves of wt, F2 and Fi nrpd1 mutants. 6 ChIP sequencing  libraries were generated from Arabidopsis leaves of wt and nrpd1 mutants.

first: Zhenxing

last: Wang

first: Nicolas

last: Butel

first: Lauriane

last: Simon

first: Cecilia

last: Wärdig

first: Claudia

last: Köhler


title: 3D-Bioprinting allows the establishment of long-term 3D culture model for Chronic Lymphocytic Leukemia cells

city: Milan

first: Anna Sofia

last: Tascini

address: Via Olgettina, 60

department: Center for Omics Science

country: Italy

institute: IRCCS, Ospedale San Raffaele

summary: Studying primary Chronic Lymphocytic Leukemia cells in vitro is very challenging due to their short survival in culture, and also due to the fact that traditional two-dimensional in vitro models lack cellular and spatial complexity present in vivo. Based on these considerations, we exploited three-dimensional (3D) bioprinting to advance in vitro models for CLL. Through RNA sequencing (RNAseq) analysis, we observed a consistent difference in gene expression profile between 2D and 3D samples, indicating a different behavior of the cells in the two different culture settings.

overall_design: Examination of the transcriptomic differences between traditional two-dimensional (2D) cultured cells and cells cultured in three-dimensional (3D) bioprinted scaffolds. RNA from bioprinted 3D cells was extracted overtime, after 7 and 14 days.

first: Francesca

middle: V

last: Sbrana

first: Riccardo

last: Pinos

first: Federica

last: Barbaglio

first: Davide

last: Ribezzi

first: Fiorella

last: Scagnoli

first: Lydia

last: Scarfò

first: Itedale

middle: N

last: Redwan

first: Hèctor

last: Martìnez

first: Silvia

last: Farè

first: Paolo

last: Ghia

first: Cristina

last: Scielzo


title: DNase-seq from activated CD4-positive, alpha-beta T cell (ENCSR255OGF)

first: ENCODE

last: DCC


title: Comparative analysis of piRNA profiles reveals cryoinjury or freezability between boar (Sus scrofa) and giant panda (Ailuropoda melanoleuca) sperm during cryopreservation

status: Public on Apr 19 2021

city: Chengdu

first: Han

middle: Yi

last: Wang

state: Sichuan

address: GongPing

department: Institute of Animal Genetics and Breeding

institute: Sichuan Agricultural University

type: Non-coding RNA profiling by high throughput sequencing

summary: In this study, differentially expressed (DE)piRNAs of fresh and frozen-thawed sperm with different freeze tolerance compacity from giant panda and boar were evaluated. The results showed 1160 (22 down-regulated and 1138 up-regulated) and 384 (110 up-regulated and 274 down-regulated) differentially expressed (DE) piRNAs were identified in giant panda and boar sperm, respectively. Gene ontology (GO) enrichment analysis revealed that the target DE mRNAs of DE piRNAs were mainly enriched in biological regulation, cellular process and metabolic process in giant panda and boar sperm. Moreover, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that the target DE mRNAs of DE piRNAs were only distributed on DNA replication and cAMP signaling pathway in giant panda, but cAMP, cGMP and MAPK signaling pathway in boar sperm which were considered as part of olfactory transduction pathway.Conclusion:Olfactory transduction related pathways maybe contributed to different freeze tolerance compacity between giant panda and boar sperm, which will benefit to further understand the molecular mechanism of sperm cryoinjury and freezability.

sample_organism:
Ailuropoda melanoleuca
Sus scrofa

platform_organism:
Ailuropoda melanoleuca
Sus scrofa

overall_design: Sperm piRNA profiles of fresh and frozen-thawed giant panda and boar sperm were generated by High-throughput sequencing.Giant pandas (n = 5) that were disease-free and exhibited normal fertility, sexual maturity and normal semen quality were selected from the Bifengxia base of China Conservation and Research. Boars (n = 11) that were disease-free and exhibited normal fertility, sexual maturity and normal semen quality were collected using an electro-ejaculation method

first: Yihan

first: Yingmin

last: Zhou

first: Malik

last: Ali

first: Jiaman

last: Zhang

first: Wencan

first: Yan

last: Huang

first: Bo

last: Luo

first: Heming

first: Ziyue

last: Qin

first: Ming

first: Guangbin

first: Changjun

last: Zeng


title: SNAT - Single cell RNA sequencing of mouse sorted Schwann cells at postnatal day 14 (P14)

first: Ge

last: Tan

overall_design: Schwann cells were acutely extracted from P14 mouse pups which, besides of beta-actin dsred, also express eYFP upon P0cre-mediated recombination. The eYFP fluorescence allows the selection of eYFP positive Schwann cells from eYFP negative debris and non-Schwann cells in the nerve.  384-well plates were used to collect one cell per well, and these individual Schwann cells were further processed for library preparation using the SmartSeq2 chemistry. Two of these plates were sequenced at P14, each plate with cells derived from independent biological samples. The cells sorted into each plate derive from an original cell suspension containing pooled cells extracted from male and female mice in a 1:1 ratio.

first: Daniel

last: Gerber

first: Jorge

last: Pereira

first: Joanne

first: Slavica

last: Dimitrieva

first: Emilio

last: Yángüez

first: Ueli

last: Suter


title: CBFB cooperates with p53 to maintain TAp73 expression and suppress breast cancer

status: Public on Apr 16 2021

city: Bethesda

first: Jing

state: MD

institute: National Cancer Institute

summary: The goal of this study is to use H3K4me3 signal to mark the promoter regions of the p73 gene. The p73 gene expresses TAp73 and DNp73 isoforms, which use two different promoters. H3K4me3 is generally associated with the promoter of a gene and, therefore, can be used to mark the promoters for TAp73 and DNp73.

overall_design: For wild type MCF10A cells, H3K4me3 were repeated twice. Other conditions were repeated once.


title: In-depth transcriptomic analyses investigating molecular mechanisms underlying diabetic retinopathy (smallRNA)

city: Biberach an der Riß

first: Kolja

last: Becker

address: Birkendorfer Str. 65

department: Global Computational Biology and Digital Sciences

country: Germany

institute: Boehringer Ingelheim Pharma GmbH & Co. KG

summary: Diabetic Retinopathy (DR) is among the major global causes for vision loss. With the rise in diabetes prevalence, an increase in DR incidence is expected. Current understanding of both the molecular etiology and pathways involved in the initiation and progression of DR is limited. Here we analyzed mRNA and miRNA expression profiles of 80 human post-mortem retinal samples from 80 patients diagnosed with various stages of DR. We found differentially expressed transcripts to be predominantly associated with late stage DR and pathways such as hippo and gap junction signaling. A multivariate regression model identified transcripts with progressive changes throughout disease stages, which in turn displayed significant overlap with sphingolipid and cGMP−PKG signaling. Combined analysis of miRNA and mRNA expression further uncovered disease-relevant miRNA/mRNA associations as potential mechanisms of post-transcriptional regulation. Finally, integrating human retinal single cell RNA-Sequencing data revealed a continuous loss of retinal ganglion cells, and Müller cell mediated changes in histidine and β-alanine signaling. Our findings offer an unprecedented insight into the development of DR and provide potential avenues for future therapeutic intervention.

overall_design:
Post-mortem human eyes from 43 donors were obtained through the Iowa Lions Eye Bank (Coralville, IA) after written informed consent of the next-of-kin was obtained. Preservation of eyes occurred within 6 hours post-mortem. From each donor group (healthy control, diabetic, NPPR, and NPDR/PDR + DME), 10 tissue samples were collected from the macula region as well as the retinal periphery. All tissue samples were taken with a 6mm biopsy punch, snap frozen in liquid nitrogen, and preserved at -80C until use.
Submitter states that raw data can't be provided due to patient privacy concerns. Raw data will be uploaded to dbGaP.

first: Holger

last: Klein

first: Eric

last: Simon

first: Coralie

last: Viollet

first: Christian

last: Haslinger

first: German

last: Leparc

last: Schultheis

first: Victor

last: Chong

first: Markus

middle: H

last: Kuehn

first: Francesc

last: Fernandez-Albert

first: Remko

last: Bakker


title: Coupled analysis of transcriptional states and somatic hypermutation in germinal center B cells reveals role for oxidative phosphorylation in positive selection

city: Hangzhou

first: Heping

last: Xu

state: Zhejiang

address: 18 Shilongshan Road

institute: Westlake University

summary: In this work we illustrate the power of coupling single cell analysis of transcriptional states with somatic hypermutation of germinal center B cells to reveal unanticipated roles of metabolic programs in the positive selection. We use massively parallel 5'-end scRNA-seq to simultaneously capture transcriptome states and mutation profiles of IgH variable genes in individual cells. Our computational analyses reveal that the OXPHOS module is enhanced in GC B cells undergoing positive selection in response to different antigens. Through deleting the Cox10 gene, which encodes a cytochrome oxidase assembly factor, specifically in GC B cells, we demonstrate that OXPHOS activity is required for cell division and positive selection. Furthermore, we show that chemical augmentation of OXPHOS activity facilitates the positive selection of GC B cells in vivo. Our findings therefore reveal that tuning of OXPHOS activity by increased affinity BCRs is critical for clonal expansion and positive selection.

overall_design: Six to eight weeks old C56BL/6J (Jax 000664) mice were immunized intraperitoneally with 100 μg NP(23)-KLH (Biosearch Technologies) or OVA (Sigma) mixed with 50% (v/v) Alum (ThermoFisher Scientific) and 1 μg LPS (Sigma). NP-specific GC B cells were sorted as 7AAD–B220+FashiGL-7hiNP+ on day 13 post immunization using MA900 (Sony) with 100 μm Chip at 4 °C. For the immunization with OVA, total GC B cells were sorted as 7AAD–B220+FashiGL-7hi for scRNA-seq. Single cells were captured via the GemCode Single Cell Platform using the GemCode Gel Bead, Chip and 5’-end Library Kits (10X Genomics), according to the manufacturer’s protocol. Libraries were sequenced on a NovaSeq (Illumina). Additionally, OVA-binding GC B cells were sorted for bulk BCR library generation and sequenced on Miseq (Illumina).

first: Dianyu

last: Chen

first: Yan

last: Wang

first: Shujie

last: Fu

first: Harinder

last: Singh


title: Role of Epigenetics in Unicellular to Multicellular Transition in Dictyostelium

city: Boston

last: Greer

state: MA

address: 320 Longwood Avenue

department: Newborn Medicine/Department of Pediatrics

institute: Boston Children's Hospital/Harvard Medical School

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

sample_organism:
Dictyostelium discoideum
Dictyostelium discoideum AX4

overall_design: Refer to individual Series


title: Differentiation reveals the plasticity of age-related change in murine muscle progenitors

city: South San Francisco

first: Jacob

middle: Cameron

last: Kimmel

address: 1170 Veterans Blvd

department: Computing

institute: Calico Life Sciences, LLC

summary: Skeletal muscle experiences a decline in lean mass and regenerative potential with age, in part due to intrinsic changes in progenitor cells. However, it remains unclear if age-related changes in progenitors persist across a differentiation trajectory or if new age-related changes manifest in differentiated cells. To investigate this possibility, we performed single cell RNA-seq on muscle mononuclear cells from young and aged mice and profiled muscle stem cells (MuSCs) and fibro/adipose progenitors (FAPs) after differentiation. Differentiation increased the magnitude of age-related change in MuSCs and FAPs, but also masked a subset of age-related changes present in progenitors. Using a dynamical systems approach and RNA velocity, we found that aged MuSCs follow the same differentiation trajectory as young cells, but stall in differentiation near a commitment decision. Our results suggest that age-related changes are plastic across differentiation trajectories and that fate commitment decisions are delayed in aged myogenic cells.

overall_design: Muscle mononuclear cells were isolated from 2 young (3 m.o.) and 2 aged (20 m.o.) C57Bl/6 mice. All cells in the muscle mononuclear compartment were transcriptionally profiled immediately after isolation using the 10X Chromium Single Cell Transcriptome v3 technology. Muscle stem cells and fibro/adipose progenitors were additionally profiled both  after a differentiation challenge using the same library preparation method.

first: David

middle: G

last: Hendrickson

middle: R

last: Kelley


title: Impact of preoperative antibiotics on integrated microbiome-host transcriptomic data generated from colorectal cancer resections.

city: Stony Brook

first: Jinyu

last: Li

address: 101 Nicolls Rd

department: Cancer Center

institute: Stony Brook University

summary: Integrative multi-omic approaches have been increasingly applied to discovery and functional studies of complex human diseases. Short-term preoperative antibiotics have been adopted to reduce site infections in colorectal cancer (CRC) resections.  We hypothesize that the antibiotics will impact analysis of multi-omic datasets generated from resection samples to investigate biological CRC risk factors. To assess the impact of preoperative antibiotics on integrated microbiome and human transcriptomic data generated from archived frozen CRC resection samples. Genomic DNA (gDNA) and RNA were extracted from 51 pairs of frozen sporadic CRC tumor and adjacent non-tumor mucosal samples from 50 CRC patients archived at a single medical center. 16S rRNA gene sequencing (V3V4 region, paired end (PE), 300 bp)  and confirmatory quantitative polymerase chain reaction (qPCR) assays were conducted on gDNA.  RNA sequencing IPE, 125bp) was performed on parallel tumor and non-tumor RNA samples with RNA Integrity Numbers (RIN) scores ≥ 6.

first: Daniel

last: Frank

first: Sarah

last: Malik

first: Chencan

last: Zhu

first: Joseph

middle: F

last: Lacomb

first: Paula

last: Denoya

first: Igor

last: Kravets

first: Joshua

middle: D

last: Miller

first: Jie

last: Yang

first: Melissa

last: Kramer

first: W

last: McCombie

first: Charles

middle: E

last: Robertson

first: Ellen


title: Neuronal ApoE Upregulates MHC-I Expression to Drive Selective Neurodegeneration in Alzheimer’s Disease

city: San Francisco

first: Kelly

last: Zalocusky

address: 1650 Owens Street, Gladstone Center for Translational Advancement

institute: Gladstone Institutes

summary: Selective neurodegeneration is a critical causal factor in Alzheimer’s disease (AD); however, the mechanisms that lead some neurons to perish while others remain resilient are unknown. We sought potential drivers of this selective vulnerability using single-nucleus RNA sequencing and discovered that apoE expression level is a substantial driver of neuronal variability. Strikingly, neuronal expression of apoE—which has a robust genetic linkage to AD—correlated strongly, on a cell-by-cell basis, with immune response pathways in neurons in the brains of wildtype mice, human apoE knock-in mice, and humans with or without AD. Elimination or over-expression of neuronal apoE revealed a causal relationship between apoE expression, neuronal MHC-I expression, Tau pathology, and neurodegeneration. Functional reduction of MHC-I ameliorated Tau pathology in apoE4-expressing primary neurons and in mouse hippocampi expressing pathological Tau. These findings suggest a mechanism linking neuronal apoE expression to MHC-I expression and, subsequently, to Tau pathology and selective neurodegeneration.

overall_design: Single-nucleus RNA sequencing of hippocampus from human APOE3 targeted replacement mice at 5, 10, 15, and 20 months, human APOE4 targeted replacement mice at 5, 10, 15, and 20 months, and neuron-specific APOE-KO (Syn-cre x floxed APOE) mice at 10 and 15 months.

first: Ramsey

last: Najm

first: Alice

last: Taubes

first: Yanxia

last: Hao

first: Seo Yeon

last: Yoon

first: Yadong

last: Huang


title: Myeloid ATP citrate lyase regulates macrophage inflammatory responses in vitro without altering inflammatory disease outcomes

city: Amsterdam

first: Menno

last: de Winther

address: Meibergdreef 9

department: Medical Biochemistry

institute: Academic Medical Center University of Amsterdam

summary: Macrophages are highly plastic, key regulators of inflammation. Deregulation of macrophage activation can lead to excessive inflammation as seen in inflammatory disorders like atherosclerosis, obesity, multiple sclerosis and sepsis. Targeting intracellular metabolism is considered as an approach to reshape deranged macrophage activation and to dampen the progression of inflammatory disorders. ATP citrate lyase (Acly) is a key metabolic enzyme and an important regulator of macrophage activation. Using a macrophage-specific Acly-deficient mouse model, we investigated the role of Acly in macrophages during acute and chronic inflammatory disorders. First, we performed RNA sequencing to demonstrate that Acly-deficient macrophages showed hyperinflammatory gene signatures in response to acute LPS stimulation in vitro. Next, we assessed endotoxin-induced peritonitis in myeloid-specific Acly-deficient mice and show that, apart from increased splenic Il6 expression, systemic and local inflammation were not affected by Acly deficiency. Also during obesity, both chronic low-grade inflammation and whole-body metabolic homeostasis remained largely unaltered in mice with Acly-deficient myeloid cells. Lastly, we show that macrophage-specific Acly deletion did not affect the severity of experimental autoimmune encephalomyelitis (EAE), an experimental model of multiple sclerosis. These results indicate that, despite increasing inflammatory responses in vitro, macrophage Acly deficiency does not worsen acute and chronic inflammatory responses in vivo. Together with our earlier observation that myeloid Acly deletion stabilizes atherosclerotic lesions, our findings highlight that therapeutic targeting of macrophage Acly can be beneficial in some, but not all, inflammatory disorders.

overall_design: RNA-seq of bone marrow-derived macrophages from female AclyM-WT and AclyM-KO mice.

first: Sanne

last: Verberk

first: Hendrik

middle: J

last: van der Zande

first: Kyra

last: de Goede

first: Jeroen

last: Baardman

first: Karl

last: Harber

first: Eelco

last: Keuning

first: Joost

last: Lambooij

first: Frank

last: Otto

first: Anna

last: Zawistowska-Deniziak

first: Helga

last: de Vries

middle: P

first: Bruno

last: Guigas

first: Jan

last: Van den Bossche


title: Identifying transcripts regulated by p53 in MCF10A cells

first: Jing

summary: Total RNA was extracted from five million wild type (WT) and p53 knockout (p53_KO) MCF10A cells using Qiagen RNAeasy kit. Ribosomal RNAs were removed and the rest of RNAs were subject to RNAseq.

overall_design: Four replicates for each genotype

first: Navdeep

last: Malik


title: SNAT - RNA sequencing of sorted Schwann cells as a single mixed population, enriched in myelinating Schwann cells, or enriched in not-myelinating Schwann cells

first: Ge

last: Tan

summary: RNA sequencing of sorted mouse Schwann cells expressing YFP due to P0Cre-mediated recombination. The plotting of side scatter versus eYFP fluorescence generates 2 semi-detached eYFP+ clouds of cells, which further enables the enriched selection of myelinating Schwann cells, and of not-myelinating Schwann cells.

overall_design: Schwann cells were acutely extracted from P5 mouse sciatic nerves. These Schwann cells, besides of beta-actin dsred, also express eYFP upon P0cre-mediated recombination. Following extraction, Schwann cells were sorted via FACS. Plotting side-scatter versus eYFP fluorescence allows the selection of eYFP positive Schwann cells (as a mixture of myelinating and not-myelinating cells) from eYFP negative debris and non-Schwann cells in the nerve. Furthermore, 2 semi-detached eYFP+ clouds of cells could be detected at this mouse age, which further enabled the selection of populations either enriched in myelinating Schwann cells, or enriched in not-myelinating Schwann cells. For each gating strategy (mixed, myelinating, and not-myelinating), 4 independent biological samples were sequenced, 2 derived from male mice and 2 derived from female mice.

first: Daniel

last: Gerber

first: Jorge

last: Pereira

first: Joanne

first: Slavica

last: Dimitrieva

first: Emilio

last: Yángüez

first: Ueli

last: Suter


title: Maternal Heat Stress Alters Expression of Genes Associated with Nutrient Transport Activity and Metabolism in Female Placentae From Mid-Gestating Pigs

status: Public on Apr 15 2021

city: Parkville

first: Weicheng

last: Zhao

state: Victoria

address: Building 184, Royal Parade

country: Australia

institute: The University of Melbourne

summary: RNA sequencing was performed to quantify differential gene expression between pig placentae exposed to thermoneutral control or cyclic heat stress conditions between d40 and d60 of gestation (early-mid gestation). Placental samples from female fetuses were collected at d60 of gestation and were subjected to sequencing library preparation and NovaSeq6000 sequencing. 150 bp paired-end reads were generated from each sample. A total of 169 genes were differentially expressed between control and heat stress placentae, of which 35 genes were upregulated and 134 genes were downregulated by maternal heat stress. Gene ontology and pathway enrichment analysis revealed the differentially expressed genes are associated with placental nutrient transporter and metabolism.

overall_design: Placental samples were collected on d60 of gestation from pregnant pigs exposed to thermoneutral control (CON; constant 20 °C; n = 5) or cyclic heat stress (HS; cyclic 28 - 33 °C; n = 5) between d40 and d60 of gestation.

first: W

first: F

last: Liu

first: C

last: Marth

first: M

last: Green

first: H

last: Le

first: B

last: Leury

first: A

middle: W

last: Bell

last: Dunshea

first: J

last: Cottrell


title: In-depth transcriptomic analyses investigating molecular mechanisms underlying diabetic retinopathy

first: Kolja

last: Becker


title: Multi-omic profiling of lung and liver tumor microenvironments of metastatic pancreatic cancer reveals site-specific immune-regulatory pathways [WES]

city: Baltimore

first: Won Jin

last: Ho

address: 1650 Orleans St. CRB I Rm 488

department: Oncology

institute: Johns Hopkins University

summary: WES was used to analyze the mutational landscape of KPC and Panc02, two murine pancreatic cancer cell lines. As expected, a relatively low mutational burden was identified in KPC cells.

overall_design: Two cells lines were submitted for WES.

first: Won


title: SNAT - Single cell RNA sequencing of mouse sorted Schwann cells at postnatal day 60 (P60)

first: Ge

last: Tan

summary: Single cell RNA sequencing of sorted mouse Schwann cells expressing eYFP due to P0Cre-mediated recombination.

overall_design: Schwann cells were acutely extracted from P60 mouse pups which, besides of beta-actin dsred, also express eYFP upon P0cre-mediated recombination. The eYFP fluorescence allows the selection of eYFP positive Schwann cells from eYFP negative debris and non-Schwann cells in the nerve.  384-well plates were used to collect one cell per well, and these individual Schwann cells were further processed for library preparation using the SmartSeq2 chemistry. Two of these plates were sequenced at P60, each plate with cells derived from independent biological samples. The cells sorted into each plate derive from an original cell suspension containing pooled cells extracted from male and female mice in a 1:1 ratio.

first: Daniel

first: Jorge

middle: A


title: SNAT - Single cell RNA sequencing of mouse sorted Schwann cells at postnatal day 1 (P1)

overall_design: Schwann cells were acutely extracted from P1 mouse pups which, besides of beta-actin dsred, also express eYFP upon P0cre-mediated recombination. The eYFP fluorescence allows the selection of eYFP positive Schwann cells from eYFP negative debris and non-Schwann cells in the nerve.  384-well plates were used to collect one cell per well, and these individual Schwann cells were further processed for library preparation using the SmartSeq2 chemistry. Two of these plates were sequenced at P1, each plate with cells derived from independent biological samples. The cells sorted into each plate derive from an original cell suspension containing pooled cells extracted from male and female mice in a 1:1 ratio.

last: Gerber

first: Joanne

first: Slavica

first: Emilio


title: Effect of single MgSO4 injection on brain transcripts in naive and ishemic 5 day-old mice

city: Rouen cedex

first: Celine

last: Derambure

address: 22 Bvd Gambetta

country: France

institute: INSERM U905

summary:
MgSO4 is given to prevent preterms neurological deficits. We have investigated proper effects and hypoxia-ischemia interfering effects of MgSO4 on transcription in neonate mice at day 5 (a brain development stage mimicking preterm maturity), at neuroprotection dose (600 mg/kg).
Pools of RNA from 6 forebrains (3 males and 3 females) were used for total RNA extraction at 5 times post single MgSO4 injection (1.5H, 3H, 6H, 12H, 24H).  Separately, MgSO4 effects were assessed post hypoxia-ischemia (3H and 12H). Co-hybridization of MgSO4-treated mRNA (labelled Cy5) and control tissues mRNA (labelled Cy3) were performed on Agilent (design 026655) micro-arrays  in 4-7  replicates. Co-hybridization of saline injected (Labelled Cy3) or MgSO4 injected (Labelled Cy5) hypoxia-ischemia (according to Rice Vannucci (RV) procedure) exposed mice brains were performed on Aglient (design 026655) microarrays in triplicates.

overall_design: Two color experiments : MgSO4 treatment (Cy5)/matched time post Phosphate buffer saline injections (Cy3) and Hypoxia-ischmia brains from saline treated (Cy3) and MgSO4 treated (Cy5) mice.

first: Bérénice

last: Le Dieu-Lugon

first: Céline

first: Nicolas

last: Dupré

first: Marret

last: Stéphane

first: Philippe

last: Leroux


title: Multi-omic profiling of lung and liver tumor microenvironments of metastatic pancreatic cancer reveals site-specific immune-regulatory features [RNA-seq]

summary: To understand the site-specific differences in how metastatic pancreatic cancer is modulated, we compared the non-immune compartments by bulk RNA-seq by mouse models of lung and liver metastatic pancreatic cancer based on Kras and Trp53 driven pancreatic cancer cells (KPC).

overall_design: Five groups are compared: In vitro culture of KPC cells (n=8); Dissociated normal lung tissue (n=5); Dissociated normal liver tissue (n=5); Non-immune cells enriched from KPC-bearing lungs (n=5); Non-immune cells enriched from KPC-bearing livers (n=7)


title: SARS-CoV-2 infection in pregnancy is associated with robust inflammatory response at the maternal-fetal interface

status: Public on Apr 14 2021

city: New Haven

first: Scott

middle: Dean

last: Pope

state: Connecticut

address: 300 Cedar St

department: Immunobiology

institute: Yale School of Medicine

summary: Pregnant women appear to be at increased risk for severe outcomes associated with COVID-19, but the pathophysiology underlying this increased morbidity and its potential impact on the developing fetus is not well understood. In this study of pregnant women with and without COVID-19, we assessed viral and immune dynamics at the placenta during maternal SARS-CoV-2 infection. Viral RNA was only rarely detected in the placentas from SARS-CoV-2-positive women in our cohort, with only 1/11 positive for infection at the maternal-fetal interface. Through bulk RNA transcriptomic analyses, we found that placentas from SARS-CoV-2-positive pregnancies exhibited inflammatory markers of immune activation, even in the majority of samples which did not show local invasion of the virus. These markers are associated with pregnancy complications such as preeclampsia and poor fetal outcomes. Overall, this study suggests that SARS-CoV-2 is associated with immune activation at the maternal-fetal interface even in the absence of detectable local viral invasion. While this likely represents a protective mechanism shielding the placenta from infection, inflammatory changes in the placenta may also contribute to poor pregnancy outcomes and thus warrant further investigation.

overall_design: mRNA profiles of placental villous tissue at term delivery from control and SARS-CoV-2-positive mothers

first: S

first: W

last: Lu-Culligan

first: A

last: Farhadian


title: Integration of genomic and transcriptomic markers improves the prognosis prediction of acute promyelocytic leukemia

city: Shanghai

first: Niu

last: Qiao

address: 197 Rui Jin Er Road

department: National Research Center for Translational Medicine (Shanghai)

institute: Shanghai Jiao Tong University

summary: Purpose: The current stratification system for acute promyelocytic leukemia (APL) is based on the white blood cell (WBC) and the platelet counts (i.e., Sanz score) over the past two decades. However, the borderlines among different risk groups are sometimes ambiguous, and for some patients, early death and relapse remained challenges. Besides, with the evolving of the treatment strategy from ATRA-chemotherapy to ATRA-ATO-based synergistic targeted therapy, the precise risk stratification with molecular markers is needed.  Patients and Methods: This study performed a systematic analysis of APL genomics and transcriptomics to identify genetic abnormalities in 348 patients mainly from the APL2012 trial (NCT01987297) to illustrate the potential molecular background of Sanz score and further optimize it. The least absolute shrinkage and selection operator (LASSO) algorithm was used to analyze the gene expression in 323 cases to establish a scoring system (i.e., APL9 score).  Results: Through combining NRAS mutations, APL9 score with WBC, 321 cases can be stratified into two groups with significantly different outcomes. The estimated 5-year overall (P = 0.00031), event-free (P < 0.0001), and disease-free (P = 0.001) survival rates in the revised standard-risk group (95.6%, 93.8%, and 98.1%, respectively) were significantly better than those in the revised high-risk group (82.9%, 77.4%, and 88.4%, respectively), which could be validated using The Cancer Genome Atlas dataset.  Conclusions: We have proposed a two-category system improving prognosis in APL patients. Molecular markers identified in this study may also provide genomic insights into the disease mechanism for improved therapy.

overall_design: A total of 348 APL patients (age 18-65 years; 54.3% males, 45.6% females) were included in an IRB-approved study, including a majority part of the patients (n = 304) coming from the APL2012 clinical trial (NCT01987297) from December 6, 2012 to December 31, 2017, and a small group of the patients (n = 44) from the historical cases between June 1, 2012 to November 31, 2012, who received the similar treatment. These above candidates were eligible to enter our study with available bone marrow (BM) samples containing blasts over 80%.     Among the 348 cases, WES was applied to 202 cases and WGS to 2 cases for the detection of genomic abnormalities; 189 out of these 204 cases had their own matched control samples (complete remission BM samples). On the other hand, 323 cases were subject to RNA-seq for transcriptome analysis.

first: Xiaojing

last: Lin

first: Yang

last: Shen

first: Hai

last: Fang

first: Qing

last: Xue

first: Bowen

last: Cui

first: Li

last: Chen

first: Hongming

last: Zhu

first: Sujiang

last: Zhang

first: Yu

first: Lu

last: Jiang

first: Shengyue

last: Wang

first: Junmin

last: Li

first: Bingshun

first: Bing

first: Zhu

first: Saijuan


title: Ribosome quality control activity potentiates vaccinia virus protein synthesis during infection

city: san diego

first: Elayanambi

last: Sundaramoorthy

state: California

address: 9500, GILMAN DRIVE, la jolla

department: Section of cell and developmental biology

institute: University of California San Diego

summary:
Viral infection both activates stress signaling pathways and redistributes ribosomes away from host mRNAs to translate viral mRNAs. The intricacies of this ribosome shuffle from host to viral mRNAs are poorly understood
Here, we uncover a role for the ribosome associated quality control (RQC) factor, ZNF598, during vaccinia virus mRNA translation. ZNF598 acts on collided ribosomes to ubiquitylate 40S subunit proteins uS10 and eS10 initiating RQC-dependent nascent chain degradation and ribosome recycling
We show that vaccinia infection in human cells enhances uS10 ubiquitylation indicating an increased burden on RQC pathways during viral propagation. Consistent with an increased RQC demand, we demonstrate that vaccinia virus replication is impaired in cells which either lack ZNF598 or express a ubiquitylation deficient version of uS10
Using SILAC-based proteomics and concurrent RNAseq analysis, we determine that translation and not transcription of vaccinia virus mRNAs is compromised in cells with deficient RQC activity. Additionally, vaccinia virus infection reduces cellular RQC activity, suggesting that co-option of ZNF598 by vaccinia virus plays a critical role in translational reprogramming that is needed for optimal viral propagation.

overall_design: 6 samples were analyzed in triplicates

first: Eric

last: Bennett


title: In-depth transcriptomic analyses investigating molecular mechanisms underlying diabetic retinopathy (totalRNA)

first: Kolja

last: Becker

summary: Diabetic Retinopathy (DR) is among the major global causes for vision loss. With the rise in diabetes prevalence, an increase in DR incidence is expected. Current understanding of both the molecular etiology and pathways involved in the initiation and progression of DR is limited. Here we analyzed mRNA and miRNA expression profiles of 80 human post-mortem retinal samples from 80 patients diagnosed with various stages of DR. We found differentially expressed transcripts to be predominantly associated with late stage DR and pathways such as hippo and gap junction signaling. A multivariate regression model identified transcripts with progressive changes throughout disease stages, which in turn displayed significant overlap with sphingolipid and cGMP−PKG signaling. Combined analysis of miRNA and mRNA expression further uncovered disease-relevant miRNA/mRNA associations as potential mechanisms of post-transcriptional regulation. Finally, integrating human retinal single cell RNA-Sequencing data revealed a continuous loss of retinal ganglion cells, and Müller cell mediated changes in histidine and β-alanine signaling. Our findings offer an unprecedented insight into the development of DR and provide potential avenues for future therapeutic intervention.

overall_design:
Post-mortem human eyes from 43 donors were obtained through the Iowa Lions Eye Bank (Coralville, IA) after written informed consent of the next-of-kin was obtained. Preservation of eyes occurred within 6 hours post-mortem. From each donor group (healthy control, diabetic, NPPR, and NPDR/PDR + DME), 10 tissue samples were collected from the macula region as well as the retinal periphery. All tissue samples were taken with a 6mm biopsy punch, snap frozen in liquid nitrogen, and preserved at -80C until use.
Submitter states that raw data can't be provided due to patient privacy concerns. Raw data will be uploaded to dbGaP.

first: Holger

last: Klein

last: Simon

first: Coralie

last: Viollet

first: Christian

last: Haslinger

first: German

last: Leparc

last: Schultheis

first: Victor

last: Chong

first: Markus

last: Kuehn

first: Francesc

last: Fernandez-Albert

first: Remko

last: Bakker


title: HMGB1 is required for virulence gene expression via configuration of genome architecture in Plasmodium falciparum

city: shanghai

first: meng

last: liu

address: 1239,SiPing Road

institute: TongJi University


title: HMGB1 is required for virulence gene expression via configuration of genome architecture in Plasmodium falciparum [TF ChIP]

summary: The mutually exclusive expression of virulence genes is critical for the immune evasion and pathogenesis of malaria parasites, Plasmodium falciparum, in human host. The three-dimensional genome structure has emerged as a new factor involved in transcriptional regulation of virulence gene families in the parasites. However, the mechanism controlling this epigenetic regulation pathway remains elusive. Here, we have identified the highly conserved high mobility group protein HMGB1 as a critical architectural regulator in establishment of high-order genome structure via interaction with centromeres in P. falciparum. Genetic manipulation of Pfhmgb1 gene and Hi-C analysis showed that the boundary of telomere and centromere clusters in an opposite spatial relationship in the nucleus was disrupted upon hmgb1 knockout. The collapse of euchromatic centromere cluster from nuclear periphery towards the opposite heterochromatic telomere cluster triggered relocation of the original active var gene, which resulted in complete silence of the entire repertoire of var gene family. ChIP-seq and fluorescence assay analysis confirmed the specific interaction between PfHMGB1 and centromeres. Meanwhile, as in other eukaryotes, PfHMGB1 was also widely present on the promoter regions of a variety of genes and co-regulated transcription, including other non-var variant gene families, suggesting multiple dimensions of epigenetic gene regulation by PfHMGB1. Finally, the natural genome organization could be reconstructed by hmgb1 gene complementation, which rescued the mutually exclusive expression of virulence genes. Taken together, our work provides new insight into the evolution of biological functions of the HMG architectural superfamily in eukaryotes.

overall_design: Genome-wide location analysis (ChIP-Seq) of  Pfhmgb1 in the P. falciparum

first: Cizhong

last: Jiang

first: Qingfeng

last: Zhang

first: Meng

last: Liu

first: Binbin

last: LU


title: HMGB1 is required for virulence gene expression via configuration of genome architecture in Plasmodium falciparum [HiC]

overall_design: Analysis of the spatial organization of the P. falciparum genome for wt, PfHMGB1-ko and Pfhmgb1-rescue parasites using chromosome conformation capture coupled with next-generation sequencing (Hi-C).


title: HMGB1 is required for virulence gene expression via configuration of genome architecture in Plasmodium falciparum [RNA-seq]

overall_design: Expression profiling by high throughput sequencing(RNA-seq) in the P. falciparum for wt ,PfHMGB1-ko and Pfhmgb1-rescue parasites


title: The transcriptome of sciatic nerves with single cell resolution

city: Zurich

first: Ge

last: Tan

address: Winterthurerstrasse 190

institute: University of Zurich

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

overall_design: Refer to individual Series


title: HMGB1 is required for virulence gene expression via configuration of genome architecture in Plasmodium falciparum [HM-ChIP]

overall_design: Genome-wide location analysis (ChIP-Seq) of h3k9me3 and h3k9ac in the P. falciparum for  wt  and PfHMGB1-ko


title: Single-cell RNA sequencing reveals tissue compartment-specific plasticity of mycosis fungoides tumor cells

status: Public on Apr 13 2021

city: Vienna

first: Katharina

last: Rindler

address: Waehringer Guertel 18-20

department: Dermatology

country: Austria

institute: Medical University of Vienna

summary: Mycosis fungoides (MF) is the most common primary cutaneous T-cell lymphoma. While initially restricted to the skin, malignant cells can appear in blood, bone marrow and secondary lymphoid organs in later disease stages. However, only little is known about phenotypic and functional properties of malignant T cells in relationship to tissue environments over the course of disease progression. We thus profiled the tumor micromilieu in skin, blood and lymph node in a patient with advanced MF using single-cell RNA sequencing combined with V-D-J T-cell receptor sequencing. In skin, we identified clonally expanded T-cells with characteristic features of tissue-resident memory T-cells (TRM, CD69+CD27-NR4A1+RGS1+AHR+). In blood and lymph node, the malignant clones displayed a transcriptional program reminiscent of a more central memory-like phenotype (KLF2+TCF7+S1PR1+SELL+CCR7+), while retaining tissuehoming receptors (CLA, CCR10). The skin tumor microenvironment contained potentially tumor-permissive myeloid cells producing regulatory (IDO1) and Th2-associated mediators (CCL13, CCL17, CCL22). Given their expression of PVR, TNFRSF14 and CD80/CD86, they might be under direct control by TIGIT+CTLA4+CSF2+TNFSF14+ tumor cells. In sum, this study highlights the adaptive phenotypic and functional plasticity of MF tumor cell clones. Thus, the TRM-like phenotype enables long-term skin residence of MF cells. Their switch to a TCM-like phenotype with persistent skin homing molecule expression in the circulation might explain the multi-focal nature of MF.

overall_design:
multi-organ single-cell RNA-seq investigation of a primary cutaneous lymphoma
>>>Raw data are unvailable due to patient privacy concerns<<<

first: Wolfgang

middle: M

last: Bauer

first: Constanze

last: Jonak

first: Matthias

last: Wielscher

first: Lisa

last: Shaw

first: Thomas

middle: B

last: Rojahn

first: Felix

last: Thaler

first: Stefanie

last: Porkert

first: Ingrid

last: Simonitsch-Klupp

last: Weninger

first: Marius

last: Mayerhoefer

last: Farlik

first: Patrick

last: Brunner


title: Multi-omic profiling of lung and liver tumor microenvironments of metastatic pancreatic cancer reveals site-specific immune-regulatory features

first: Won Jin

last: Ho


title: Expression data from stabilized epithelial pancreatic cancer cells

city: Houston

first: Raghu

last: Kalluri

state: TX

address: 1881 East Road

department: Cancer Biology

institute: MD Anderson Cancer Center

summary:
Pancreatic ductal adenocarcinoma is therapeutically recalcitrant and metastatic. Epithelial to mesenchymal transition (EMT) is associated with metastasis, however, a causal connection needs further unraveling. We explored the impact of stabilized EMT states on PDAC metastasis through the use of genetically-engineered mouse models that exhibit a stabilized epithelial phenotype through the deletion of EMT-driving transcription factors Snail and Twist together
We examined the cancer cell-intrinsic pathways associated with stabilized epithelial pancreatic adenocarcinoma cells.

overall_design: YFP+ cancer cells were freshly sorted from the primary pancreatic tumors and the most common metastatic sites, liver and lung, of the KPC and KPC;Snai1cKO; Twist1cKO mice for global expression profiling using the Clariom D mouse whole transcriptome array.

first: Julienne

middle: L

last: Carstens


title: NKX3.1 localization to mitochondria suppresses prostate cancer initiation

city: Newark

first: Antonina

last: Mitrofanova

state: NJ

address: 65 Bergen Street, Rm 923B

institute: Rutgers University

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design:
Refer to individual Series

For queries, please contact Cory Abate-Shen at cabateshen@columbia.edu


title: RNA-seq of the fruits of Curculigo latifolia and Curculigo capitulata

city: Kyoto

first: Satoshi

last: Okubo

address: Yamashina-ku

country: Japan

institute: Nippon Shinyaku Co., Ltd.

summary:
Background
Curculigo latifolia is a perennial plant endogenous to Southeast Asia whose fruits contain the taste-modifying protein neoculin, which binds to sweet receptors and makes sour fruits taste sweet. Although similar to snowdrop (Galanthus nivalis) agglutinin (GNA), which contains mannose-binding sites in its sequence and 3D structure, neoculin lacks such sites and has no lectin activity. Whether the fruits of C. latifolia and other Curculigo plants contain neoculin and/or GNA family members was unclear.
Results
Through de novo RNA-seq assembly of the fruits of C. latifolia and the related C. capitulata and detailed analysis of the expression patterns of neoculin and neoculin-like genes in both species, we assembled 85,697 transcripts from C. latifolia and 76,775 from C. capitulata using Trinity and annotated them using public databases. We identified 70,371 unigenes in C. latifolia and 63,704 in C. capitulata. In total, 38.6% of unigenes from C. latifolia and 42.6% from C. capitulata shared high similarity between the two species. We identified ten neoculin-related transcripts in C. latifolia and 15 in C. capitulata, encoding both the basic and acidic subunits of neoculin in both plants. We aligned these 25 transcripts and generated a phylogenetic tree. Many orthologs in the two species shared high similarity, despite the low number of common genes, suggesting that these genes likely existed before the two species diverged. The relative expression levels of these genes differed considerably between the two species: the transcripts per million (TPM) values of neoculin genes were 60 times higher in C. latifolia than in C. capitulata, whereas those of GNA family members were 15,000 times lower in C. latifolia than in C. capitulata.
Conclusions
The genetic diversity of neoculin-related genes strongly suggests that neoculin genes underwent duplication during evolution. The marked differences in their expression profiles between C. latifolia and C. capitulata may be due to mutations in regions involved in transcriptional regulation. Comprehensive analysis of the genes expressed in the fruits of these two Curculigo species helped elucidate the origin of neoculin at the molecular level.

sample_organism:
Molineria latifolia
Molineria capitulata

overall_design: total RNA of each one fruit of Curculigo latifolia and C. capitulata

first: Kaede

last: Terauchi

first: Shinji

last: Okada

first: Yoshikazu

last: Saito

first: Takao

last: Yamaura

first: Takumi

last: Misaka

first: Ken-ichiro

last: Nakajima

first: Keiko

last: Abe

first: Tomiko

last: Asakura


title: NKX3.1 localization to mitochondria suppresses prostate cancer initiation  (Human RWPE1 RNASeq)

summary:
The NKX3.1 homeobox gene functions in mitochondria to regulate oxidative stress
To investigate the role of NKX3.1 in regulation of oxidative stress, we employed transcriptome analysis of mouse prostate ( from 4 month old Nkx3.1+/+ and Nkx3.1-/- mice treated with paraquat), and human prostate cells ( RWPE1 cells engineered with empty vector (altered pTRIPZ), NKX3.1 wild type over-expression, and NKX3.1 (R52C) over-expression treated with paraquat). Mouse tissue or human cells were snap frozen for subsequent molecular analysis.

overall_design:
Analysis of transcriptome of human RWPE1 cells
Human RWPE1 cells were engineered with empty vector (altered pTRIPZ)  or NKX3.1 wild type over-expression or NKX3.1(R52C) overexpression, and treated with paraquat . Cells were snap frozen for subsequent molecular analysis
Total RNA obtained from RWPE1 cells. Engineered RWPE1 cells were harvested and processed for RNA isolation and transcriptome analysis using the MagMAX RNA isolation kit (Ambion).

For queries, please contact Cory Abate-Shen at cabateshen@columbia.edu

first: Aditya

last: Dutta

first: Cory

last: Abate-Shen

first: Alexandros

last: Papachristodoulou


title: MarR type regulator PA3458 is involved in osmoadaptation control in Pseudomonas aeruginosa (ChIP-seq)

status: Public on Apr 12 2021

city: Warszawa

first: Adam

last: Kawałek

address: Pawinskiego 5A

department: Department of Microbial Biochemistry

country: Poland

institute: Institute of Biochemistry and Biophysics, PAS

summary: Pseudomonas aeruginosa is a common bacterium, but also a facultative human pathogen, especially fatal for immunocompromised patients. It is dangerous due to its high adaptability and intrinsic antibiotic resistance mechanisms making treatment of P. aeruginosa infections particularly difficult. Sophisticated, complex, multilevel regulatory systems engaging huge repertoire of transcriptional regulators (TRs) are the main factors that direct cellular processes to keep cellular homeostasis and adapt to changeable conditions. The PA3458 gene encodes a putative MarR-type TR. Most representatives of MarR family are described as repressors involved in response to various environmental signals and control of different processes e.g. adhesion, virulence, antibiotic resistance. Transcriptional profiling of P. aeruginosa PAO1161 overexpressing PA3458 showed changes in mRNA level of 133 genes, among them 100 was down-regulated, pointing out the role of PA3458 as a repressor. ChIP-seq analysis identified multiple PA3458 binding sites in P. aeruginosa genome suggesting its role as a global regulator. The preferred sequence motif recognised by PA3458 was identified. Many genes involved in stress response are under control of PA3458. The PA3459-PA3461 operon, divergent to PA3458 gene is regulated by PA3458. It encodes: asparagine synthase, GNAT-family acetyltransferase and glutamyl aminopeptidase, respectively engaged in the production of potent osmoprotectant an N-acetylglutaminylglutamine amide (NAGGN). Overall, the PA3458 is engaged in osmoadaptation control in P. aeruginosa.

overall_design: Pseudomonas aeruginosa PAO1161 (leu-, r-, RifR) derivative of PAO1, was used in the experiment (Kawalek et al., 2020; BMC Genomics, 21:14). Chromatin immunoprecipitation and sequencing (ChIP-seq) analysis was performed on P. aeruginosa PAO1161 ΔPA3458 / pKKB2.12 (araC araBADp-PA3458-flag) (hereafter referred to as PA3458-F) as well as PAO1161 / pABB28.3 (araC araBADp-flag), empty vector control (hereafter called EV-F) strains. Cells were grown under selection in L broth with 0.02% arabinose until OD600 = 0.5). For each biological replicate, two independent cultures of each strain were pooled together. The immunoprecipitation was performed with commercially available polyclonal anti-FLAG antibodies (DYKDDDDK Tag polyclonal  antibodies; PA1-985B; Invitrogen).

first: Karolina

last: Kotecka

last: Kawalek

first: Aneta

last: Bartosik


title: Single-cell transcriptomics of human intestinal organoids infected with  SARS-CoV-2

city: Heidelberg

first: Sergio

last: Triana

address: Meyerhofstr. 1

department: Structural and Computational biology

institute: EMBL

summary: In this work we have employed a single cell sequencing approach of both ileum and colon organoids using 10x Genomics scRNAseq and TAP-seq targeted single-cell RNA-seq.

overall_design: 10x Genomics single-cell RNA sequencing V3.1 and targeted single-cell RNA-seq (TAP) was perfomed on Colon and Ilean organoids infected with SARS-CoV-2 at mock condition and after 12hpi and 24hpi


title: Polycomb factor Phf19 controls cell growth and differentiation towards erythroid pathway in chronic myeloid leukemia cells

city: Barcelona

first: Enrique

last: Blanco

address: Dr. Aiguader 88

department: Gene Regulation, Stem Cells and Cancer

country: Spain

institute: Center for Genomic Regulation (CRG)

summary: Polycomb group (PcG) of proteins are a group of highly conserved epigenetic regulators involved in many biological functions, such as embryonic development, cell proliferation and adult stem cell determination. PHD finger protein 19 (PHF19) is an associated factor of Polycomb Repressor Complex 2 (PRC2) up-regulated in different human cancers. In particular, myeloid leukemia cell lines show increased levels of PHF19, yet little is known about its function. Here, we have characterized the role of PHF19 in cell lines of a type of myeloid leukemia named chronic myeloid leukemia (CML). Thus, we have demonstrated that PHF19 depletion decreases cell proliferation and promotes differentiation. Mechanistically, we have shown how PHF19 regulates the proliferation of CML through its epigenetic regulation of the cell cycle regulator p21. Furthermore, we have observed that MTF2, a PHF19 homolog, compensates at chromatin level for PHF19 depletion, instructing specific erythroid differentiation. Taken together, our results show that PHF19 is a key transcriptional regulator for cell fate determination and could be a potential target for myeloid leukemia treatment.

overall_design:
ChIP-seq (6 samples with fly spike-in) of K562 cells. shCT means shRNA Control, sh1 and sh2 are two different knock-downs of PHF19 long isoform.
RNA-seq (6 samples, 3 conditions with 2 replicates per condition) of K562 cells. shCT means shRNA Control, sh1 and sh2 are two different knock-downs of PHF19 long isoform.

first: Marc

last: García-Montolio

first: Cecilia

last: Ballaré

first: Pedro

last: Vizán


title: DNMT3A haploinsufficiency causes dichotomous DNA methylation defects at enhancers in mature human immune cells

city: Irvine

first: Minji

last: Byun

address: 829 Health Science Rd, 311

department: Microbiology and Molecular Genetics

institute: University of California Irvine

type: Methylation profiling by genome tiling array


title: NKX3.1 localization to mitochondria suppresses prostate cancer initiation  (Mouse 4M Prostate RNASeq)

first: Antonina

last: Mitrofanova

overall_design:
Analysis of transcriptome of prostate tissue from 4 month old mouse tissue
Prostate tissue from 4 month old Nkx3.1+/+ and Nkx3.1-/- mice  treated with paraquat was harvested, and snap frozen for subsequent molecular analysis
Total RNA obtained from prostate tissues. Prostate tissues were harvested and processed for RNA isolation and transcriptome analysis using the MagMAX RNA isolation kit (Ambion).

For queries, please contact Cory Abate-Shen at cabateshen@columbia.edu


title: Overlapping roles of spliceosomal components SF3B1 and PHF5A in rice splicing regulation

status: Public on Apr 11 2021

city: Jeddah

first: Haroon

last: Butt

state: Makkah

address: King Abdullah University of Science and Technology (KAUST) Thuwal, 23955-6900

department: BESE

country: Saudi Arabia

institute: KAUST

summary: The SF3B complex, a multiprotein component of the U2 snRNP of the spliceosome, mediates branch point selection and facilitates spliceosome assembly and activation. Several splicing modulators bind the SF3B1 and PHF5A subunits of the SF3B complex and globally inhibit splicing. Engineered mutant variants of SF3B1 and PHF5A conferred tolerance to splicing inhibitors with only minor effects on gene expression and AS.

overall_design: 7-day-old seedlings of SF3B1, PHF5A and WT are treated for six hours with splicing inhibitor GEX1A

first: Jeremie

last: Bazin

first: Sahar

last: Alshareef

first: Ayman

last: Eid

first: Moussa

last: Benhamed

first: Anireddy S

middle: N

last: Reddy

first: Martin

last: Crespi

first: Magdy

last: Mahfouz


title: Astrocytes differentiation is modulated by the NF-KB pathway

city: Belvaux

first: Luc

last: Grandbarbe

address: 7, Avenue des Hauts Fourneaux

department: Life Sciences Research Unit

country: Luxembourg

institute: University of Luxembourg

summary: We demonstrate that persistent NF-KB activation affects neural progenitor cells-derived astrocytes differentiation

overall_design: time series from 0 to 72h of control (FCS) versus TNF treatment, 3 biological replicates

first: Cindy

last: Birck


title: LY6K-AS lncRNA is a lung adenocarcinoma prognostic biomarker and regulator of mitotic progression

status: Public on Apr 07 2021

city: Gothenburg

first: Subazini

last: TK

address: Medicineragatan 9A

institute: Gothenburg university

summary:
Purpose: Lung adenocarcinoma tumors acquire resistance to the newly-developed as well as existing therapies that restricts life quality improvements. The goal of the current study is to investigate the noncoding portion of the human transcriptome in search of actionable targets for lung adenocarcinoma treatment.
Methods: The identified actionable targets (LY6K-AS lncRNA and YWHAG) were transiently downregulated in A549 cell line using either LNA-GapmeRs or siRNA. RNA was extracted from each sample and analyzed in respect to the corresponding control.
Results: LY6K-AS lncRNA regulated mitotic progression in A549 cell line through the interaction with YWHAG to orchestrate the expression of several mitosis-promoting factors.
Conclusions: Our study indicates that LY6K-AS silencing is a promising therapeutic option for LUAD that inhibits oncogenic mitotic progression.

overall_design: RNA profiles of LY6K-Asdepleted A549 cells and YWHAG-depleted A549 cells were analyzed using illumina whole RNA-seq analysis.

first: Chandrasekhar

last: Kanduri

first: Mohamad

last: Ali

middle: T

last: Kosalai


title: The chromatin accessibility landscape reveals distinct transcriptional regulation in the induction of human primordial germ cell-like cells from pluripotent stem cells

city: Munster

first: Veeramohan

last: Veerapandian

state: North Rhine-Westphalia

address: Röntgenstr. 20

department: Department Tissue Morphogenesis

institute: Max Planck Institute for Molecular Biomedicine

summary: The  accessibility chromatin patterns during hPGCLCs undergo a diverse changes in absence of SOX15. The consequence of these changes lead to a somatic gene network activation that leads to decrease hPGCLC at late stage

overall_design: We analyzed the transcription factors binding profiles using cut-tag sequencing in human primordial germ cell like cells (hPGCLCs) comparing to SOX15-/-


title: Human KIT+ myeloid cells facilitate visceral metastasis by melanoma

status: Public on Apr 08 2021

city: Farmington

first: Carolyn

last: Paisie

state: CT

address: 10 Discovery Dr

institute: The Jackson Laboratory for Genomic Medicine

summary: Metastasis of melanoma significantly worsens prognosis and therefore therapeutic interventions that prevent, or slow metastasis could improve patient outcomes. Here, we show using humanized mice that colonization of distant visceral organs with melanoma is dependent upon a human CD33+CD11b+CD117+ progenitor cell subset comprising <4% of the human CD45+ leukocytes. Metastatic tumor-infiltrating CD33+ cells from patients and humanized (h)NSG-SGM3 mice showed converging transcriptional profiles. Single-cell RNAseq analysis identified a gene signature of a KIT/CD117 expressing CD33+ subset that correlated with decreased overall survival in TCGA melanoma samples. Thus, human CD33+CD11b+CD117+ myeloid cells represent a novel candidate biomarker as well as a therapeutic target for metastatic melanoma.

overall_design: We examed the transcriptomic of CD33pos cells in NSG-SGM3 mice transplated with human hematopoietic stem cells for their capacity to facilitate human melanoma metastasis

first: Chun

middle: I

last: Yu

first: Jan

last: Martinek

first: Te-Chia

last: Wu

first: KyungIn

last: Kim

first: Joshy

last: George

first: Elaheh

last: Ahmadzadeh

first: Rick

last: Maser

first: Florentina

last: Marches

first: Patrick

last: Metang

first: Pierre

last: Authie

first: Vanessa

middle: K

last: Oliveira

first: Victor

last: Wang

first: Jeffrey

middle: H

last: Chuang

first: Paul

last: Robson

first: Jacques

last: Banchereau

first: Karolina

last: Palucka


title: The genome-wide analysis of H3K4me3 in human umbilical cord blood

city: Rennes

first: Fatima

last: SMAGULOVA

address: 9 av. Prof. Léon Bernard

institute: Irset - U1085

summary: We hypothesised that gestational exposure to chlordecone (CD) can lead to alteration of epigenetic landscape, specifically marks associated with transcriptional activity of the genes, such as H3K4me3 marks. We performed ChIP using anti-H3K4me3 commercial antibody (Millipore - 07-473). DNA-protein complexes were immunoprecipitated, eluted and then DNA were purified. We prepared libraries using NEBNext Ultra II DNA Library Prep Kit for Illumina. 13 libraries were prepared: 6 control, 6 CD-exposed and 1 input. After pre-processing of the sequencing data, we performed a comparison of peaks occupancy between control and exposed samples.

overall_design: H3K4me3 ChIP-seq of human umbilical cord blood.

last: Smagulova

first: Louis

last: Legoff


first: Veeramohan

last: Veerapandian

overall_design: We analyzed the acessible genome profiles in human primordial germ cell like cells (hPGCLCs) comparing to SOX15-/-


title: COVID-19 tissue atlases reveal SARS-COV-2 pathology and cellular targets

status: Public on Apr 09 2021

city: Cambridge

first: Caroline

last: Porter

address: 415 Main Street

department: Klarman Cell Observatory

institute: Broad Institute

summary: COVID-19, caused by SARS-CoV-2, can result in acute respiratory distress syndrome and multiple-organ failure, but little is known about its pathophysiology. Here, we generated single-cell atlases of 23 lung, 16 kidney, 15 liver and 18 heart COVID-19 autopsy donor tissue samples, and spatial atlases of 14 lung donors. Integrated computational analysis uncovered substantial remodeling in the lung epithelial, immune and stromal compartments, with evidence of multiple paths of failed tissue regeneration, including defective alveolar type 2 differentiation and expansion of myofibroblasts and putative TP63+ intrapulmonary basal-like progenitor cells. Viral RNAs were enriched in mononuclear phagocytic and endothelial lung cells which induced specific host programs. Spatial analysis in lung distinguished inflammatory host responses in lung regions with and without viral RNA. Analysis of the other tissue atlases showed transcriptional alterations in multiple cell types in COVID-19 donor heart tissue, and mapped cell types and genes implicated with disease severity based on COVID-19 GWAS. Our foundational dataset elucidates the biological impact of severe SARS-CoV-2 infection across the body a key step towards new treatments.

overall_design:
We developed a large cross-body COVID-19 autopsy biobank of 420 autopsy specimens, spanning 11 organs and 17 donors and used it to generate a single cell atlas of COVID-19 lung, kidney, liver and heart from up to 16 donors, and a lung spatial atlas. For our single-cell and single-nucleus RNA-Seq data, we provide both Cellranger raw counts matrices and counts matrices following ambient and emtpy drop removal using Cellbender remove-background for all lung, heart, liver, and kidney samples included in our published atlases as well as for a some airway and lymph node samples that we generated data for but did not analyze or include in our publication. We provide a metadata file including a list of barcodes that passed QC, basic QC metrics, and annotations for the lung, heart, liver, and kidney atlases. We  provide an RSEM countsmatrix for our bulk RNA-sequencing samples, including data for the lung samples we analyzed and included in our publication as well as one heart and one brain sample that we did not include in our publication.
NOTE from submitter: This submission does not contain raw data files as the fastq files contain protected patient information. Fastq files will be deposited to DUOS.

first: Toni

last: Delorey

first: Carly

middle: G

last: Ziegler

first: Graham

last: Heimberg

first: Rachelly

last: Normand

first: Yiming

last: Yang

first: Åsa

last: Segerstolpe

first: Domenic

last: Abbondanza

first: Stephen

last: Fleming

first: Ayshwarya

last: Subramanian

first: Daniel

last: Montoro

first: Karthik

last: Jagadeesh

first: Kushal

last: Dey

first: Pritha

last: Sen

first: Michal

last: Slyper

first: Yered

last: Pita-Juárez

first: Devan

last: Phillips

first: Jana

last: Biermann

first: Zohar

last: Bloom-Ackermann

first: Nick

last: Barkas

first: Andrea

last: Ganna

first: James

last: Gomez

first: Johannes

middle: C

last: Melms

first: Igor

last: Katsyv

first: Erica

last: Normandin

first: Pourya

last: Naderi

first: Yury

middle: V

last: Popov

first: Siddharth

middle: S

last: Raju

first: Sebastian

last: Niezen

first: Linus

last: Tsai

first: Katherine

last: Siddle

first: Malika

last: Sud

first: Victoria

last: Tran

first: Shamsudheen

last: Vellarikkal

first: Yiping

first: Liat

last: Amir-Zilberstein

first: Deepak

last: Atri

first: Joseph

last: Beechem

first: Olga

middle: R

last: Brook


title: Single-cell RNA sequencing of human nasal swab from healthy donors

status: Public on Apr 06 2021

city: Daejeon

first: JUNGMO

last: KIM

state: -- None selected --

address: 291 Daehak-ro, Yuseong-gu

department: Center for Vascular Research

country: South Korea

institute: Institute for Basic Science

summary: Understanding on pathogenesis of COVID-19 is rapidly growing, but primary target cells of SARS-CoV-2 infection is still not known. Here, we performed single cell RNA sequencing on human nasal swab from healthy donors to investigate the expression patterns of host cell entry factors of SARS-CoV-2.

overall_design: Single cells from healthy donors' nasal swabs  were isolated and single-cell transcriptome libraries were generated

first: Gou-Young

last: Koh

first: JungMo

last: Kim


title: MeRIP-sequencing in lung adenocarcinoma cells

city: BeiJing

first: Xueying

last: Yang

address: No. 17, Nanli, Panjiayuan, Chaoyang District, Beijing

institute: Cancer Hospital, Chinese Academy of Medical Sciences

summary: IP with m6A-specific antibodies and input sequencing for every sample.

overall_design:
Examining 2 conditions, H322 cells with or without FTO depletion, m6A-sequencing
[Contributor]  cloudseq


first: Veeramohan

last: Veerapandian

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

overall_design: Refer to individual Series


title: De novo Epstein-Barr virus infection of pseudostratified nasopharynx epithelial cells differentiated at the air-liquid interface (ALI)

city: PITTSBURGH

first: Yulong

last: Bai

state: Pennsylvania

address: Public Health Building, 130 De Soto St,, 3121

department: Human Genetics

institute: University of Pittsburgh

summary: This donor NP-H10 was susceptible to EBV infection and produced a lytic infection as determined by Zebra and gp350 immunostaining.

overall_design: Primary nasopharynx-derived epithelial cells were differentiated in ALI conditions and then infected with recombinant EBV (Akata strain). The recombinant EBV expresses the GFP marker gene inserted into the BXLF1 locus (PMID 11562531). Expression of EBV BamHI A RNA transcripts (BARTs) is retained (PMID 16611410).

first: Kathy

last: Shair


title: Dichotomous roles of Arid5a augment the immunosuppressive microenvironment of mesenchymal malignant tumors

city: Suita

first: Daisuke

last: Okuzaki

state: Osaka

address: Yamadaoka 3-1

department: Immunology Frontier Research Center

institute: Osaka univ.

summary: Although mesenchymal subtypes of pancreatic ductal adenocarcinoma (PDAC) and colorectal cancer (CRC) are known as “immunologically cold” tumors, the molecular link between tumor immune evasiveness and mesenchymal phenotype remains largely unknown. Here, we show that AT-rich interaction domain-containing protein 5a (Arid5a), an RNA-binding protein, is involved in immune evasion in PDAC and CRC mouse models. Mass cytometry demonstrated that in tumors from Arid5a-deficient cells, the infiltration of granulocytic myeloid-derived suppressor cells and regulatory T cells is suppressed, but cytotoxic T-lymphocyte recruitment is enhanced. Mechanistically, Arid5a augmented Ido1 and Ccl2 expression by stabilizing these mRNAs in the PDAC model, but not Ido1 in the CRC model. Furthermore, Arid5a expression was substantially increased in mesenchymal subtypes of PDAC and CRC, mediated by ZEB1, and Arid5a promoted TGF-b-induced and IL6-induced epithelial-mesenchymal transition and acquisition of invasiveness in PDAC model cells. Thus, our findings demonstrate that Arid5a is a promising target for immunotolerant malignant tumors.

overall_design: Comparison of gene expression profiles between WT and Arid5a knockout (KO) in KPC and MC38 cells by RNA sequencing

first: Shigeru

last: Hashimoto


title: Familial Thrombocyotpenia due to a WAC-ANKRD26 Gene Fusion

status: Public on Apr 05 2021

city: Boston

first: Vijay

last: Sankaran

address: 1 Blackfan Cr

institute: Boston Children's Hospital

summary: Human peripheral blood mononuclear cells from patients carrying a WAC-ANKRD26 gene fusion caused by a duplication-inversion-duplication and healthy controls

overall_design: 3 individuals affected with dup-inv-dup, 3 healthy controls. RNA was isolated using a RNeasy Micro kit (Qiagen) according to the manufacturer’s instructions. An on-column DNase digestion was performed before RNA was quantified using a Qubit RNA HS Assay kit (Invitrogen). ~10 ng of RNA was used as input to a modified SMART-seq2 protocol and after reverse transcription, 10 cycles of PCR were used to amplify transcriptome library12,14,15. Quality of whole transcriptome libraries was validated using a High Sensitivity DNA Chip run on a Bioanalyzer 2100 system (Agilent), followed by library preparation using the Nextera XT kit (Illumina) and custom index primers according to the manufacturer’s instructions. Final libraries were quantified using a Qubit dsDNA HS Assay kit (Invitrogen) and a High Sensitivity DNA chip run on a Bioanalyzer 2100 system (Agilent). All libraries were sequenced using Nextseq High Output Cartridge kits and a Nextseq 500 sequencer (Illumina).

first: Lara

last: Wahlster

first: Jeffrey

last: Verboon