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Series GSE269849 Query DataSets for GSE269849
Status Public on Jun 20, 2024
Title bHLH transcription factors cooperate with chromatin remodelers to regulate cell fate decisions during Arabidopsis stomatal development
Organism Arabidopsis thaliana
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Summary The development of multi-cellular organisms requires coordinated changes in gene expression that are often mediated by the interaction between transcription factors (TFs) and their corresponding cis-regulatory elements (CREs). During development and differentiation, the accessibility of CREs is dynamically modulated by the epigenome. How the epigenome, CREs and TFs together exert control over cell fate commitment remains to be fully understood. In the Arabidopsis leaf epidermis, meristemoids undergo a series of stereotyped cell divisions, then switch fate to commit to stomatal differentiation. Newly created or reanalyzed scRNA-seq and ChIP-seq data confirm that stomatal development involves distinctive phases of transcriptional regulation and that differentially regulated genes are bound by the stomatal basic-helix-loop-helix (bHLH) TFs. Targets of the bHLHs often reside in repressive chromatin before activation. MNase-seq evidence further suggests that the repressive state can be overcome and remodeled upon activation by specific stomatal bHLHs. We propose that chromatin remodeling is mediated through the recruitment of a set of physical interactors that we identified through proximity labeling – the ATPase-dependent chromatin remodeling SWI/SNF complex and the histone acetyltransferase HAC1. The bHLHs and chromatin remodelers localize to overlapping genomic regions in a hierarchical order. Furthermore, plants with stage-specific knock-down of the SWI/SNF components or HAC1 fail to activate specific bHLH targets and display stomatal development defects. Together these data converge on a model for how stomatal TFs and epigenetic machinery cooperatively regulate transcription and chromatin remodeling during progressive fate specification.
 
Overall design Chromatin Immunoprecipitation DNA sequencing (ChIP-seq) for FAMA with anti-MYC antibody using a MYC tagged FAMA line, and control WT line that does not contain the transgene. Micrococcal Nuclease digestion with deep sequencing (MNase-seq) in seedlings with MUTE induced with estradiol or mock control. Replicates were pooled.
 
Contributor(s) Liu A, Matos JL, Bergmann DC
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BioProject PRJNA1053499
Submission date Jun 14, 2024
Last update date Jun 20, 2024
Contact name Dominique C. Bergmann
E-mail(s) dbergmann@stanford.edu
Organization name Stanford University
Department Biology
Street address 371 Jane Stanford Way
City Stanford
ZIP/Postal code 94305
Country USA
 
Platforms (2)
GPL13222 Illumina HiSeq 2000 (Arabidopsis thaliana)
GPL19580 Illumina NextSeq 500 (Arabidopsis thaliana)
Samples (5)
GSM8328865 Col, FAMA ChIP
GSM8328866 FAMApro::FAMA-MYC/fama-1, FAMA ChIP
GSM8328867 FAMApro::FAMA-MYC/fama-1, input

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE269849_FAMA_ChIP_fold_enrichment.bw 320.5 Mb (ftp)(http) BW
GSE269849_control.bw 41.9 Mb (ftp)(http) BW
GSE269849_estrodial.bw 45.0 Mb (ftp)(http) BW
SRA Run SelectorHelp
Raw data are available in SRA

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