GSE185388
ChIP-seq of a transcriptional regulator AtSDR4L
Repression of embryonic traits during the seed-to-seedling phase transition requires the inactivation of master transcription factors associated with embryogenesis. How the timing of such inactivation is controlled is unclear. Here, we report on a novel transcriptional co-repressor, Arabidopsis thaliana SDR4L, that forms a feedback inhibition loop with the master transcription factors LEC1 and ABI3 to repress post-germinative embryonic traits. LEC1 and ABI3 regulate their own expression by inducing AtSDR4L during mid- to late embryogenesis. AtSDR4L directly binds to the promoter of LEC1. Atsdr4l mutant seedlings phenocopy the LEC1 overexpressors, and their embryonic traits could be partially rescued by impairing LEC1 or ABI3. The penetrance and expressivity of the Atsdr4l phenotypes depend on both developmental and external cues, demonstrating the broad regulatory potential offered by AtSDR4L during the seed-to-seedling phase transition. Overall design: ChIP was carried out using two biological replicates of ß-Estradiol induced AtSDR4-HA seedlings. A control ChIP was carried out using uninduced AtSDR4-HA seedlings.  ß-Estradiol induced treament samples and  uninduced control sample were harvested at 4 days after imbibition. Libraries were sequenced on Illumina NextSeq2000. Peaks were called by MACS2 (v2.2.7.1) between the treatment and control samples using demultiplexed and adatper-trimmed pair-end reads.