APC/CCCS52A2 repressed phytosulfokine signaling restricts root QC cell proliferation through ERF115 degradation
The quiescent center (QC) plays an essential role during root development by creating a  microenvironment that preserves the stem cell fate of its surrounding cells. Strikingly, in  order to retain root structure, QC cells only occasionally self-renew, displaying a  proliferation rate far below that of all other cells within the root meristem. Previously, the  APC/CCCS52A2 ubiquitine ligase and brassinosteroid signaling pathways have been found to  antagonistically control Arabidopsis thaliana QC cell proliferation. Here, we demonstrate  that both pathways converge on the ERF115 transcription factor that acts as a rate-limiting  factor of QC cell division through transcriptional control of the autocrine phytosulfokine  PSK5 peptide hormone. ERF115 marks QC cell division but is restrained through  proteolysis by the APC/CCCS52A2 ubiquitine ligase, whereas QC proliferation is driven by  brassinosteroid-dependent ERF115 expression. Combined, these two antagonistic  mechanisms delimit the ERF115-PSK5 activity and QC renewal. Our results reveal a  unique cell cycle regulatory mechanism that accounts for the low proliferation rate of QC  cells within a surrounding population of highly mitotic active cells. Overall design: ChIP-seq analysis of genes bound by the ERF115 transcription factor, using mock ChIP with wild type cells as negative control. Analyzed by Illumina HiSeq