ERF115 Controls Root Quiescent Center Cell Division and Stem Cell Replenishment

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Science  15 Nov 2013:
Vol. 342, Issue 6160, pp. 860-863
DOI: 10.1126/science.1240667

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The Root of the Problem

The quiescent center (QC) within the root meristem plays a key role as a stem cell organizer to sustain the root stem cell niche. The QC cells execute a dual role: prevention of the differentiation of neighboring stem cells, and maintenance of the root structure by undergoing only occasional cell division. The mechanisms that account for the low QC proliferation are unclear, although the anaphase-promoting complex/cyclosome (APC/C) E3 ubiquitin ligase is known to suppress QC cell division. Through a systematic functional analysis of APC/C-copurifying proteins, Heyman et al. (p. 860) characterized a transcription factor ERF115 as a rate-limiting factor for QC cell division. ERF115 needs to be destroyed to retain QC cells in a resting state. ERF115 operates in a brassinosteroid-dependent manner and controls QC cell division through transcriptional activation of phytosulfokine signaling.


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. Despite being surrounded by highly mitotic active cells, QC cells self-renew at a low proliferation rate. Here, we identified the ERF115 transcription factor as a rate-limiting factor of QC cell division, acting as a transcriptional activator of the phytosulfokine PSK5 peptide hormone. ERF115 marks QC cell division but is restrained through proteolysis by the APC/CCCS52A2 ubiquitin ligase, whereas QC proliferation is driven by brassinosteroid-dependent ERF115 expression. Together, these two antagonistic mechanisms delimit ERF115 activity, which is called upon when surrounding stem cells are damaged, revealing a cell cycle regulatory mechanism accounting for stem cell niche longevity.

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