DNA double-strand breaks enhance brassinosteroid signaling to activate quiescent center cell division in Arabidopsis.

Abstract

In Arabidopsis roots, the quiescent center (QC), a group of slowly dividing cells located at the center of the stem cell niche, functions as an organizing center to maintain the stemness of neighboring cells. Recent studies have shown that they also act as a reservoir for backup cells, which replenish DNA-damaged stem cells by activating cell division. The latter function is essential for maintaining stem cells under stressful conditions, thereby guaranteeing post-embryonic root development in fluctuating environments. In this study, we show that one of the brassinosteroid receptors in Arabidopsis, BRASSINOSTEROID INSENSITIVE1-LIKE3 (BRL3), plays a major role in activating QC division in response to DNA double-strand breaks. SUPPRESSOR OF GAMMA RESPONSE 1, a master transcription factor governing DNA damage response, directly induces BRL3. DNA damage-induced QC division was completely suppressed in brl3 mutants, whereas QC-specific overexpression of BRL3 activated QC division. Our data also showed that BRL3 is required to induce the AP2-type transcription factor ETHYLENE RESPONSE FACTOR 115, which triggers regenerative cell division. We propose that BRL3-dependent brassinosteroid signaling plays a unique role in activating QC division and replenishing dead stem cells, thereby enabling roots to restart growing after recovery from genotoxic stress.