DNA double-strand breaks enhance brassinosteroid signaling to activate quiescent center cell division in Arabidopsis.
BRL3
Brassinosteroid
DNA damage
ERF115
quiescent center
regeneration
Journal
Journal of experimental botany
ISSN: 1460-2431
Titre abrégé: J Exp Bot
Pays: England
ID NLM: 9882906
Informations de publication
Date de publication:
26 Oct 2023
26 Oct 2023
Historique:
received:
31
07
2023
medline:
26
10
2023
pubmed:
26
10
2023
entrez:
26
10
2023
Statut:
aheadofprint
Résumé
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.
Identifiants
pubmed: 37882240
pii: 7330313
doi: 10.1093/jxb/erad424
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email: journals.permissions@oup.com.