Bacillus subtilis RecA, DisA, and RadA/Sms Interplay Prevents Replication Stress by Regulating Fork Remodeling

Reviving Bacillus subtilis spores require the recombinase RecA, the DNA damage checkpoint sensor DisA, and the DNA helicase RadA/Sms to prevent a DNA replication stress. When a replication fork stalls at a template lesion, RecA filaments onto the lesion-containing gap and the fork is remodeled (fork...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Rubén Torres, Juan C. Alonso
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	DNA repair c-di-AMP fork stalling fork reversal template switching Holliday junction Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/a065527f7ef94034b1e1c709760c5bba
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:a065527f7ef94034b1e1c709760c5bba
record_format	dspace
spelling	oai:doaj.org-article:a065527f7ef94034b1e1c709760c5bba2021-11-22T06:19:52ZBacillus subtilis RecA, DisA, and RadA/Sms Interplay Prevents Replication Stress by Regulating Fork Remodeling1664-302X10.3389/fmicb.2021.766897https://doaj.org/article/a065527f7ef94034b1e1c709760c5bba2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fmicb.2021.766897/fullhttps://doaj.org/toc/1664-302XReviving Bacillus subtilis spores require the recombinase RecA, the DNA damage checkpoint sensor DisA, and the DNA helicase RadA/Sms to prevent a DNA replication stress. When a replication fork stalls at a template lesion, RecA filaments onto the lesion-containing gap and the fork is remodeled (fork reversal). RecA bound to single-strand DNA (ssDNA) interacts with and recruits DisA and RadA/Sms on the branched DNA intermediates (stalled or reversed forks), but DisA and RadA/Sms limit RecA activities and DisA suppresses its c-di-AMP synthesis. We show that RecA, acting as an accessory protein, activates RadA/Sms to unwind the nascent lagging-strand of the branched intermediates rather than to branch migrate them. DisA limits the ssDNA-dependent ATPase activity of RadA/Sms C13A, and inhibits the helicase activity of RadA/Sms by a protein-protein interaction. Finally, RadA/Sms inhibits DisA-mediated c-di-AMP synthesis and indirectly inhibits cell proliferation, but RecA counters this negative effect. We propose that the interactions among DisA, RecA and RadA/Sms, which are mutually exclusive, contribute to generate the substrate for replication restart, regulate the c-di-AMP pool and limit fork restoration in order to maintain cell survival.Rubén TorresJuan C. AlonsoFrontiers Media S.A.articleDNA repairc-di-AMPfork stallingfork reversaltemplate switchingHolliday junctionMicrobiologyQR1-502ENFrontiers in Microbiology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	DNA repair c-di-AMP fork stalling fork reversal template switching Holliday junction Microbiology QR1-502
spellingShingle	DNA repair c-di-AMP fork stalling fork reversal template switching Holliday junction Microbiology QR1-502 Rubén Torres Juan C. Alonso Bacillus subtilis RecA, DisA, and RadA/Sms Interplay Prevents Replication Stress by Regulating Fork Remodeling
description	Reviving Bacillus subtilis spores require the recombinase RecA, the DNA damage checkpoint sensor DisA, and the DNA helicase RadA/Sms to prevent a DNA replication stress. When a replication fork stalls at a template lesion, RecA filaments onto the lesion-containing gap and the fork is remodeled (fork reversal). RecA bound to single-strand DNA (ssDNA) interacts with and recruits DisA and RadA/Sms on the branched DNA intermediates (stalled or reversed forks), but DisA and RadA/Sms limit RecA activities and DisA suppresses its c-di-AMP synthesis. We show that RecA, acting as an accessory protein, activates RadA/Sms to unwind the nascent lagging-strand of the branched intermediates rather than to branch migrate them. DisA limits the ssDNA-dependent ATPase activity of RadA/Sms C13A, and inhibits the helicase activity of RadA/Sms by a protein-protein interaction. Finally, RadA/Sms inhibits DisA-mediated c-di-AMP synthesis and indirectly inhibits cell proliferation, but RecA counters this negative effect. We propose that the interactions among DisA, RecA and RadA/Sms, which are mutually exclusive, contribute to generate the substrate for replication restart, regulate the c-di-AMP pool and limit fork restoration in order to maintain cell survival.
format	article
author	Rubén Torres Juan C. Alonso
author_facet	Rubén Torres Juan C. Alonso
author_sort	Rubén Torres
title	Bacillus subtilis RecA, DisA, and RadA/Sms Interplay Prevents Replication Stress by Regulating Fork Remodeling
title_short	Bacillus subtilis RecA, DisA, and RadA/Sms Interplay Prevents Replication Stress by Regulating Fork Remodeling
title_full	Bacillus subtilis RecA, DisA, and RadA/Sms Interplay Prevents Replication Stress by Regulating Fork Remodeling
title_fullStr	Bacillus subtilis RecA, DisA, and RadA/Sms Interplay Prevents Replication Stress by Regulating Fork Remodeling
title_full_unstemmed	Bacillus subtilis RecA, DisA, and RadA/Sms Interplay Prevents Replication Stress by Regulating Fork Remodeling
title_sort	bacillus subtilis reca, disa, and rada/sms interplay prevents replication stress by regulating fork remodeling
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/a065527f7ef94034b1e1c709760c5bba
work_keys_str_mv	AT rubentorres bacillussubtilisrecadisaandradasmsinterplaypreventsreplicationstressbyregulatingforkremodeling AT juancalonso bacillussubtilisrecadisaandradasmsinterplaypreventsreplicationstressbyregulatingforkremodeling
_version_	1718418118070501376

Bacillus subtilis RecA, DisA, and RadA/Sms Interplay Prevents Replication Stress by Regulating Fork Remodeling

Ejemplares similares