Title
Overproduction of a dominant mutant of the conserved era GTPase inhibits cell division in escherichia coli
Date Issued
08 October 2020
Access level
open access
Resource Type
journal article
Author(s)
Zhou X.
Peters H.K.
Li X.
Costantino N.
Kumari V.
Shi G.
Tu C.
Cameron T.A.
Haeusser D.P.
Ji X.
Margolin W.
Court D.L.
McGovern Medical School
Publisher(s)
American Society for Microbiology
Abstract
Cell growth and division are coordinated, ensuring homeostasis under any given growth condition, with division occurring as cell mass doubles. The signals and controlling circuit(s) between growth and division are not well understood; however, it is known in Escherichia coli that the essential GTPase Era, which is growth rate regulated, coordinates the two functions and may be a checkpoint regulator of both. We have isolated a mutant of Era that separates its effect on growth and division. When overproduced, the mutant protein Era647 is dominant to wildtype Era and blocks division, causing cells to filament. Multicopy suppressors that prevent the filamentation phenotype of Era647 either increase the expression of FtsZ or decrease the expression of the Era647 protein. Excess Era647 induces complete delocalization of Z rings, providing an explanation for why Era647 induces filamentation, but this effect is probably not due to direct interaction between Era647 and FtsZ. The hypermorphic ftsZ∗allele at the native locus can suppress the effects of Era647 overproduction, indicating that extra FtsZ is not required for the suppression, but another hypermorphic allele that accelerates cell division through periplasmic signaling, ftsL∗, cannot. Together, these results suggest that Era647 blocks cell division by destabilizing the Z ring.
Volume
202
Issue
21
Language
English
OCDE Knowledge area
Biología celular, Microbiología
Scopus EID
2-s2.0-85092749893
PubMed ID
Source
Journal of Bacteriology
ISSN of the container
0021-9193
Sponsor(s)
This work was supported by National Institutes of Health grants GM61074 and GM131705 to W.M.; in part by the Intramural Research Program of the National Institutes of Health, National Cancer Institute, Center for Cancer Research; and by federal funds from the National Cancer Institute, National Institutes of Health, under contract N01-CO-12400, to D.L.C. and X.J.
Sources of information: Directorio de Producción Científica Scopus