Novel mechanism of cell division inhibition associated with the SOS response in Escherichia coli.
AUTOR(ES)
D'Ari, R
RESUMO
Certain Escherichia coli strains were shown to possess a novel system of cell division inhibition, called the SfiC+ phenotype. SfiC+ filamentation had a number of properties similar to those of sfiA-dependent division inhibition previously described: (i) both are associated with the SOS response induced by expression of the recA(Tif) mutation, (ii) both are associated with cell death, (iii) both are amplified in mutants lacking the Lon protease, and (iv) both are suppressed by sfiB mutations. SfiC+ filamentation and sfiA-dependent division inhibition differed in (i) the physiological conditions under which loss of viability is observed, (ii) the extent of amplification in lon mutants, (iii) their genetic regulation (SfiC+ filamentation is not under direct negative control of the LexA repressor), and (iv) their genetic determinants (SfiC+ filamentation depends on a locus, sfiC+, near 28 min on the E. coli map and distinct from sfiA).
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=215076Documentos Relacionados
- Reversibility of SOS-associated division inhibition in Escherichia coli.
- SOS-associated division inhibition gene sfiC is part of excisable element e14 in Escherichia coli.
- SOS-independent coupling between DNA replication and cell division in Escherichia coli.
- Bactericidal activities of five quinolones for Escherichia coli strains with mutations in genes encoding the SOS response or cell division.
- Mutations in uvrD induce the SOS response in Escherichia coli.
