2006
DOI: 10.2323/jgam.52.91
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RcsA-dependent and -independent growth defects caused by the activated Rcs phosphorelay system in the Escherichia coli pgsA null mutant

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Cited by 24 publications
(14 citation statements)
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“…An lpp mutation is necessary to prevent accumulation of the nascent major outer membrane lipoprotein, which requires PG for its modification (10,20,21). The Rcs phosphorelay system is constitutively activated in ⌬pgsA mutants resulting in the cell lyses at 37-42°C, which is prevented by a ⌬rcsF mutation (22). We compared the growth rates of UE54 lacking PG and CL and its two parental pgsA ϩ strains, MG1655 and UE53 (lpp-2 ⌬rcsF), with wild-type phospholipid composition.…”
Section: Lack Of Pg and CL Decreases The Length Of The Ue54 Mutantmentioning
confidence: 99%
“…An lpp mutation is necessary to prevent accumulation of the nascent major outer membrane lipoprotein, which requires PG for its modification (10,20,21). The Rcs phosphorelay system is constitutively activated in ⌬pgsA mutants resulting in the cell lyses at 37-42°C, which is prevented by a ⌬rcsF mutation (22). We compared the growth rates of UE54 lacking PG and CL and its two parental pgsA ϩ strains, MG1655 and UE53 (lpp-2 ⌬rcsF), with wild-type phospholipid composition.…”
Section: Lack Of Pg and CL Decreases The Length Of The Ue54 Mutantmentioning
confidence: 99%
“…E-mail: koumatsu@molbiol.saitama-u.ac.jp is lacking, a null pgsA mutant is viable, by substituting indispensable roles of PG with other acidic phospholipids (Kikuchi et al, 2000;Matsumoto, 2001;Mileykovskaya et al, 2009). In null pgsA cells the lack of PG is, however, an envelope stress that activates the Rcs phosphorelay signal transduction system to cause thermosensitive growth (Shiba et al, 2004;Nagahama et al, 2006).…”
Section: Introductionmentioning
confidence: 99%
“…Null mutants in the pssA gene are viable, have defects in cell division and secondary solute transporters, and lack amine-containing and zwitterionic lipids downstream of the left branch of the pathway (17). Null mutants in the pgsA gene (18) are also viable, require second site repressor mutations for viability; show reduced rates of protein translocation across the inner membrane; and have Ͻ10% anionic phospholipids, which are mainly the precursors to PGP. Placing the pssA gene under the control of an inducible promoter allows synthesis and membrane assembly of a target membrane protein in the absence of PE, followed by induction of PE synthesis to study the effects of changes in the lipid environment post-assembly of protein in vivo (6,8,11).…”
Section: Engineering Changes In Membrane Lipid Compositionmentioning
confidence: 99%