Affiliation:
1. Departamento de Microbiologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, SP, Brazil
2. Department of Biochemistry and Molecular Biology, Tel-Aviv University, Tel-Aviv, Israel
Abstract
ABSTRACT
Mutations that cause the constitutive expression of the PHO regulon of
Escherichia coli
occur either in the
pst
operon or in the
phoR
gene, which encode, respectively, a high-affinity P
i
transport system and a histidine kinase sensor protein. These mutations are normally selected on glycerol-2-phosphate (G2P) as the carbon source in the presence of excess P
i
. The emergence of early PHO-constitutive mutants, which appear after growth for up to 48 h on selective medium, depends on the presence of
phoA
, which codes for a periplasmic alkaline phosphatase, while late mutants, which appear after 48 h, depend both on
phoA
and on the
ugp
operon, which encodes a glycerophosphodiester transport system. The emergence of the late mutants hints at an adaptive mutation process. PHO-constitutive
phoR
mutants appear only in a host that is mutated in
pitA
, which encodes an alternative P
i
transport system that does not belong to the PHO regulon. The conserved Thr
217
residue in the PhoR protein is essential for PHO repression.
IMPORTANCE
One of the principal ways in which bacteria adapt to new nutrient sources is by acquiring mutations in key regulatory genes. The inability of
E. coli
to grow on G2P as a carbon source is used to select mutations that derepress the PHO regulon, a system of genes involved in the uptake of phosphorus-containing molecules. Mutations in the
pst
operon or in
phoR
result in the constitutive expression of the entire PHO regulon, including alkaline phosphatase, which hydrolyzes G2P. Here we demonstrate that the
ugp
operon, another member of the PHO regulon, is important for the selection of PHO-constitutive mutants under prolonged nutritional stress and that
phoR
mutations can be selected only in bacteria lacking
pitA
, which encodes a secondary P
i
transport system.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
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