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Gene position within a long transcript as a determinant for stochastic switching in bacteria
Author(s) -
Veening JanWillem,
Kuipers Oscar P.
Publication year - 2010
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2010.07113.x
Subject(s) - biology , operon , sigma factor , gene , rna polymerase , flagellum , motility , genetics , bacillus subtilis , gene expression , caulobacter crescentus , processivity , regulation of gene expression , rna , microbiology and biotechnology , polymerase , bacteria , cell cycle , escherichia coli
Summary How cultures of genetically identical cells bifurcate into distinct phenotypic subpopulations under uniform growth conditions is an important question in developmental biology of relevance even to relatively simple developmental systems, such as spore formation in bacteria. A growing Bacillus subtilis culture consists of either cells that are motile and can swim or cells that are non‐motile and are chained together. In this issue of Molecular Microbiology , Cozy and Kearns show that the probability of a cell to become motile depends on the position of the sigD gene within the long (27 kb) motility operon. sigD encodes the alternative sigma factor σ D that, together with RNA polymerase, drives expression of genes required for cell separation and the assembly of flagella. sigD is the penultimate gene of the B. subtilis motility operon and, in the control strain approximately, 70% of the cells are motile. When sigD was moved upstream within the operon, a larger fraction of cells became motile (up to 100%). This study highlights that the position of a gene within an operon can have a large impact on the control of gene expression. Furthermore, it suggests that RNA polymerase processivity or mRNA turnover can play important roles as sources of noise in bacterial development, and that gene position might be an unrecognized and possibly widespread mechanism to regulate phenotypic variation.