A differential effect of sigmaS on the expression of the PHO regulon genes of Escherichia coli.

نویسندگان

  • Natalia Pasternak Taschner
  • Ezra Yagil
  • Beny Spira
چکیده

The RNA polymerase core associated with sigma(S) transcribes many genes related to stress or to the stationary phase. When cells enter a phase of phosphate starvation, the transcription of several genes and operons, collectively known as the PHO regulon, is strongly induced. The promoters of the PHO genes hitherto analysed are recognized by sigma(D)-associated RNA polymerase. A mutation in the gene that encodes sigma(S), rpoS, significantly increases the level of alkaline phosphatase activity and the overproduction of sigma(S) inhibits it. Other PHO genes such as phoE and ugpB are likewise affected by sigma(S). In contrast, pstS, which encodes a periplasmic phosphate-binding protein and is a negative regulator of PHO, is stimulated by sigma(S). The effect of sigma(S) on the PHO genes is at the transcriptional level. It is shown that a cytosine residue at position -13 is important for the positive effect of sigma(S) on pst. The interpretation of these observations is based on the competition between sigma(S) and sigma(D) for the binding to the core RNA polymerase.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Genome-wide analysis of the general stress response network in Escherichia coli: sigmaS-dependent genes, promoters, and sigma factor selectivity.

The sigmaS (or RpoS) subunit of RNA polymerase is the master regulator of the general stress response in Escherichia coli. While nearly absent in rapidly growing cells, sigmaS is strongly induced during entry into stationary phase and/or many other stress conditions and is essential for the expression of multiple stress resistances. Genome-wide expression profiling data presented here indicate ...

متن کامل

The Pho regulon and the pathogenesis of Escherichia coli.

During the course of infection, bacteria must coordinately regulate gene expression in response to environmental stimuli. The phosphate (Pho) regulon is controlled by the two component-regulatory system PhoBR. PhoBR is activated during starvation and regulates genes involved in phosphate homeostasis. Several studies have highlighted the importance of the Pho regulon in bacterial pathogenesis, s...

متن کامل

PhoB Activates Escherichia coli O157:H7 Virulence Factors in Response to Inorganic Phosphate Limitation

Enterohemorrhagic Escherichia coli (EHEC), an emerging food- and water-borne hazard, is highly pathogenic to humans. In the environment, EHEC must survive phosphate (Pi) limitation. The response to such Pi starvation is an induction of the Pho regulon including the Pst system that senses Pi variation. The interplay between the virulence of EHEC, Pho-Pst system and environmental Pi remains unkno...

متن کامل

Decreased expression of type 1 fimbriae by a pst mutant of uropathogenic Escherichia coli reduces urinary tract infection.

The pstSCAB-phoU operon encodes the phosphate-specific transport system (Pst). Loss of Pst constitutively activates the Pho regulon and decreases bacterial virulence. However, specific mechanisms underlying decreased bacterial virulence through inactivation of Pst are poorly understood. In uropathogenic Escherichia coli (UPEC) strain CFT073, inactivation of pst decreased urinary tract colonizat...

متن کامل

The phosphate-binding protein of Escherichia coli is not essential for P(i)-regulated expression of the pho regulon.

Disruption of pstS encoding the P(i)-binding protein in Escherichia coli generally leads to the constitutive expression of the pho regulon. We demonstrate that P(i)-controlled expression is restored when the activity of the P(i) transporter PitA or PitB is increased. Apparently, PstS is not an essential component of the signal transduction pathway.

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Microbiology

دوره 150 Pt 9  شماره 

صفحات  -

تاریخ انتشار 2004