The fim switch in Escherichia coli is the mechanism by which the fim gene cluster, encoding Type I Pili [1], is transcriptionally controlled.
These pili are virulence factors involved in adhesion, especially important in u ropathogenic Escherichia coli. The gene undergoes phase variation mediated via two recombinases and is a model example of site specific inversion.
The operon consists of the promoter region fim S, the main constituent fim A, forming a rod like structure and fim H, the adhesin at the tip, to name just a few important elements. The fim S region is flanked by 9bp repeats that are mirror images of each other [2]. These mirror images serve as substrates for two ATP-dependent recombinases, fim B and fim E. These recombinases can invert the orientation of the fim S region and only one orientation allows for 3' to 5' transcription.
fim B "flips" the promoter region both ways, from the "on" position to the "off" position and vice versa, whereas fim E can only facilitate recombination from "on" to "off". This equilibrium, shifted towards maintaining the "off" position, due to higher fim E activity [3], serves as a mode of expressing pili only when adhesion is needed. Another level of transcriptional control in E. coli is mediated by the sensitivity of the recombinases to pH and osmolarity [4], further ensuring appropriate expression levels of type-I pili. Type-I pili are expressed by many species of Enterobacteriaceae. However, it is to be noted that the transcriptional control can differ widely between species [5], in S almonella typhimurium, for example much influence is exerted by a l eucine-responsive regulatory protein and there is no fim S element [5].
{{
cite journal}}
: Check date values in: |date=
(
help)
{{
cite journal}}
: Check date values in: |date=
(
help)
{{
cite journal}}
: Check date values in: |date=
(
help)
{{
cite journal}}
: Check date values in: |date=
(
help)
The fim switch in Escherichia coli is the mechanism by which the fim gene cluster, encoding Type I Pili [1], is transcriptionally controlled.
These pili are virulence factors involved in adhesion, especially important in u ropathogenic Escherichia coli. The gene undergoes phase variation mediated via two recombinases and is a model example of site specific inversion.
The operon consists of the promoter region fim S, the main constituent fim A, forming a rod like structure and fim H, the adhesin at the tip, to name just a few important elements. The fim S region is flanked by 9bp repeats that are mirror images of each other [2]. These mirror images serve as substrates for two ATP-dependent recombinases, fim B and fim E. These recombinases can invert the orientation of the fim S region and only one orientation allows for 3' to 5' transcription.
fim B "flips" the promoter region both ways, from the "on" position to the "off" position and vice versa, whereas fim E can only facilitate recombination from "on" to "off". This equilibrium, shifted towards maintaining the "off" position, due to higher fim E activity [3], serves as a mode of expressing pili only when adhesion is needed. Another level of transcriptional control in E. coli is mediated by the sensitivity of the recombinases to pH and osmolarity [4], further ensuring appropriate expression levels of type-I pili. Type-I pili are expressed by many species of Enterobacteriaceae. However, it is to be noted that the transcriptional control can differ widely between species [5], in S almonella typhimurium, for example much influence is exerted by a l eucine-responsive regulatory protein and there is no fim S element [5].
{{
cite journal}}
: Check date values in: |date=
(
help)
{{
cite journal}}
: Check date values in: |date=
(
help)
{{
cite journal}}
: Check date values in: |date=
(
help)
{{
cite journal}}
: Check date values in: |date=
(
help)