Regulation in the Escherichia coli lee pathogenicity island

Alsharif, Ghadah Saleh (2016). Regulation in the Escherichia coli lee pathogenicity island. University of Birmingham. Ph.D.

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Abstract

Enterohaemorrhagic Escherichia coli (EHEC) pathogens represent major difficulties to health as they cause infections and in the gastrointestinal tracts of animals. Previous studies revealed that the locus of enterocyte effacement (LEE) pathogenicity island is the major player in triggering the attaching and effacing lesions that induce death of host cells. The first step in its expression is activation of the LEE1 promoter that controls expression of the LEE encoded regulator (Ler) that activates LEE expression. The global regulator of LEE activator (GrlA) transcription is considered to be especially important in this process.

Although GrlA binds to the LEE1 promoter and activates transcription initiation in vitro, the fold of activation was only ~ 1.5 fold. The aim of this work was to discover the factors that trigger GrlA activity. Thus, in chapter 3, it is shown how bacterial attachment to host cells triggers GrlA activity to an extent not seen during planktonic growth, with up to ~20 fold activation. Data also show that the level of free unbound GrlA defines the activity of the LEE promoter by GrlA, and the previously characterised GrlR anti-GrlA protein merely serves to buffer the level of GrlA.

Type of Work:

Thesis (Doctorates > Ph.D.)

Award Type:

Doctorates > Ph.D.

Supervisor(s):