Substitution of fifty four homologue (Ffh) in escherichia coli with the mammalian 54-kda protein of signal-recognition particle

Patel, Sarju and Austen, Brian M. 1996. Substitution of fifty four homologue (Ffh) in escherichia coli with the mammalian 54-kda protein of signal-recognition particle. European Journal of Biochemistry 238 (3) , pp. 760-768. 10.1111/j.1432-1033.1996.0760w.x

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Abstract

The fifty four homologue (Ffh) of Escherichia coli promotes the translocation of a subset of periplasmic, membrane and secreted proteins across the cytoplasmic membrane. The ffh gene product is essential for cell viability and efficient protein export. Here we show that the mammalian homologue signal-recognition particle (SRP) 54 kDa is not able to suppress the translocation defect in an Ffh conditional mutant Wam 113 [Phillips, G. J. & Silhavy, T. J. (1992) Nature 359, 744–746], The expression of SRP 54 kDa, which is increased when Ffh is suppressed in the Wam 113 strain, causes a pleiotropic defect characterised by cell elongation, and increased accumulation of precursor proteins. The accumulation of precursors of outer membrane protein A (Omp A) and maltose-binding protein (MBP), Sec-B dependent pre-proteins, was less than the Ffh-dependent proteins ribose-binding protein (RBP) and β-lactamase. Sec B expression was suppressed by Ffh expression. The recombinant SRP 54 kDa, which forms a ribonucleoprotein complex in E. coli, was shown to bind to precursor proteins, but is unable to interact with the filamentous temperature-sensitive Y (Fts Y) membrane receptor of the translocation machinery.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Schools > Medicine
Publisher:	Federation of European Biochemical Societies
ISSN:	0014-2956
Last Modified:	11 Apr 2025 14:20
URI:	https://orca.cardiff.ac.uk/id/eprint/175611

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