Cargando…

Piliation changes in transformation-defective gonococci

Recombination-dependent alterations of their expressed pilin gene (pilE) enable gonococci to synthesize a myriad of structurally/antigenically different pili and to reversibly switch their pilus production on and off. These changes have been ascribed both to DNA transformation and to intragenomic re...

Descripción completa

Detalles Bibliográficos
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1990
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187963/
https://www.ncbi.nlm.nih.gov/pubmed/1972181
_version_ 1782146296977555456
collection PubMed
description Recombination-dependent alterations of their expressed pilin gene (pilE) enable gonococci to synthesize a myriad of structurally/antigenically different pili and to reversibly switch their pilus production on and off. These changes have been ascribed both to DNA transformation and to intragenomic recombination between pilE and silent pilin genes (pilS). We examined the pilus changes in gonococci that are incompetent for transformation because of their DNA uptake deficiency (dud) mutation, pilus- (P-) phenotype, or both. Though incompetent for DNA transformation, dud cells displayed pilus antigenic variation and underwent reversible pilus variations much like their wild-type parent. Wild-type P- with a pilE nonsense mutation were also virtually nontransformable, but they reverted to P+ at high frequencies. The pilin mRNA sequence changes that accompanied pilus transitions in these nontransformable dud and P- gonococci represent insertion of pilS stretches into their respective pilE, apparently via intragenomic recombination.
format Text
id pubmed-2187963
institution National Center for Biotechnology Information
language English
publishDate 1990
publisher The Rockefeller University Press
record_format MEDLINE/PubMed
spelling pubmed-21879632008-04-17 Piliation changes in transformation-defective gonococci J Exp Med Articles Recombination-dependent alterations of their expressed pilin gene (pilE) enable gonococci to synthesize a myriad of structurally/antigenically different pili and to reversibly switch their pilus production on and off. These changes have been ascribed both to DNA transformation and to intragenomic recombination between pilE and silent pilin genes (pilS). We examined the pilus changes in gonococci that are incompetent for transformation because of their DNA uptake deficiency (dud) mutation, pilus- (P-) phenotype, or both. Though incompetent for DNA transformation, dud cells displayed pilus antigenic variation and underwent reversible pilus variations much like their wild-type parent. Wild-type P- with a pilE nonsense mutation were also virtually nontransformable, but they reverted to P+ at high frequencies. The pilin mRNA sequence changes that accompanied pilus transitions in these nontransformable dud and P- gonococci represent insertion of pilS stretches into their respective pilE, apparently via intragenomic recombination. The Rockefeller University Press 1990-06-01 /pmc/articles/PMC2187963/ /pubmed/1972181 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Piliation changes in transformation-defective gonococci
title Piliation changes in transformation-defective gonococci
title_full Piliation changes in transformation-defective gonococci
title_fullStr Piliation changes in transformation-defective gonococci
title_full_unstemmed Piliation changes in transformation-defective gonococci
title_short Piliation changes in transformation-defective gonococci
title_sort piliation changes in transformation-defective gonococci
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187963/
https://www.ncbi.nlm.nih.gov/pubmed/1972181