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MG 428 is a novel positive regulator of recombination that triggers mgpB and mgpC gene variation in M ycoplasma genitalium
Author(s) -
Burgos Raul,
Totten Patricia A.
Publication year - 2014
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12760
Subject(s) - biology , gene , homologous recombination , antigenic variation , gene isoform , genetics , recombination , regulator , mutant , regulation of gene expression , mycoplasma genitalium , gene expression , microbiology and biotechnology , chlamydia trachomatis , immunology
Summary The human pathogen M ycoplasma genitalium employs homologous recombination to generate antigenic diversity in the immunodominant MgpB and MgpC proteins. Only recently, some of the molecular factors involved in this process have been characterized, but nothing is known about its regulation. Here, we show that M . genitalium expresses N ‐terminally truncated RecA isoforms via alternative translation initiation, but only the full‐length protein is essential for gene variation. We also demonstrate that overexpression of MG 428 positively regulates the expression of recombination genes, including recA , ruvA , ruvB and ORF 2, a gene of unknown function co‐transcribed with ruvAB . The co‐ordinated induction of these genes correlated with an increase of mgpBC gene variation. In contrast, cells lacking MG 428 were unable to generate variants despite expressing normal levels of RecA . Similarly, deletion analyses of the recA upstream region defined sequences required for gene variation without abolishing RecA expression. The requirement of these sequences is consistent with the presence of promoter elements associated with MG 428‐dependent recA induction. Sequences upstream of recA also influence the relative abundance of RecA isoforms, possibly through translational regulation. Overall, these results suggest that MG 428 is a positive regulator of recombination and that precise control of recA expression is required to initiate mgpBC variation.