A Homologue of the Recombination-Dependent Growth Gene, rdgC, Is Involved in Gonococcal Pilin Antigenic Variation

• Published in: Genetics (Austin) 2000-02, Vol.154 (2), p.523-532
• Main Authors: Mehr, Ian J, Long, Cynthia D, Serkin, Carla D, Seifert, H. Steven
• Format: Article
• Language: English
• Subjects: AGc gene; Amino Acid Sequence; Amino acids; Antigens, Bacterial - genetics; Bacterial Proteins - genetics; Base Sequence; Cloning, Molecular; Deoxyribonucleic acid; DNA; DNA Primers; DNA Transposable Elements; engA gene; EngA protein; Escherichia coli Proteins; Fimbriae Proteins; Gc gene; Genes; Genes, Essential; Genetic Complementation Test; Genetics; Membrane Proteins - immunology; Microscopy, Electron; Molecular Sequence Data; Mutation; Neisseria gonorrhoeae; Neisseria gonorrhoeae - genetics; Neisseria gonorrhoeae - growth & development; Neisseria gonorrhoeae - immunology; Operon; Phenotype; pilE gene; pilin; pilS gene; rdgC gene; Recombination, Genetic
• ISSN: 0016-6731; 1943-2631; 1943-2631
• DOI: 10.1093/genetics/154.2.523

Neisseria gonorrhoeae pilin undergoes high-frequency changes in primary amino acid sequence that aid in the avoidance of the host immune response and alter pilus expression. The pilin amino acid changes reflect nucleotide changes in the expressed gene, pilE, which result from nonreciprocal recombination reactions with numerous silent loci, pilS. A series of mini-transposon insertions affecting pilin antigenic variation were localized to three genes in one region of the Gc chromosome. Mutational analysis with complementation showed that a Gc gene with sequence similarity to the Escherichia coli rdgC gene is involved in pilus-dependent colony phase variation and in pilin antigenic variation. Furthermore, we show that the Gc rdgC homologue is transcriptionally linked in an operon with a gene encoding a predicted GTPase. The inability to disrupt expression of this gene suggests it is an essential gene (engA, essential neisserial GTPase). While some of the transposon mutations in rdgC and insertions in the 5'-untranslated portion of engA showed a growth defect, all transposon insertions investigated conferred an aberrant cellular morphology. Complementation analysis showed that the growth deficiencies are due to the interruption of RdgC expression and not that of EngA. The requirement of RdgC for efficient pilin variation suggests a role for this protein in specialized DNA recombination reactions.