{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T09:25:59Z","timestamp":1790933159570,"version":"4.1.0"},"reference-count":47,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2005,7,25]],"date-time":"2005-07-25T00:00:00Z","timestamp":1122249600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Microbiology"],"published-print":{"date-parts":[[2005,9]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>The <jats:italic>penC<\/jats:italic> resistance gene was previously characterized in an FA19 <jats:italic>penA mtrR penB<\/jats:italic> gonococcal strain (PR100) as a spontaneous mutation that increased resistance to penicillin and tetracycline. We show here that antibiotic resistance mediated by <jats:italic>penC<\/jats:italic> is the result of a Glu\u2010666 to Lys missense mutation in the\u200a<jats:italic>pilQ<\/jats:italic>\u200a gene\u200a that\u200a interferes\u200a with\u200a the\u200a formation\u200a of the SDS\u2010resistant high\u2010molecular\u2010mass PilQ secretin complex, disrupts piliation and decreases transformation frequency by 50\u2010fold. Deletion of <jats:italic>pilQ<\/jats:italic> in PR100 confers the same level of antibiotic resistance as the <jats:italic>penC<\/jats:italic> mutation, but increased resistance was\u200a observed\u200a only\u200a in\u200a strains\u200a containing\u200a the\u200a<jats:italic>mtrR<\/jats:italic> and <jats:italic>penB<\/jats:italic> resistance determinants. Site\u2010saturation mutagenesis of Glu\u2010666 revealed that only acidic or amidated amino acids at this position preserved PilQ function. Consistent with early studies suggesting the importance of cysteine residues for stability of the PilQ multimer, mutation of either of the two cysteine residues in FA19 PilQ led to a similar phenotype as <jats:italic>penC<\/jats:italic>: increased antibiotic resistance, loss of piliation, intermediate levels of transformation competence and absence of SDS\u2010resistant PilQ oligomers. These data show that a functional secretin complex can enhance the entry of antibiotics into the cell and suggest that the PilQ oligomer forms a pore in the outer membrane through which antibiotics diffuse into the periplasm.<\/jats:p>","DOI":"10.1111\/j.1365-2958.2005.04752.x","type":"journal-article","created":{"date-parts":[[2005,8,5]],"date-time":"2005-08-05T14:40:01Z","timestamp":1123252801000},"page":"1238-1251","source":"Crossref","is-referenced-by-count":74,"title":["The <i>penC<\/i> mutation conferring antibiotic resistance in <i>Neisseria gonorrhoeae<\/i> arises from a mutation in the PilQ secretin that interferes with multimer stability"],"prefix":"10.1111","volume":"57","author":[{"given":"Shuqing","family":"Zhao","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deborah M.","family":"Tobiason","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mei","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. 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