Premium
Internalin‐mediated invasion of epithelial cells by Listeria monocytogenes is regulated by the bacterial growth state, temperature and the pleiotropic activator prfA
Author(s) -
Dramsi S.,
Kocks C.,
Forestier C.,
Cossart P.
Publication year - 1993
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/j.1365-2958.1993.tb01223.x
Subject(s) - biology , listeria monocytogenes , locus (genetics) , operon , activator (genetics) , gene , virulence , promoter , listeria , transcription (linguistics) , bacteria , gene expression , microbiology and biotechnology , genetics , escherichia coli , linguistics , philosophy
Summary Entry of Listeria monocytogenes into epithelial cells requires expression of inlA , the first gene of an operon comprising two genes: inlA , which encodes internalin, a 800‐amino‐acid protein, and inlB , which encodes a 630‐amino‐acid protein. We report here that the inl locus is transcribed on two transcripts in constant relative ratio: a 5 kb transcript spanning inlA and inlB , and a 2.9 kb transcript that covers only inlA. The promoter is located 397 bp from the GTG initiator of inlA and displays in its ‐35 region a palindrome similar to that found in promoters controlled by the pleiotropic activator prfA. Transcription of the inl locus is, as are several other L. monocytogenes virulence genes, activated by prfA and regulated by temperature—with higher expression at 37°C versus 25°C — and bacterial growth state. It is maximal during exponential growth and correlates with maximal invasivity of the bacteria in the human epithelial cell line Caco‐2. It also correlates with maximum amounts of internalin present on the bacterial surface. Internalin is also detected in substantial amounts in culture supernatants. Taken together, these data suggest that surface‐bound internalin plays an important role in bacterial entry but do not exclude a role for the released form.