.png){kind=icon}
.png){kind=icon}
Return
MntR Mediates LiaSR-Regulated gadT2/gadD2 Expression and Acid Resistance in Listeria monocytogenes 10403S
.png){kind=icon}
OA
AI
Y
M
X
J
J
L
S
X
C
DOI：10.3390/microorganisms14081765.png)
.png){kind=icon}
Original request for help.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
Listeria monocytogenes is a foodborne pathogen capable of persisting under acid, osmotic, oxidative, thermal, and other environmental stresses. The glutamate decarboxylase (GAD) system is a major determinant of survival under acidic conditions. Previous work showed that the two-component system LiaSR negatively regulates the gadT2/gadD2 locus in L. monocytogenes 10403S, but the intervening regulator was unknown. Here, we combined transcription-factor mutant screening, promoter-reporter assays, RT-qPCR, Western blotting, acid-survival assays, and electrophoretic mobility shift assays to define this regulatory relationship. Deletion of mntR reduced PgadT2-gfp activity, gadD2 transcript abundance, and GadD2 protein levels at pH 4.5, 7, and 9, whereas complementation restored expression toward the wild-type level. The ΔmntR strain also showed reduced survival under inorganic and organic acid stresses. LiaSR deletion increased PmntR-gfp activity, and LiaR bound directly to PmntR. Conversely, mntR deletion increased LiaR abundance, although MntR did not bind to PliaSR, indicating indirect feedback regulation. The liaSR/mntR double mutant showed reduced gadT2/gadD2 expression under acidic conditions and impaired acid survival. Together, these findings support a LiaSR-MntR-gadT2/gadD2 pathway in which MntR promotes GAD-mediated acid resistance.
Keywords:
<i>Listeria monocytogenes</i>
two-component system
transcription factor
glutamate decarboxylase
acid resistance
Journal
M
IF:
4.2
Papers:
1.8W
Citations:
5.2W
Organization
Cited Papers