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Glucose induces delocalization of a flagellar biosynthesis protein from the flagellated pole
Author(s) -
Park Soyoung,
Park YoungHa,
Lee ChangRo,
Kim YeonRan,
Seok YeongJae
Publication year - 2016
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.13424
Subject(s) - motility , biology , flagellum , chemotaxis , biosynthesis , bacteria , psychological repression , microbiology and biotechnology , biochemistry , downregulation and upregulation , gene , receptor , genetics , gene expression
Summary To survive in a continuously changing environment, bacteria sense concentration gradients of attractants or repellents, and purposefully migrate until a more favourable habitat is encountered. While glucose is known as the most effective attractant, the flagellar biosynthesis and hence chemotactic motility has been known to be repressed by glucose in some bacteria. To date, the only known regulatory mechanism of the repression of flagellar synthesis by glucose is via downregulation of the cAMP level, as shown in a few members of the family Enterobacteriaceae . Here we show that, in Vibrio vulnificus , the glucose‐mediated inhibition of flagellar motility operates by a completely different mechanism. In the presence of glucose, EIIA Glc is dephosphorylated and inhibits the polar localization of FapA (flagellar assembly protein A) by sequestering it from the flagellated pole. A loss or delocalization of FapA results in a complete failure of the flagellar biosynthesis and motility. However, when glucose is depleted, EIIA Glc is phosphorylated and releases FapA such that free FapA can be localized back to the pole and trigger flagellation. Together, these data provide new insight into a bacterial strategy to reach and stay in the glucose‐rich area.