Glucose induces delocalization of a flagellar biosynthesis protein from the flagellated pole

Abstract

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.

FlhF regulates the number and configuration of periplasmic flagella in Borrelia burgdorferi

“…The rest of the three are hypothetical proteins (HP). Blast and protein domain search revealed that BB0267 is a homolog of flagella assembly protein A (FapA) (Figure c), a protein that controls Vibrio vulnificus flagellar biosynthesis and polar location (Park, Park, Lee, Kim, & Seok, ). There were no functional domains or motifs identified in BB0266 and BB0265.…”

“…Interestingly, BLAST search using SflA as a query reveals that the genome of B. burgdorferi encodes three putative DnaJ homologs (BB0517, BB0602 and BB0655); thus, it is likely that B. burgdorferi adopts a similar mechanism as V. alginolyticus to control the flagella polarity by suppressing formation of peritrichous flagella. In addition, a recent report reveals that FapA (flagellar assembly protein A) controls the flagellar polarity and biosynthesis in V. vulnificus (Park et al, ). BB0267, a protein downstream of FlhF Bb , belongs to the family of FapA (Figure c).…”

A GntR Family Transcription Factor (VPA1701) for Swarming Motility and Colonization of Vibrio parahaemolyticus

“…The second messenger c-di-GMP directly binds to the flagellar master regulator FlrA and inhibits the motility of Vibrio cholerae [26]. Glucose regulates the synthesis of flagellum by inhibiting the polar localization of FapA in V. vulnificus [27]. Furthermore, a global transcriptional regulator, CalR, downregulates the expression of laf genes to inhibit the swarming motility of V. parahaemolyticus [25].…”

Identification of fliC and flagella expression in Salmonella enterica subspecies enterica serovar Gallinarum biovar gallinarum

“…An interesting example of these mechanisms is offered by V. vulnificus, who in the presence of glucose, in vitro, 87% of the microorganisms do not present flagellum and 13% do develop it but in a short form. In this event, dephosphorylated EIIAGlc is involved and interacts with FapA, which avoids the biosynthesis of the flagellum and allows the bacteria to remain in the niche rich in glucose; the mechanism is developed through an independent cAMP pathway (Park et al, 2016). On the other hand, it has been reported that in Saccharomyces cerevisiae, glucose represses the transcription of a series of genes responsible for respiration, the use of other carbon sources (galactose, maltose, sucrose) and genes encoding enzymes of the gluconeogenic pathway.…”