Vibrio fischeri is a bioluminescent bacterium that works in a symbiosis with the squid Euprymna scolopes. While the E.scolopes provides shelter and nutrients for the V.fischeri, the V.fischeri allows the E.scolopeses underside to mimic the moonlight during the night to protect itself from predators.
It has been found that one of the main nutrients that V.fischeri is provided with is chitin, which must be broken down by enzymes as it is not soluble. The chitin is broken down by exochitinases into N-acetyl-D-glucosamine (GlcNAc) and chitobiose (GlcNAc)2. V.fischeri have a nag locus which regulates the uptake and metabolism of GlcNAc. The nag locus is made up of a number of genes including nagE and nagBAC. nagE encodes enzyme involved in transporting GlcNAc from outside the cell into the cytoplasm. During the transportation the GlcNAc is phosphorylated becoming N-acetylD-glucosamine-6-phosphate (GlcNAc-6P). nagA encodes for the deacetylase NagA which removes the acetyl group, giving glucosamine-6P. The deaminase Nag B, encoded by nagB, then removes the amino group. Nag C represses the nag locus by binding to operon sites. The Nag C is only released when GlcNAc-6P binds to the operon site.
One of the things that are not fully understood in the symbiosis of E.scolopes and V.fischeri is how E.scolopes is able to only allow V.fischeri to infect its light organ. We know that juvenile E.scolopeses have a complex ciliated epithelium around the pores of the light organ and that when the epithelium is stimulated by peptidoglycan from bacteria that colonise the squid produces mucus that stimulates V.fischeri, which then form aggregates. The V.fischeri somehow out-competes other, non-symbiotic bacteria and then migrates through the pores to colonise tissue within the light organ. It is thought that the expression of certain genes in the V.fischeri may act as an indicator to E.scolopes, informing the squid of which bacteria present would be suitable for the light organ.
This study tests the role of the gene nagC in colonisation. They tested the ability of both wild-type V.fischeri and a mutant strain that had a faulty NagC gene to colonise Euprymna scolopes and found that when both strains were present the wild-type did not facilitate the colonisation of the mutant strain but that the mutant strain did not hinder the wild-types ability to colonise either. This suggests that the squid is able to select symbionts that have a functional NagC , ensuring that the bacteria is able to regulate the expression of the nag locus and take advantage of the chitin present to the best of its ability. It would be interesting if a further experiment were conducted, looking into how the squid is able to be so selective about which bacteria colonise its light organ but such an experiment would be difficult to conduct.
Reference: Miyashiro, T et al (2011), The N-acetyl-d-glucosamine repressor NagC of Vibrio fischeri facilitates colonization of Euprymna scolopes. Molecular Microbiology, 82: 894–903
2 comments:
Fascinating extra twist to the story, and interesting that they have returned to good old mutant competition assays. Do the authors say what host mechanism the host might have to detect this gene function? There are so many situations where chitin is involved in regulating gene function in marine bacteria. In the lectures, we will be looking at the role of chitin in virulence and genetic exchange of Vibrio cholerae.
Sorry for the very late reply. No they don't go into any detail how the host detects the gene function. The paper seems to be entirely focused on which gene expression, or lack of, causes the host to reject the bacteria. There is no speculation in the introduction or the discussion. I could see how the host could possibly tell if the nagE was not working correctly as there would be a higher concentration of GlcNAc around but that wouldn't account for a mutation in any of the other genes. I'm also not sure how quickly the host detects a mutation, whether it's before the bacteria would have a chance to take in GlcNAc anyway.
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