2 Matching Annotations
  1. Jul 2018
    1. On 2017 Oct 26, Martine Crasnier-Mednansky commented:

      This paper reinforces –perhaps validates– the authors’ previous work (Mondal M, 2014) indicating PTS-transported GlcNAc is utilized by Vibrio cholerae in the mucus layer, as further explained.

      Data in Meibom KL, 2004, particularly supplemental figure 7, clearly indicate chiA2 (VCA0027) is not upregulated by GlcNAc. Therefore, in agreement with the present work, GlcNAc utilization by V. cholerae in the mucus may rely on the periplasmic activation of ChiS for production of ChiA2. Because chiS mutant strains do not produce extracellular chitinases in the presence of chitin oligomers (Li X, 2004), they are unlikely to produce chitinases in the presence of mucin (the authors report ChiS is activated in the presence of mucin). Thus, both chiA2 and chiS mutant strains may prevent colonization of the intestine because they are both unable to cause mucin hydrolysis by ChiA2 and subsequent release of GlcNAc, which, according to the authors’ original 2014 proposal, is necessary for growth and survival in the mucus. The mucin-derived 'inducer' for ChiS activation is possibly (GlcNAc)3, as the authors reported (GlcNAc)3 is released upon mucin hydrolysis by ChiA2.


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  2. Feb 2018
    1. On 2017 Oct 26, Martine Crasnier-Mednansky commented:

      This paper reinforces –perhaps validates– the authors’ previous work (Mondal M, 2014) indicating PTS-transported GlcNAc is utilized by Vibrio cholerae in the mucus layer, as further explained.

      Data in Meibom KL, 2004, particularly supplemental figure 7, clearly indicate chiA2 (VCA0027) is not upregulated by GlcNAc. Therefore, in agreement with the present work, GlcNAc utilization by V. cholerae in the mucus may rely on the periplasmic activation of ChiS for production of ChiA2. Because chiS mutant strains do not produce extracellular chitinases in the presence of chitin oligomers (Li X, 2004), they are unlikely to produce chitinases in the presence of mucin (the authors report ChiS is activated in the presence of mucin). Thus, both chiA2 and chiS mutant strains may prevent colonization of the intestine because they are both unable to cause mucin hydrolysis by ChiA2 and subsequent release of GlcNAc, which, according to the authors’ original 2014 proposal, is necessary for growth and survival in the mucus. The mucin-derived 'inducer' for ChiS activation is possibly (GlcNAc)3, as the authors reported (GlcNAc)3 is released upon mucin hydrolysis by ChiA2.


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.