Expression of the blood-group-related glycosyltransferase B4galnt2 influences the intestinal microbiota in mice
Glycans on mucosal surfaces have an important role in host–microbe interactions. The locus encoding the blood-group-related glycosyltransferase β- 1,4-N-acetylgalactosaminyltransferase 2 ( B4galnt2 ) is subject to strong selective forces in natural house-mouse populations that contain a common allel...
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Veröffentlicht in: | The ISME Journal 2012-07, Vol.6 (7), p.1345-1355 |
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Sprache: | eng |
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Zusammenfassung: | Glycans on mucosal surfaces have an important role in host–microbe interactions. The locus encoding the blood-group-related glycosyltransferase β-
1,4-N-acetylgalactosaminyltransferase 2
(
B4galnt2
) is subject to strong selective forces in natural house-mouse populations that contain a common allelic variant that confers loss of
B4galnt2
gene expression in the gastrointestinal (GI) tract. We reasoned that altered glycan-dependent intestinal host–microbe interactions may underlie these signatures of selection. To determine whether
B4galnt2
influences the intestinal microbial ecology, we profiled the microbiota of wild-type and
B4galnt2-
deficient siblings throughout the GI tract using 16S rRNA gene pyrosequencing. This revealed both distinct communities at different anatomic sites and significant changes in composition with respect to genotype, indicating a previously unappreciated role of
B4galnt2
in host–microbial homeostasis. Among the numerous
B4galnt2-
dependent differences identified in the abundance of specific bacterial taxa, we unexpectedly detected a difference in the pathogenic genus,
Helicobacter
, suggesting
Helicobacter
spp. also interact with B4galnt2 glycans. In contrast to other glycosyltransferases, we found that the host intestinal
B4galnt2
expression is not dependent on presence of the microbiota. Given the long-term maintenance of alleles influencing
B4galnt2
expression by natural selection and the GI phenotypes presented here, we suggest that variation in
B4galnt2
GI expression may alter susceptibility to GI diseases such as infectious gastroenteritis. |
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ISSN: | 1751-7362 1751-7370 |
DOI: | 10.1038/ismej.2011.204 |