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We began analyzing https://link.springer.com/article/10.1007/s00248-010-9787-2, but it redirected us to https://link.springer.com/article/10.1007/s00248-010-9787-2. The analysis below is for the second page.

Title[redir]:
Genotype Is a Stronger Determinant than Sex of the Mouse Gut Microbiota | Microbial Ecology
Description:
The mammalian gut microbiota is considered to be determined mostly by diet, while the effect of genotype is still controversial. Here, we examined the effect of genotype on the gut microbiota in normal populations, exhibiting only natural polymorphisms, and evaluated this effect in comparison to the effect of sex. DNA fingerprinting approaches were used to profile the gut microbiota of eight different recombinant inbred mouse lines of the collaborative cross consortium, whose level of genetic diversity mimics that of a natural human population. Analyses based on automated ribosomal internal transcribed spacer analysis demonstrated significant higher similarity of the gut microbiota composition within mouse lines than between them or within same-gender groups. Thus, genetic background significantly impacts the microbiota composition and is a stronger determinant than gender. These findings imply that genetic polymorphisms help shape the intestinal microbiota of mammals and consequently could affect host susceptibility to diseases.

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Keywords {🔍}

article, google, scholar, pubmed, cas, microbiota, gut, microbiol, human, microbial, gophna, analysis, intestinal, genetics, environ, genotype, mouse, composition, bacterial, disease, appl, aviv, privacy, cookies, content, data, ecology, genetic, access, microbiome, community, bowel, proc, usa, nature, publish, research, search, sex, kovacs, effect, diversity, host, health, subjects, crohns, differences, gastroenterology, fecal, immunol,

Topics {✒️}

irritable bowel syndrome month download article/chapter pardo-manuel de villena genome-wide resequencing data human intestinal microbiota akkermans-van vliet wm intestinal microbial ecology adherent-invasive escherichia coli high-fat diet determines th1/th2 cytokine production gut microbiota composition full article pdf core gut microbiome human gut microbes mouse gut microbiota mammalian systems genetics polymorphism architecture privacy choices/manage cookies mammalian gut microbiota human gut bacteria soil microbial richness human gastronintestinal tract microbial community imbalances colonic microbiota signatures invasive escherichia coli natural human population culture independent analysis pcr-based estimates intestinal microbiota freshwater bacterial communities estimating bacterial richness article kovacs intraepithelial escherichia coli host genotype affects check access instant access de vos wm a-chip profiling gut microbiome related subjects de visser jagm microbiota composition european economic area affect host susceptibility ng tze chiang northern european countries turnbaugh pj differential interleukin-10 production double-edged sword safra bioinformatics program

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         description:The mammalian gut microbiota is considered to be determined mostly by diet, while the effect of genotype is still controversial. Here, we examined the effect of genotype on the gut microbiota in normal populations, exhibiting only natural polymorphisms, and evaluated this effect in comparison to the effect of sex. DNA fingerprinting approaches were used to profile the gut microbiota of eight different recombinant inbred mouse lines of the collaborative cross consortium, whose level of genetic diversity mimics that of a natural human population. Analyses based on automated ribosomal internal transcribed spacer analysis demonstrated significant higher similarity of the gut microbiota composition within mouse lines than between them or within same-gender groups. Thus, genetic background significantly impacts the microbiota composition and is a stronger determinant than gender. These findings imply that genetic polymorphisms help shape the intestinal microbiota of mammals and consequently could affect host susceptibility to diseases.
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