News | Can the Genes of People You Live With ‘Move Into’ Your Gut? Study Reveals Social Transmission of Genetic Effects Through Microbes
The genes of people you live with may be quietly influencing the bacteria in your gut. A study published in Nature Communications shows that living together not only shapes an individual's gut microbiome, but can also allow genetic effects to “spread” through a population via microbes.
The study, a collaboration between the Center for Genomic Regulation (CRG) in Barcelona and the University of California, San Diego, examined more than 4,000 laboratory mice. It found that the composition of a mouse's gut microbiome was influenced both by its own genes and significantly by the genes of its cage mates.
The researchers explained that genes themselves do not transfer between individuals, but commensal microbes shaped by those genes can spread through close social contact. Some genes selectively promote the growth of particular gut bacteria, which can pass between animals living together and cause genetic effects to “spill over” into other individuals.
“This is not magic, but the result of genetic influences being transmitted through social contact. Genes shape the gut microbiome, and we found that an individual's own genes are not the only ones at work,” said corresponding author Dr. Amelie Baud, a researcher at CRG.
The gut microbiome consists of trillions of microorganisms and plays key roles in digestion, immunity and overall health. Although diet and medications are considered major influences, the genetic contribution has long been difficult to define precisely. In human studies, only the lactase gene and ABO blood group gene have so far been reliably linked to the gut microbiome.
Researchers noted that nature and nurture are tightly intertwined in natural settings: genes influence diet and lifestyle, while family members and social contacts share food, living environments and microbes, making genetic effects difficult to isolate. The team therefore used genetically diverse laboratory mice raised under tightly controlled conditions and fed the same diet.
The 4,000 mice came from four independent populations at four U.S. facilities with different husbandry procedures. By combining whole-genome and gut microbiome data, researchers identified three gene–microbe association regions that remained stable across different environmental conditions.
The strongest association involved the St6galnac1 gene, which adds sugar molecules to intestinal mucus. Researchers believe the gut bacterium Paraprevotella feeds on these sugars. The association was observed in all four populations. A second genetic region contained several mucin genes and was associated with the abundance of Firmicutes bacteria. The third involved the Pip gene, which encodes an antimicrobial molecule, and was associated with bacteria in the Muribaculaceae family, common in mice and also present in humans.
The large sample allowed researchers to quantify for the first time how much of the laboratory mice's gut microbiome was determined by their own genes and how much arose from the genetic influence of cage mates. This phenomenon is called an “indirect genetic effect,” similar to classic examples in which maternal genes affect offspring growth or immunity through the nurturing environment.
The team built computational models to distinguish direct genetic effects from indirect effects mediated by social contact. Some Muribaculaceae bacteria were influenced by both. When these social effects were incorporated into the model, the overall strength of genetic influence in the three newly identified gene–microbe associations increased 4- to 8-fold. Researchers believe this may represent only a small part of the true picture.
“We may only be seeing the tip of the iceberg,” Dr. Baud said. “At present, we can detect the bacteria with the strongest signals. As microbiome sequencing improves, we may find many more microbes influenced by social genetic effects.”
The study further suggests that if similar mechanisms exist in humans, large population studies may systematically underestimate the effects of genes on health. Genes may not only determine an individual's disease risk, but also affect the health of others in their social network through microbial transmission.
At the mechanistic level, researchers noted that St6galnac1 in mice is functionally closely related to the human gene ST6GAL1, and earlier studies have also linked ST6GAL1 to Paraprevotella. This suggests that different species may share a biological mechanism in which glycosylation of the intestinal mucus surface determines which microbes can colonize and proliferate in the gut.
The team also proposed potential medical hypotheses. Other studies have associated ST6GAL1 with breakthrough SARS-CoV-2 infection after vaccination, while Paraprevotella has been shown to promote degradation of a digestive enzyme required for the virus to enter host cells. Genetic variants might indirectly affect infection risk by regulating the abundance of this bacterium.
Paraprevotella may also affect the structure of IgA antibodies. IgA protects the gut, but abnormal IgA may enter the bloodstream and accumulate in the kidneys, causing IgA nephropathy. Researchers speculated that this pathway could explain why some people develop the autoimmune disease.
The team next plans to investigate how St6galnac1 regulates Paraprevotella in laboratory mice and trace the downstream effects on the gut and whole-body physiology.
“I am almost obsessed with this bacterium now,” Dr. Baud said. “Our findings were replicated in four independent facilities, giving us an exceptionally rare opportunity for follow-up research.”
News | Can the Genes of People You Live With ‘Move Into’ Your Gut? Study Reveals Social Transmission of Genetic Effects Through Microbes
News | Can the Genes of People You Live With ‘Move Into’ Your Gut? Study Reveals Social Transmission of Genetic Effects Through Microbes
The genes of people you live with may be quietly influencing the bacteria in your gut. A study published in Nature Communications shows that living together not only shapes an individual's gut microbiome, but can also allow genetic effects to “spread” through a population via microbes.
The study, a collaboration between the Center for Genomic Regulation (CRG) in Barcelona and the University of California, San Diego, examined more than 4,000 laboratory mice. It found that the composition of a mouse's gut microbiome was influenced both by its own genes and significantly by the genes of its cage mates.
The researchers explained that genes themselves do not transfer between individuals, but commensal microbes shaped by those genes can spread through close social contact. Some genes selectively promote the growth of particular gut bacteria, which can pass between animals living together and cause genetic effects to “spill over” into other individuals.
“This is not magic, but the result of genetic influences being transmitted through social contact. Genes shape the gut microbiome, and we found that an individual's own genes are not the only ones at work,” said corresponding author Dr. Amelie Baud, a researcher at CRG.
The gut microbiome consists of trillions of microorganisms and plays key roles in digestion, immunity and overall health. Although diet and medications are considered major influences, the genetic contribution has long been difficult to define precisely. In human studies, only the lactase gene and ABO blood group gene have so far been reliably linked to the gut microbiome.
Researchers noted that nature and nurture are tightly intertwined in natural settings: genes influence diet and lifestyle, while family members and social contacts share food, living environments and microbes, making genetic effects difficult to isolate. The team therefore used genetically diverse laboratory mice raised under tightly controlled conditions and fed the same diet.
The 4,000 mice came from four independent populations at four U.S. facilities with different husbandry procedures. By combining whole-genome and gut microbiome data, researchers identified three gene–microbe association regions that remained stable across different environmental conditions.
The strongest association involved the St6galnac1 gene, which adds sugar molecules to intestinal mucus. Researchers believe the gut bacterium Paraprevotella feeds on these sugars. The association was observed in all four populations. A second genetic region contained several mucin genes and was associated with the abundance of Firmicutes bacteria. The third involved the Pip gene, which encodes an antimicrobial molecule, and was associated with bacteria in the Muribaculaceae family, common in mice and also present in humans.
The large sample allowed researchers to quantify for the first time how much of the laboratory mice's gut microbiome was determined by their own genes and how much arose from the genetic influence of cage mates. This phenomenon is called an “indirect genetic effect,” similar to classic examples in which maternal genes affect offspring growth or immunity through the nurturing environment.
The team built computational models to distinguish direct genetic effects from indirect effects mediated by social contact. Some Muribaculaceae bacteria were influenced by both. When these social effects were incorporated into the model, the overall strength of genetic influence in the three newly identified gene–microbe associations increased 4- to 8-fold. Researchers believe this may represent only a small part of the true picture.
“We may only be seeing the tip of the iceberg,” Dr. Baud said. “At present, we can detect the bacteria with the strongest signals. As microbiome sequencing improves, we may find many more microbes influenced by social genetic effects.”
The study further suggests that if similar mechanisms exist in humans, large population studies may systematically underestimate the effects of genes on health. Genes may not only determine an individual's disease risk, but also affect the health of others in their social network through microbial transmission.
At the mechanistic level, researchers noted that St6galnac1 in mice is functionally closely related to the human gene ST6GAL1, and earlier studies have also linked ST6GAL1 to Paraprevotella. This suggests that different species may share a biological mechanism in which glycosylation of the intestinal mucus surface determines which microbes can colonize and proliferate in the gut.
The team also proposed potential medical hypotheses. Other studies have associated ST6GAL1 with breakthrough SARS-CoV-2 infection after vaccination, while Paraprevotella has been shown to promote degradation of a digestive enzyme required for the virus to enter host cells. Genetic variants might indirectly affect infection risk by regulating the abundance of this bacterium.
Paraprevotella may also affect the structure of IgA antibodies. IgA protects the gut, but abnormal IgA may enter the bloodstream and accumulate in the kidneys, causing IgA nephropathy. Researchers speculated that this pathway could explain why some people develop the autoimmune disease.
The team next plans to investigate how St6galnac1 regulates Paraprevotella in laboratory mice and trace the downstream effects on the gut and whole-body physiology.
“I am almost obsessed with this bacterium now,” Dr. Baud said. “Our findings were replicated in four independent facilities, giving us an exceptionally rare opportunity for follow-up research.”
Story source:
Collected online