Do we have/need a name for this process?
It’s a firmly established fact straight from Biology 101: Traits such as eye color and height are passed from one generation to the next through the parents’ DNA.
As firmly established as Darwinism itself (natural selection acting on random mutation, neo-Darwinism, the neo-Darwinian synthesis, the extended synthesis, whatever …). Actually, the only thing that is firmly established these days is that what ain’t so will continue to be taught in school, by court order if necessary. Oh, and walking dead legacy media will continue to hound American Republican politicians about what they believe about “evolution.” But not about science topics that are relevant to governing a country.
But now, a new study in mice by researchers at Washington University School of Medicine in St. Louis has shown that the DNA of bacteria that live in the body can pass a trait to offspring in a way similar to the parents’ own DNA. According to the authors, the discovery means scientists need to consider a significant new factor — the DNA of microbes passed from mother to child — in their efforts to understand how genes influence illness and health.
“We have kept bacteria on one side of a line separating the factors that shape our development — the environmental side of that line, not the genetic side,” said co-senior author Herbert W. Virgin IV, MD, PhD. “But our results show bacteria stepping over the line. This suggests we may need to substantially expand our thinking about their contributions, and perhaps the contributions of other microorganisms, to genetics and heredity.”
Bacteria are most familiar through their roles in harmful infections. But scientists have realized that such bacteria are only a tiny fraction of the bacterial communities that live in and on our bodies. Most bacteria are commensal, which means they do not cause harm and often confer benefits.
The study is the first to show that bacterial DNA can pass from parent to offspring in a manner that affects specific traits such as immunity and inflammation.
The researchers linked commensal bacteria in mice to the animals’ susceptibility to a gut injury. Mice with certain inherited bacteria are susceptible to the injury, which is caused by exposure to a chemical. Female mice pass the bacteria to their offspring, making them vulnerable to the injury. Others carrying different bacteria are less susceptible.
In the short term, the findings may help scientists eliminate a significant “bug” in studies of genetically engineered mice. In several fields of research, scientists have been confronted intermittently with the sudden, unexplained appearance of new or altered traits in mice. The traits often spread from one mouse habitat to the next, suggesting a spreading microbial infection is responsible. But the traits also consistently pass from mother to offspring, suggesting a genetic cause.
The latter explanation involves a major change in thinking because it suggests that traits affected by bacteria can pass from mothers to their offspring in the same manner as traits affected by mouse DNA.
“The implications for mouse experiments are profound and could help us cut through some persistent sources of confusion,” Stappenbeck said. “When we study mice, we have to account for the possibility that inherited bacteria and their genes could be influencing the trait we’re trying to learn about.”
These are lab mice, of course. It would certainly be good to know whether this also happens in nature, where the mice may be somewhat hardier. Here’s the abstract from Nature:
The proliferation of genetically modified mouse models has exposed phenotypic variation between investigators and institutions that has been challenging to control1, 2, 3, 4, 5. In many cases, the microbiota is the presumed cause of the variation. Current solutions to account for phenotypic variability include littermate and maternal controls or defined microbial consortia in gnotobiotic mice6, 7. In conventionally raised mice, the microbiome is transmitted from the dam2, 8, 9. Here we show that microbially driven dichotomous faecal immunoglobulin-A (IgA) levels in wild-type mice within the same facility mimic the effects of chromosomal mutations. We observe in multiple facilities that vertically transmissible bacteria in IgA-low mice dominantly lower faecal IgA levels in IgA-high mice after co-housing or faecal transplantation. In response to injury, IgA-low mice show increased damage that is transferable by faecal transplantation and driven by faecal IgA differences. We find that bacteria from IgA-low mice degrade the secretory component of secretory IgA as well as IgA itself. These data indicate that phenotypic comparisons between mice must take into account the non-chromosomal hereditary variation between different breeders. We propose faecal IgA as one marker of microbial variability and conclude that co-housing and/or faecal transplantation enables analysis of progeny from different dams. (paywall)
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