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Baines, J. F.

Publications and source records attributed to Baines, J. F..

2 recordsLinked to original sources

The Neutral Metaorganism

Almost all animals and plants are inhabited by diverse communities of microorganisms, the microbiota. The hosts often pose highly selective environments, which only a subset of the environmentally available microbes are able to colonize. From the hosts perspective it seems useful to shape the community composition of these allowed microbes to promote a beneficial host-microbe symbiosis. In contrast to this, neutral models assume that the structure of the microbiota is entirely shaped by random population dynamics and dispersal. We here show that microbiota community structure from a wide range of host organisms, in particular including previously understudied invertebrates, is in almost all cases consistent with neutral expectations. Moreover, we demonstrate that apparent discrepancies with the neutral model can be due to transient community states rather than host selection. In conclusion, even though hosts are often assumed to control microbiota composition to ensure beneficial interactions, our broad-scale analysis highlights that following colonization, it could rather be neutral processes that determine microbial community structure.

ecology

Low-level mitochondrial heteroplasmy modulates DNA replication, glucose metabolism and lifespan in mice

Mutations in mitochondrial DNA (mtDNA) lead to heteroplasmy, i.e. the intracellular coexistence of wild-type and mutant mtDNA strands, which impact a wide spectrum of diseases but also physiological processes, including endurance exercise performance in athletes. However, the phenotypic consequences of limited levels of naturally-arising heteroplasmy have not been experimentally studied to date. We hence generated a conplastic mouse strain carrying the mitochondrial genome of a AKR/J mouse strain (B6-mtAKR) together with a C57BL/6J nuclear genomic background, leading to >20% heteroplasmy in the origin of light-strand DNA replication (OriL). These conplastic mice demonstrate a shorter lifespan as well as dysregulation of multiple metabolic pathways, culminating in impaired glucose metabolism, compared to wild-type C57BL/6J mice carrying lower levels of heteroplasmy. Our results indicate that physiologically relevant differences in mtDNA heteroplasmy levels at a single, functionally important site impair metabolic health and lifespan in mice.\n\nHighlightsO_LIWe identify heteroplasmy of the adenine-repeat variation (9 to 13A) in nt5172 in the origin of light-strand DNA replication (OriL) in inbred mice.\nC_LIO_LIB6-mtAKR mice carry >20% 12A heteroplasmy in the OriL, while B6 mice carry only [~] 10% heteroplasmy.\nC_LIO_LIThe level of 12A heteroplasmy correlates to mtDNA copy number, glucose metabolism, and lifespan in mice.\nC_LIO_LIGiven the established role of mtDNA heteroplasmy in regards to endurance exercise performance in athletes, these findings may impact our understanding of metabolism and aging in humans.\nC_LI

genetics