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Loss of a-actinin-3 during human evolution provides superior cold resilience and muscle heat generation

ABSTRACT: To examine if the loss of alpha-actinin-3, a fast skeletal muscle protein, modifies core body temperture following acute cold exposure in humans and a mice Using an Actn3 KO mice model we explore the effects of cold exposure on brown adipose tissue function following exposure to cold (4oC) for 5 hours, compared to control mice housed at either thermoneutrality (30oC) or standard room temperature (22oC)

ORGANISM(S): Mus musculus

PROVIDER: GSE164936 | GEO | 2021/01/16

REPOSITORIES: GEO

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Loss of α-actinin-3 during human evolution provides superior cold resilience and muscle heat generation

Project description:The fast skeletal muscle protein α-actinin-3 is absent in 1.5 billion people worldwide due to homozygosity for a nonsense polymorphism in the ACTN3 gene (R577X). The prevalence of the 577X allele increased as modern humans moved to colder climates, suggesting a link between α-actinin-3 deficiency and improved cold tolerance. Here, we show that humans lacking α-actinin-3 (XX) are superior in maintaining core body temperature during cold-water immersion due to changes in skeletal muscle thermogenesis. Muscles of XX individuals displayed a shift towards more slow-twitch isoforms of myosin heavy chain (MyHC) and sarcoplasmic reticulum (SR) proteins, accompanied by altered neuronal muscle activation resulting in increased tone rather than overt shivering. Experiments on Actn3 knockout mice showed no alterations in brown adipose tissue (BAT) properties that could explain the improved cold tolerance in XX individuals. Thus, this study provides a clear mechanism for the positive selection of the ACTN3 X-allele in cold climates and supports a key thermogenic role of skeletal muscle during cold exposure in humans.

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Loss of a-actinin-3 during human evolution provides superior cold resilience and muscle heat generation

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