Mitonuclear interactions alter sex-specific longevity in a species without sex chromosomes
Mitonuclear interactions alter sex-specific longevity in a species without sex chromosomes
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DOI：
10.1098/rspb.2021.1813
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发表时间：
2021-11-10
影响因子：
4.7
通讯作者：
Edmands, Suzanne
中科院分区：
文献类型：
--
作者：
Flanagan, Ben A.;Li, Ning;Edmands, Suzanne
线粒体功能受损可导致衰老和衰老表型。理论预测，由于在大多数真核生物中观察到的线粒体DNA的母系遗传模式，退行性衰老表型和线粒体病理可能在男性中发生得更频繁。在这里，我们估计了来自两个线粒体DNA差异超过20%的异地加州虎种群的近交系亲本和正反交F1的性别特定寿命。卡氏锥虫缺乏性染色体，因此可以更直接地测试线粒体在性别特有的衰老过程中的功能。为了更好地了解衰老机制，我们在寿命的两个时间点估计了两种与年龄相关的表型(线粒体DNA含量和8-羟基-20-脱氧鸟苷(8-OH-DG)DNA损伤)。寿命上的性别差异取决于线粒体和核背景，包括正反交F1之间的差异，这些F1正反交具有不同的线粒体单倍型，核背景为50：50，核贡献来自替代亲本。幼雌鱼线粒体DNA含量最高，且随年龄增长而下降，雄鱼DNA损伤随年龄增长而增加，并在孵化后56d超过雌鱼。成人性比偏向男性，并归因于复杂的有丝分裂核相互作用。结果表明，在没有性染色体的情况下，衰老过程中的性别差异取决于有丝分裂核的相互作用。
Impaired mitochondrial function can lead to senescence and the ageing phenotype. Theory predicts degenerative ageing phenotypes and mitochondrial pathologies may occur more frequently in males due to the matrilineal inheritance pattern of mitochondrial DNA observed in most eukaryotes. Here, we estimated the sex-specific longevity for parental and reciprocal F1 hybrid crosses for inbred lines derived from two allopatric Tigriopus californicus populations with over 20% mitochondrial DNA divergence. T. californicus lacks sex chromosomes allowing for more direct testing of mitochondrial function in sex-specific ageing. To better understand the ageing mechanism, we estimated two age-related phenotypes (mtDNA content and 8-hydroxy-20-deoxyguanosine (8-OH-dG) DNA damage) at two time points in the lifespan. Sex differences in lifespan depended on the mitochondrial and nuclear backgrounds, including differences between reciprocal F1 crosses which have different mitochondrial haplotypes on a 50 : 50 nuclear background, with nuclear contributions coming from alternative parents. Young females showed the highest mtDNA content which decreased with age, while DNA damage in males increased with age and exceed that of females 56 days after hatching. The adult sex ratio was male-biased and was attributed to complex mitonuclear interactions. Results thus demonstrate that sex differences in ageing depend on mitonuclear interactions in the absence of sex chromosomes.