Telomere length (TL) is increasingly recognized as a molecular marker that reflects how reproductive aging affects intergenerational transmissions. Here, we investigated the effects of parental age on offspring survival and the regulation of TL by examining the telomere-elongating activity of telomerase in the Pacific oyster. We assessed the classical hallmarks of aging in parents at three age classes (young, middle-aged, and old) and crossbred them using a split-brood design to examine the consequences of the nine maternal-by-paternal age combinations on their offspring. Reproductive aging leads to increased larval mortality and accelerated telomere shortening in spats, rendering them more susceptible to infection by the Ostreid herpesvirus. Viral exposure stimulates telomerase activity, a response that we identified as adaptive, but weakened by parental aging. While telomerase lengthens a spat’s telomere, paradoxically, longer individual TL predicts higher mortality in adults. The telomerase-telomere complex appeared as a conservative biomarker for distinguishing survivors and losers upon exposure to polymicrobial diseases.

中文翻译：

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生殖衰老削弱了太平洋牡蛎后代的存活率并限制了端粒酶对疱疹病毒的反应


端粒长度 （TL） 越来越被认为是反映生殖衰老如何影响代际传递的分子标志物。在这里，我们通过检查太平洋牡蛎端粒酶的端粒延长活性，研究了父母年龄对后代存活和 TL 调节的影响。我们评估了三个年龄段 （年轻、中年和老年） 父母的典型衰老特征，并使用分体育雏设计对它们进行杂交，以检查九种母体对父系年龄组合对其后代的影响。生殖衰老导致幼虫死亡率增加和卵状物端粒加速缩短，使它们更容易受到 Ostreid 疱疹病毒的感染。病毒暴露会刺激端粒酶活性，我们确定这种反应是适应性的，但会因父母衰老而减弱。虽然端粒酶会延长 spite 的端粒，但矛盾的是，较长的个体 TL 预示着成人的死亡率更高。端粒酶-端粒复合物作为一种保守的生物标志物出现，用于区分暴露于多种微生物疾病的幸存者和失败者。