Maternal age effect on mouse oocytes: new biological insight from proteomic analysis.
Maternal age effect on mouse oocytes: new biological insight from proteomic analysis.
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DOI：
10.1530/rep-14-0126
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发表时间：
2014-07
期刊：
影响因子：
3.8
通讯作者：
C. Schwarzer;Marcin Siatkowski;M. Pfeiffer;Nicole Baeumer;H. Drexler;Bingyuan Wang;G. Fuellen;M. Boia
中科院分区：
文献类型：
--
作者：
C. Schwarzer;Marcin Siatkowski;M. Pfeiffer;Nicole Baeumer;H. Drexler;Bingyuan Wang;G. Fuellen;M. Boia
长期存在的“不朽生殖系vs致命体细胞”的观点提出了一个关于卵母细胞如何在分子方面老化的生物学基本问题。一个主流的假设是，母体卵母细胞的老化有其基因转录的根源。研究mRNA翻译产生的蛋白质将揭示功能可用蛋白质水平与mRNA的相关性，并将为母亲衰老过程中卵母细胞所经历的变化提供新的见解。基因本体（GO）语义分析显示，检测到的蛋白质组（2324个蛋白质）与转录组（22334个mRNA）高度相似，尽管并非所有蛋白质都具有同源mRNA。在它们的动态方面，蛋白质组的丰度变化（3%）比转录组（0.05%）更频繁，但没有相关性。而与细胞核相关的蛋白质（例如染色体的结构维护和纺锤体组装检查点）在母体衰老过程中主要出现在卵母细胞的变化中；与氧化应激/损伤相关的蛋白质（如超氧化物歧化酶）很少出现。这些数量上的变化要么使人贫穷，要么使人富足。使用氧化石墨烯分析，这些变化与从体细胞组织中已知的衰老的经典特征没有任何简单的联系。鉴于缺乏相关性，我们得出结论，小鼠卵母细胞的蛋白质组分析可能无法替代转录组分析。此外，我们得出结论，衰老的经典特征可能不会以一对一的方式从体细胞组织转移到卵母细胞。总的来说，母体卵母细胞的衰老不仅仅是细胞退化，减数分裂非整倍体的臭名昭著的增加就是例证。
The long-standing view of 'immortal germline vs mortal soma' poses a fundamental question in biology concerning how oocytes age in molecular terms. A mainstream hypothesis is that maternal ageing of oocytes has its roots in gene transcription. Investigating the proteins resulting from mRNA translation would reveal how far the levels of functionally available proteins correlate with mRNAs and would offer novel insights into the changes oocytes undergo during maternal ageing. Gene ontology (GO) semantic analysis revealed a high similarity of the detected proteome (2324 proteins) to the transcriptome (22 334 mRNAs), although not all proteins had a cognate mRNA. Concerning their dynamics, fourfold changes of abundance were more frequent in the proteome (3%) than the transcriptome (0.05%), with no correlation. Whereas proteins associated with the nucleus (e.g. structural maintenance of chromosomes and spindle-assembly checkpoints) were largely represented among those that change in oocytes during maternal ageing; proteins associated with oxidative stress/damage (e.g. superoxide dismutase) were infrequent. These quantitative alterations are either impoverishing or enriching. Using GO analysis, these alterations do not relate in any simple way to the classic signature of ageing known from somatic tissues. Given the lack of correlation, we conclude that proteome analysis of mouse oocytes may not be surrogated with transcriptome analysis. Furthermore, we conclude that the classic features of ageing may not be transposed from somatic tissues to oocytes in a one-to-one fashion. Overall, there is more to the maternal ageing of oocytes than mere cellular deterioration exemplified by the notorious increase of meiotic aneuploidy.