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在异常的亮灰蜻(双翅目,摇蚊科)精母细胞中,着丝粒组蛋白 H2AT120 的磷酸化丧失伴随着体细胞染色体失活。

Loss of centromeric histone H2AT120 phosphorylation accompanies somatic chromosomes inactivation in the aberrant spermatocytes of Acricotopus lucidus (Diptera, Chironomidae).

机构信息

Institute of Genetics (240), University of Hohenheim, Garbenstrasse 30, 70599, Stuttgart, Germany.

出版信息

Protoplasma. 2016 Jan;253(1):211-6. doi: 10.1007/s00709-015-0801-x. Epub 2015 Mar 28.

DOI:10.1007/s00709-015-0801-x
PMID:25820679
Abstract

In the germ line of the chironomid Acricotopus lucidus, two cells with quite different chromosome constitutions result from the last unequal gonial mitosis. In the male, the future primary spermatocyte receives all the germ line-limited chromosomes (=Ks) together with somatic chromosomes (=Ss), and later on undergoes meiotic divisions, while the connected aberrant spermatocyte gets only Ss and remains undivided with chromosomes inactivated in a metaphase-like condensed state. This raises the question whether the centromeres of the permanently condensed Ss of the aberrant spermatocyte remain active during meiosis of the connected regular spermatocyte. Active centromeres exhibit an epigenetic phosphorylation mark at threonine 120 of histone H2A. To visualise the centromeric H2A phosphorylation of the Ss in the aberrant spermatocyte, meiotic stages were immunostained with different anti-phospho histone H2AT120 antibodies. Clear H2AT120ph signals appear at the centromeres of the Ss during prophase, persist on the metaphase-like condensed Ss during meiosis I of the connected primary spermatocyte and disappear during transition to meiosis II. The centromeres of the Ss and Ks of the regular spermatocytes display H2AT120ph signals from prophase I to anaphase II. The loss of the H2AT120 phosphorylation detected on the centromeres of the Ss of the aberrant spermatocyte indicating their deactivation supports the idea of a programmed inactivation of the Ss to block the entry of the germ line-derived aberrant spermatocyte, lacking Ks, into meiosis, and thus to prevent the generation of sperms possessing only Ss. This mechanism would ensure the presence of the Ks in the germ line.

摘要

在摇蚊 Acricotopus lucidus 的生殖系中,最后一次不均等的精巢有丝分裂会导致两个具有截然不同染色体组成的细胞。在雄性中,未来的初级精母细胞接收所有生殖系限制染色体(=Ks)以及体细胞染色体(=Ss),随后进行减数分裂,而相连的异常精母细胞仅接收 Ss 并保持未分裂状态,染色体处于类似于中期的浓缩状态失活。这就提出了一个问题,即异常精母细胞中永久浓缩的 Ss 的着丝粒在相连的正常精母细胞的减数分裂过程中是否保持活跃。活跃的着丝粒在苏氨酸 120 处表现出组蛋白 H2A 的表观遗传磷酸化标记。为了可视化异常精母细胞中 Ss 的着丝粒组蛋白 H2A 磷酸化,使用不同的抗磷酸化组蛋白 H2AT120 抗体对减数分裂阶段进行免疫染色。在前期,Ss 的着丝粒处出现明显的 H2AT120ph 信号,在相连的初级精母细胞的第一次减数分裂中期类似于浓缩的 Ss 上持续存在,并在向第二次减数分裂过渡时消失。正常精母细胞的 Ss 和 Ks 的着丝粒在从前期 I 到后期 II 都显示 H2AT120ph 信号。异常精母细胞的 Ss 着丝粒上检测到的 H2AT120 磷酸化的丧失表明它们失活,这支持了 Ss 被程序性失活以阻止缺乏 Ks 的生殖系衍生的异常精母细胞进入减数分裂的观点,从而防止产生仅具有 Ss 的精子。该机制将确保生殖系中存在 Ks。

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