Kumar Anita, Dumasia Kushaan, Deshpande Sharvari, Gaonkar Reshma, Balasinor N H
Department of Neuroendocrinology, National Institute for Research in Reproductive Health (ICMR), Parel, Mumbai 400012, India.
Confocal Facility, National Institute for Research in Reproductive Health (ICMR), Parel, Mumbai 400012, India.
Biochim Biophys Acta. 2016 Aug;1863(8):1996-2005. doi: 10.1016/j.bbamcr.2016.04.022. Epub 2016 Apr 23.
Actin remodeling is a vital process for signaling, movement and survival in all cells. In the testes, extensive actin reorganization occurs at spermatid-Sertoli cell junctions during sperm release (spermiation) and at inter Sertoli cell junctions during restructuring of the blood testis barrier (BTB). During spermiation, tubulobulbar complexes (TBCs), rich in branched actin networks, ensure recycling of spermatid-Sertoli cell junctional molecules. Similar recycling occurs during BTB restructuring around the same time as spermiation occurs. Actin related protein 2/3 complex is an essential actin nucleation and branching protein. One of its subunits, Arpc1b, was earlier found to be down-regulated in an estrogen-induced rat model of spermiation failure. Also, Arpc1b was found to be estrogen responsive through estrogen receptor beta in seminiferous tubule culture. Here, knockdown of Arpc1b by siRNA in adult rat testis led to defects in spermiation caused by failure in TBC formation. Knockdown also compromised BTB integrity and caused polarity defects of mature spermatids. Apart from these effects pertaining to Sertoli cells, Arpc1b reduction perturbed ability of germ cells to enter G2/M phase thus hindering cell division. In summary, Arpc1b, an estrogen responsive gene, is a regulator of spermiation, mature spermatid polarity, BTB integrity and cell division during adult spermatogenesis.
肌动蛋白重塑是所有细胞中信号传导、运动和存活的重要过程。在睾丸中,精子释放(精子形成)过程中,在精子细胞-支持细胞连接处以及血睾屏障(BTB)重塑期间的支持细胞间连接处会发生广泛的肌动蛋白重组。在精子形成过程中,富含分支肌动蛋白网络的微管球复合体(TBCs)可确保精子细胞-支持细胞连接分子的循环利用。在与精子形成同时发生的BTB重塑过程中也会出现类似的循环利用。肌动蛋白相关蛋白2/3复合体是一种重要的肌动蛋白成核和分支蛋白。其亚基之一Arpc1b,早前在雌激素诱导的精子形成失败大鼠模型中被发现表达下调。此外,在生精小管培养中发现Arpc1b通过雌激素受体β对雌激素有反应。在此,在成年大鼠睾丸中通过小干扰RNA(siRNA)敲低Arpc1b会导致由于TBC形成失败而引起的精子形成缺陷。敲低还会损害BTB的完整性,并导致成熟精子细胞的极性缺陷。除了这些与支持细胞相关的影响外,Arpc1b的减少还会干扰生殖细胞进入G2/M期的能力,从而阻碍细胞分裂。总之,Arpc1b作为一个雌激素反应基因,是成年精子发生过程中精子形成、成熟精子细胞极性、BTB完整性和细胞分裂的调节因子。