Palladin is a regulator of actin filament bundles at the ectoplasmic specialization in adult rat testes.

Palladin is a regulator of actin filament bundles at the ectoplasmic specialization in adult rat testes.
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DOI:
10.1210/en.2012-2269
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发表时间:
2013-04
期刊:
影响因子:
4.8
通讯作者:
Xiaojing Qian;Xiaojing Qian;D. Mruk;Elissa W P Wong;Pearl P Y Lie;C. Cheng
Xiaojing Qian;Xiaojing Qian;D. Mruk;Elissa W P Wong;Pearl P Y Lie;C. Cheng
中科院分区:
医学2区
文献类型:
--
作者:
Xiaojing Qian;Xiaojing Qian;D. Mruk;Elissa W P Wong;Pearl P Y Lie;C. Cheng

文献摘要

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在大鼠睾丸中,支持细胞-支持细胞和支持细胞-精子细胞界面处的外质特化(ES)分别称为血-睾丸屏障处的基底ES和近腔室中的顶端ES,是睾丸特异性粘附连接。电镜下可见内质网池与质膜之间夹有肌动蛋白纤维束。虽然这些肌动蛋白丝束进行广泛的重组,以转换之间的捆绑和解开状态,以促进血-睾丸屏障重建和精子细胞的粘附/运输,这些事件背后的调控分子仍然未知。在这里,我们报告的肌动蛋白丝交联/捆绑蛋白palladin,在上皮细胞周期的顶端和基底ES显示限制性时空表达的研究结果。Palladin在结构上与Eps 8(表皮生长因子受体途径底物8,一种肌动蛋白倒刺末端加帽和捆绑蛋白)和Arp 3(肌动蛋白相关蛋白3,其与Arp 2一起形成Arp 2/3复合物以诱导分支肌动蛋白成核,将捆绑的肌动蛋白丝转化为未捆绑/分支网络)相互作用并共定位,说明其在ES调节肌动蛋白丝束动力学中的作用。在体外建立紧密连接(TJ)渗透性屏障的支持细胞中,palladin的敲除被发现会破坏TJ功能,这与影响TJ蛋白分布的肌动蛋白丝的解体有关。它在体内的敲除也扰乱了F-肌动蛋白的组织,导致精子细胞极性和粘附力的丧失,导致精子细胞运输和精子形成的缺陷。总之,palladin是ES的肌动蛋白丝调节剂。
In rat testes, the ectoplasmic specialization (ES) at the Sertoli-Sertoli and Sertoli-spermatid interface known as the basal ES at the blood-testis barrier and the apical ES in the adluminal compartment, respectively, is a testis-specific adherens junction. The remarkable ultrastructural feature of the ES is the actin filament bundles that sandwiched in between the cisternae of endoplasmic reticulum and apposing plasma membranes. Although these actin filament bundles undergo extensive reorganization to switch between their bundled and debundled state to facilitate blood-testis barrier restructuring and spermatid adhesion/transport, the regulatory molecules underlying these events remain unknown. Herein we report findings of an actin filament cross-linking/bundling protein palladin, which displayed restrictive spatiotemporal expression at the apical and the basal ES during the epithelial cycle. Palladin structurally interacted and colocalized with Eps8 (epidermal growth factor receptor pathway substrate 8, an actin barbed end capping and bundling protein) and Arp3 (actin related protein 3, which together with Arp2 form the Arp2/3 complex to induce branched actin nucleation, converting bundled actin filaments to an unbundled/branched network), illustrating its role in regulating actin filament bundle dynamics at the ES. A knockdown of palladin in Sertoli cells in vitro with an established tight junction (TJ)-permeability barrier was found to disrupt the TJ function, which was associated with a disorganization of actin filaments that affected protein distribution at the TJ. Its knockdown in vivo also perturbed F-actin organization that led to a loss of spermatid polarity and adhesion, causing defects in spermatid transport and spermiation. In summary, palladin is an actin filament regulator at the ES.