顶体
生物
细胞骨架
细胞生物学
精子
顶体反应
自噬
肌动蛋白
生物发生
支架蛋白
高尔基体
电容
肌动蛋白细胞骨架
精子发生
转录组
蛋白质组学
蛋白质亚单位
信号转导衔接蛋白
蛋白质亚细胞定位预测
信号转导
细胞
支持细胞
细胞器生物发生
蛋白质组
作者
Andjela Kovacevic,Eva Ordziniak,Naila Umer,Lena Arévalo,Leo Daniel Hinterlang,Sanaz Ziaeipour,Sara Suvilla,Gina Esther Merges,Hubert Schorle
出处
期刊:Development
[The Company of Biologists]
日期:2026-02-01
卷期号:153 (3)
摘要
Actin-related protein T3 (ACTRT3) is localized in the perinuclear theca (PT) of murine spermatids. We generated Actrt3-/- male mice and showed that they are subfertile, with defects of the acrosome first observed during cap phase. Actrt3 deficiency causes reduced protein levels of the trans-Golgi network markers TGN46 and GOPC and mislocalization of the cis-Golgi protein GM130. Reduction of the autophagy markers LC3B, CTSB and mTOR indicates that loss of ACTRT3 leads to impaired Golgi trafficking and autophagic flux, which are required for acrosome biogenesis. In addition, levels of PFN3, a protein involved in acrosome biogenesis, were significantly reduced. Further, co-immunoprecipitation revealed interaction of ACTRT3 with the PT proteins ACTRT1, ACTRT2, ACTL7A, SPEM2 and the sperm surface protein ZPBP. This suggested that ACTRT3 is a part of the complex 3D scaffold of the PT and contributes to ZPBP localization. Mass spectrometry revealed enrichment of cytoskeletal regulators such as CFL1 and CNN1. Expression of Actrt3 caused changes in HEK239T cell shape and F-actin filament distribution, suggesting a role in cytoskeletal shaping. We conclude that lack of ACTRT3 affects acrosome biogenesis, PT structure and actin remodeling.
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