Ueffing Mareike, Langeheine Marion, Gniesmer Sarah, Rode Kristina, Staggenborg Sarah, Wirth Gudrun, Rohn Kerstin, Koch Rüdiger, Blume Ines, Pfarrer Christiane, Wrede Christoph, Brehm Ralph
Institute for Anatomy, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany.
Department of Pathology, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany.
PLoS One. 2025 Apr 24;20(4):e0321292. doi: 10.1371/journal.pone.0321292. eCollection 2025.
Genetically induced loss of the gap-junction protein Connexin 43 (Cx43) in murine Sertoli cells leads to an arrest of spermatogenesis at the level of spermatogonia, highly vacuolated tubules, and intratubular cell clusters. Transmission electron microscopy as well as 3D-reconstruction of Sertoli cells based on serial block-face scanning electron microscopy imaging revealed severe cell shape changes in Cx43 deficient Sertoli cells. Since the cytoskeleton is important for the transport of germ cells within the seminiferous epithelium and for keeping the cell shape, the study at hand aimed to reveal correlations of Cx43 loss and changes of cytoskeletal components and their spatial organization in the seminiferous epithelium. Immunohistochemistry, immunofluorescence, conventional transmission electron microcopy and immunogold labeling indicated alterations in microtubule and actin filament distribution patterns in Cx43 deficient Sertoli cells compared to wildtype mice. Firstly, microtubules seemed to be misoriented in mutant Sertoli cells. Secondly, the actin filament based basal ectoplasmic specializations were increased in spatial extension, but the apical ectoplasmic specialization was missing. Lastly, Sertoli cells of both genotypes immunostained positive for vimentin, the prevalent intermediate filament of Sertoli cells, but not for keratins, markers for Sertoli cell immaturity or dedifferentiation. In conclusion, Cx43 deficiency in Sertoli cells correlates not only with severe cell shape alterations but also with changes in microtubule and actin filament distribution patterns, while intermediate filament expression seems to be only negligibly influenced.
在小鼠支持细胞中,基因诱导的缝隙连接蛋白连接蛋白43(Cx43)缺失会导致精子发生在精原细胞水平停滞,出现高度空泡化的小管和管内细胞簇。基于连续块面扫描电子显微镜成像的透射电子显微镜以及支持细胞的三维重建显示,Cx43缺陷型支持细胞存在严重的细胞形态变化。由于细胞骨架对于生精上皮内生殖细胞的运输以及维持细胞形态很重要,因此本研究旨在揭示Cx43缺失与生精上皮中细胞骨架成分变化及其空间组织之间的相关性。免疫组织化学、免疫荧光、传统透射电子显微镜和免疫金标记表明,与野生型小鼠相比,Cx43缺陷型支持细胞中微管和肌动蛋白丝的分布模式发生了改变。首先,突变型支持细胞中的微管似乎方向错误。其次,基于肌动蛋白丝的基底外质特化在空间上有所增加,但顶端外质特化缺失。最后,两种基因型的支持细胞对波形蛋白(支持细胞中普遍存在的中间丝)免疫染色均呈阳性,但对角蛋白(支持细胞不成熟或去分化标志物)免疫染色呈阴性。总之,支持细胞中Cx43缺陷不仅与严重的细胞形态改变有关,还与微管和肌动蛋白丝分布模式的变化有关,而中间丝表达似乎仅受到微不足道的影响。