Division of Natural Sciences, College of Mt St Vincent, Bronx, NY 10471, USA
Division of Natural Sciences, College of Mt St Vincent, Bronx, NY 10471, USA.
Biol Open. 2020 Feb 26;9(2):bio049080. doi: 10.1242/bio.049080.
Individual sperm cells are resolved from a syncytium during late step of spermiogenesis known as individualization, which is accomplished by an Individualization Complex (IC) composed of 64 investment cones. encodes Tubulin-binding cofactor E-like (TBCEL), suggesting a role for microtubule dynamics in individualization. Indeed, a population of ∼100 cytoplasmic microtubules fails to disappear in mutant testes during spermatogenesis. This persistence, detected using epi-fluorescence and electron microscopy, suggests that removal of these microtubules by TBCEL is a prerequisite for individualization. Immunofluorescence reveals TBCEL expression in elongated spermatid cysts. In addition, testes from mutant males were rescued to wild type using to drive TBCEL expression, indicating that the mutant phenotype is caused by the lack of TBCEL. Finally, RNAi driven by -GAL4 successfully phenocopied , confirming that is required in the germline for individualization. We propose a model in which the cytoplasmic microtubules serve as alternate tracks for investment cones in mutant testes.This article has an associated First Person interview with the first author of the paper.
个体精子细胞是在精子发生的晚期阶段从合胞体中分离出来的，这个过程被称为个体化，由一个由 64 个投资锥组成的个体化复合物（IC）完成。 编码微管结合辅助因子 E 样（TBCEL），表明微管动力学在个体化过程中起作用。事实上，在 突变体睾丸的精子发生过程中，大约 100 个细胞质微管未能消失。这种持久性，通过 epi-荧光和电子显微镜检测到，表明 TBCEL 通过去除这些微管是个体化的前提。免疫荧光显示 TBCEL 在伸长的精子细胞囊中表达。此外，使用 驱动 TBCEL 表达挽救了 突变体雄性的睾丸，表明突变表型是由 TBCEL 的缺乏引起的。最后，由 -GAL4 驱动的 RNAi 成功地模拟了 ，证实 在线粒体中是个体化所必需的。我们提出了一个模型，其中细胞质微管作为 突变体睾丸中投资锥的替代轨道。本文有与论文第一作者的相关第一人称采访。
