关键词: Drosophila RDC complex female hybrid sterility oogenesis piRNA pathway speciation whole-transcriptome libraries

Mesh : Animals Female Drosophila melanogaster / genetics Male Drosophila simulans / genetics Drosophila Proteins / genetics metabolism RNA, Small Interfering / genetics DNA Transposable Elements / genetics Ovary / metabolism Hybridization, Genetic Oogenesis / genetics Infertility / genetics Crosses, Genetic DEAD-box RNA Helicases

来  源:   DOI:10.3390/ijms25115681   PDF(Pubmed)

Abstract:
Species of the genus Drosophila have served as favorite models in speciation studies; however, genetic factors of interspecific reproductive incompatibility are under-investigated. Here, we performed an analysis of hybrid female sterility by crossing Drosophila melanogaster females and Drosophila simulans males. Using transcriptomic data analysis and molecular, cellular, and genetic approaches, we analyzed differential gene expression, transposable element (TE) activity, piRNA biogenesis, and functional defects of oogenesis in hybrids. Premature germline stem cell loss was the most prominent defect of oogenesis in hybrid ovaries. Because of the differential expression of genes encoding piRNA pathway components, rhino and deadlock, the functional RDCmel complex in hybrid ovaries was not assembled. However, the activity of the RDCsim complex was maintained in hybrids independent of the genomic origin of piRNA clusters. Despite the identification of a cohort of overexpressed TEs in hybrid ovaries, we found no evidence that their activity can be considered the main cause of hybrid sterility. We revealed a complicated pattern of Vasa protein expression in the hybrid germline, including partial AT-chX piRNA targeting of the vasasim allele and a significant zygotic delay in vasamel expression. We arrived at the conclusion that the hybrid sterility phenotype was caused by intricate multi-locus differences between the species.
摘要:
果蝇属的物种已成为物种形成研究中最喜欢的模型;但是,种间生殖不相容性的遗传因素研究不足。这里,我们通过杂交果蝇雌性和果蝇雄性对杂种雌性不育进行了分析。使用转录组学数据分析和分子,细胞,和遗传方法,我们分析了差异基因表达,转座因子(TE)活性,piRNA生物发生,和杂种卵子发生的功能缺陷。生殖细胞早逝是杂交卵巢中最突出的缺陷。由于编码piRNA通路组分的基因表达差异,犀牛和僵局,杂种卵巢中的功能性RDCmel复合物未组装。然而,RDCsim复合物的活性在杂交体中得以维持,而与piRNA簇的基因组起源无关.尽管在杂交卵巢中发现了一组过度表达的TEs,我们发现没有证据表明它们的活性可以被认为是杂种不育的主要原因。我们揭示了杂交种系中Vasa蛋白表达的复杂模式,包括Vasim等位基因的部分AT-chXpiRNA靶向和血管内表达的显著合子延迟。我们得出的结论是,杂种不育表型是由物种之间复杂的多位点差异引起的。
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