Insights into the mechanism of bovine spermiogenesis based on comparative transcriptomic studies

Abstract

To reduce the reproductive loss caused by semen quality and provide theoretical guidance for the eradication of human male infertility, differential analysis of the bovine transcriptome among round spermatids, elongated spermatids, and epididymal sperm was carried out with the reference of the mouse transcriptome, and the homology trends of gene expression to the mouse were also analysed. First, to explore the physiological mechanism of spermiogenesis that profoundly affects semen quality, homological trends of differential genes were compared during spermiogenesis in dairy cattle and mice. Next, the Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, protein-protein interaction network (PPI network), and bioinformatics analysis uncovered the regulation network of acrosome formation during the transition from round to elongated spermatids. In addition, processes that regulate gene expression during spermiogenesis from elongated spermatid to epididymal sperm, such as ubiquitination, acetylation, deacetylation, glycosylation, and the functional gene ART3 may play an important role during spermiogenesis. Therefore, its localisation in the seminiferous tubule was investigated by immunofluorescent analysis, and its structure and function were also predicted. This study provides important data for revealing the mystery of life during spermiogenesis resulting from acrosome formation, histone replacement, and the fine regulation of gene expression.

Dysregulation of the Acrosome Formation Network by 8-oxoguanine (8-oxoG) in Infertile Sperm: A Case Report with Advanced Techniques

“…The evolutional conservation of spermatogenesis is reported in the mammalian species. The irregularity of spermatogenic gene expression reduces the quality of semen and may lead to the failure of fertilization both in cattle and humans [ 1 ]. Environmental and genetic effects have been associated with decreased male fertility, which is known to contribute to a dysregulated spermatogenic gene network, abnormal spermatogenesis, and eventually, impaired sperm fertility [ 2 ].…”