Creation of mutants that affect spermatogenesis is very challenging in most experimental systems, especially mammals. The main reason this is true is because "absence of successful mating" is a negative result that can occur for a wide variety of trivial, irrelevant reasons. The C. elegans hermaphroditic mode of reproduction has unusual features that facilitate analysis of spermatogenesis. Normally, hermaphrodites are virtually 100% self-fertile and spermatogenesis defective mutants are self-sterile. A candidate spermatogenesis defective mutant will produce cross-progeny after mating to a wild type male, showing that the presence of sperm is both necessary and sufficient to restore fertility to the sterile hermaphrodite. This has allowed selection of a large number of spermatogenesis defective mutants. In this article, I will review spermatogenesis, how mutants are made and what has been learned about the identified genes and their roles during development and fertilization.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.mce.2009.01.008 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Platelet Mitochondrial Function and Endogenous Coenzyme Q Levels Could Be Used as Markers of Mitochondrial Health in Infertile Men: A Pilot Study.
Int J Mol Sci
December 2024
Faculty of Medicine, Slovak Medical University, Limbová 12, 833 03 Bratislava, Slovakia.
Fertility disorders are a worldwide problem affecting 8-12% of the population, with the male factor substantially contributing to about 40-50% of all infertility cases. Mitochondria, crucial organelles for cellular viability, play a pivotal role in the processes of spermatogenesis and significantly affect sperm quality and their fertilizing ability. Mitochondrial oxidative phosphorylation (OXPHOS) dysfunction, reduced energy supply for sperm, reduced endogenous coenzyme Q (CoQ) levels, and oxidative stress are among the main factors that contribute to male infertility.
View Article and Find Full Text PDFComprehensive analysis of poly(A) tails in mouse testes and ovaries using Nanopore Direct RNA Sequencing.
Sci Data
January 2025
Laboratory of RNA Biology, International Institute of Molecular and Cell Biology, Warsaw, 02-109, Poland.
Gametogenesis is a process in which dysfunctions lead to infertility, a growing health and social problem worldwide. In both spermatogenesis and oogenesis, post-transcriptional gene expression regulation is crucial. Essentially, all mRNAs possess non-templated poly(A) tails, whose composition and dynamics (elongation, shortening, and modifications) determine the fate of mRNA.
View Article and Find Full Text PDFA recurrent loss-of-function variant in DRC1 causes non-syndromic severe asthenozoospermia with favorable intracytoplasmic sperm injection and pregnancy outcomes.
Andrology
January 2025
Institute for Advanced Biosciences, Team Genetics Epigenetics and Therapies of Infertility, University of Grenoble Alpes, Grenoble, France.
Background: Asthenozoospermia, characterized by reduced sperm motility, is a common cause of male infertility. Multiple morphological abnormalities of the sperm flagella (MMAF) represent a severe and genetically heterogeneous form of asthenozoospermia. Over 50 genes have been associated, but approximately half of MMAF cases remain unexplained.
View Article and Find Full Text PDFExploring the impact of environmental factors on male reproductive health through epigenetics.
Reprod Toxicol
January 2025
Reproductive and Genetic Center, The Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China. Electronic address:
Male infertility has become an increasingly severe global health issue, with its incidence significantly rising over the past few decades. This paper delves into the crucial role of epigenetics in male reproductive health, focusing particularly on the effects of DNA methylation, histone modifications, chromatin remodeling and non-coding RNAs regulation on spermatogenesis. Exposure to various environmental factors can cause sperm DNA damage, leading to epigenetic abnormalities.
View Article and Find Full Text PDFCep78 knockout causes sterility and oligoasthenoteratozoospermia in male mice.
Sci Rep
January 2025
The Affiliated Taian City Central Hospital of Qingdao University, 29 Longtan Rd, Taishan District, Taian, 271000, Shandong, China.
Oligoasthenoteratozoospermia (OAT) is a common cause of infertility among males, and the majority of cases of idiopathic OAT are thought to be attributed to genetic defects. In this study, the role of the CEP78 protein in spermatogenesis was initially investigated using Cep78 knockout (Cep78) mice. Notably, the male Cep78 mice exhibited the OAT phenotype and sterility.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!