ArticleReproduction, fertility, and development2019
Analysis of spermatogenesis and fertility in adult mice with a hypomorphic mutation in the Mtrr gene.
Article in Reproduction, fertility, and development, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Hyperhomocysteinemia lowers serum testosterone concentration via impairing testosterone production in Leydig cells.Cell biology and toxicology · 2023Article
- One-carbon metabolism is required for epigenetic stability in the mouse placenta.Frontiers in cell and developmental biology · 2023Article
- Defective folate metabolism causes germline epigenetic instability and distinguishes Hira as a phenotype inheritance biomarker.Nature communications · 2021Article
- The Guangsi Yulin Decoction Inhibits Oxidative Stress and Inflammation-Induced Spermatogenesis DysfunctionAmerican journal of men's healthArticle
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Recent research has focussed on the significance of folate metabolism in male fertility. Knocking down the mouse gene Mtrr impedes the progression of folate and methionine metabolism and results in hyperhomocysteinaemia, dysregulation of DNA methylation and developmental phenotypes (e.g. neural tube, heart and placenta defects). The Mtrrgt mouse line is a model of transgenerational epigenetic inheritance (TEI), the hypothesised cause of which is the inheritance of a yet-to-be determined epigenetic factor via the germline. We investigated Mtrrgt/gt testes and sperm function compared with control C57Bl/6J testes to explore potential defects that might confound our understanding of TEI in the Mtrrgt model. Histological analysis revealed that adult Mtrrgt/gt testes are more spherical in shape than C57Bl/6J testes, though serum testosterone levels were normal and spermatogenesis progressed in a typical manner. Spermatozoa collected from the cauda epididymis showed normal morphology, counts, and viability in Mtrrgt/gt males. Correspondingly, Mtrrgt spermatozoa contributed to normal pregnancy rates. Similar parameters were assessed in Mtrr+/+ and Mtrr+/gt males, which were normal compared with controls. Overall, our data showed that the Mtrrgt allele is unlikely to alter spermatogenesis or male fertility. Therefore, it is improbable that these factors confound the mechanistic study of TEI in Mtrrgt mice.
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