論文

査読有り 招待有り 筆頭著者 最終著者 責任著者
2022年3月

The phenotype of PLCζ1-deficient mice.

Reproduction
  • Yuhkoh Satouh

記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1530/rep-21-0438
出版者・発行元
Bioscientifica

In 2002, a report suggested that oocyte activation is induced by Plcz1 in mouse oocytes, which prompted great interest on exploring the role of sperm PLCζ1. Thus, PLCζ1 loss-of-function experiments became a crucial tool for addressing this subject. Although the only option to completely delete a target protein in fully functional spermatozoa is to use gene-deficient animals, Plcz1-deficient mice were not reported until 2017. Challenges to obtain suitable in vivo models have been related to altered expression of Capza3, a neighbor gene to Plcz1 locus in mammalian genomes that is required for spermatogenesis. With the advancement of genome-editing technologies, two groups independently and simultaneously produced Plcz1 mutant mouse lines, which were the first animal models to be artificially and reliably deficient for sperm PLCζ1. All Plcz1 mutant mouse lines display normal spermatogenesis and, surprisingly, subfertility rather than complete infertility. Moreover, analysis of oocyte Ca2+ dynamics indicate that mouse PLCζ1 is an essential sperm-derived oocyte activation factor via intracytoplasmic sperm injection, as PLCζ1 deficiency causes complete lack of Ca2+ oscillations. This seemingly contradictory phenotype can be explained by atypical Ca2+ oscillations that are provoked slowly and less frequently in the case of fertilization accompanied by physiological sperm-egg fusion. These findings not only raise new questions concerning the sperm basic biology, by clearly demonstrating the existence of a PLCζ1-independent oocyte activation mechanism in mice, but also have implications for the treatment and phenotypic interpretation of patients presenting oocyte activation failure.

リンク情報
DOI
https://doi.org/10.1530/rep-21-0438
共同研究・競争的資金等の研究課題
哺乳類卵子活性化に伴う表在タンパク質動態のプロテオミクス解析
共同研究・競争的資金等の研究課題
哺乳類の胚発生を司る新規卵活性化機構の解明
URL
https://rep.bioscientifica.com/view/journals/rep/aop/rep-21-0438/rep-21-0438.xml
URL
https://rep.bioscientifica.com/downloadpdf/journals/rep/aop/rep-21-0438/rep-21-0438.xml
ID情報
  • DOI : 10.1530/rep-21-0438
  • ISSN : 1470-1626
  • eISSN : 1741-7899

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