ArticleDevelopmental biology2021
Mutations in non-muscle myosin 2A disrupt the actomyosin cytoskeleton in Sertoli cells and cause male infertility.
Article in Developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- The membrane skeleton density of red blood cells in MYH9-related disease patients is decreased.Bioscience reports · 2026Article
- Role of the nonhelical tailpiece of myosin-II in regulating filament architecture and function.The Journal of cell biology · 2026Article
- Nonmuscle myosin IIA (NMIIA) regulates anisotropic cell tension to maintain the hexagonal packing of mouse lens meridional row cells.Molecular biology of the cell · 2025Article
- Human congenital cataract mutation inInternational journal of ophthalmology · 2025Article
- Structure, regulation, and mechanisms of nonmuscle myosin-2.Cellular and molecular life sciences : CMLS · 2024Review
- Nonmuscle Myosin IIA Regulates the Precise Alignment of Hexagonal Eye Lens Epithelial Cells During Fiber Cell Formation and Differentiation.Investigative ophthalmology & visual science · 2023Article
- The sperm-interacting proteome in the bovine isthmus and ampulla during the periovulatory period.Journal of animal science and biotechnology · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in non-muscle myosin 2A (NM2A) encompass a wide spectrum of anomalies collectively known as MYH9-Related Disease (MYH9-RD) in humans that can include macrothrombocytopenia, glomerulosclerosis, deafness, and cataracts. We previously created mouse models of the three mutations most frequently found in humans: R702C, D1424N, and E1841K. While homozygous R702C and D1424N mutations are embryonic lethal, we found homozygous mutant E1841K mice to be viable. However the homozygous male, but not female, mice were infertile. Here, we report that these mice have reduced testis size and defects in actin-associated junctions in Sertoli cells, resulting in inability to form the blood-testis barrier and premature germ cell loss. Moreover, compound double heterozygous (R702C/E1841K and D1424/E1841K) males show the same abnormalities in testes as E1841K homozygous males. Conditional ablation of either NM2A or NM2B alone in Sertoli cells has no effect on fertility and testis size, however deletion of both NM2A and NM2B in Sertoli cells results in infertility. Isolation of mutant E1841K Sertoli cells reveals decreased NM2A and F-actin colocalization and thicker NM2A filaments. Furthermore, A
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