Scientists from the University Hospital Bonn and the University of Bonn have discovered that a loss of the structural protein ACTL7B prevents the development of mature sperm cells in male mice. These cells are typically characterized by their elongated shape, which allows them to move. However, without ACTL7B, the cells remain round and cannot function properly, leading to infertility in the mice. The researchers created a mouse model with a mutation in the Actl7b gene to investigate the role of the protein in spermatogenesis. They found that ACTL7B is necessary for the reorganization of the cytoskeleton of the developing sperm cells. Without the protein, other proteins involved in this process are not properly localized. This disruption in the protein network prevents the sperm cells from taking on their characteristic shape. The study suggests that mutations in the Actl7b gene could be responsible for male infertility in some cases. Future research will aim to further understand the role of ACTL7B and develop potential treatments for infertility. The findings were published in the journal Development.
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