Reviewed by Lily Ramsey, LLMOct 27 2023 Mature spermatozoa are characterized by an head, midpiece and a long tail for locomotion. Now, researchers from the University Hospital Bonn and the Transdisciplinary Research Unit "Life & Health" at the University of Bonn have found that a loss of the structural protein ACTL7B blocks spermatogenesis in male mice. The cells can no longer develop their characteristic shape and remain in a rather round form. The animals are infertile.
Male sperm cells are constantly produced in large quantities in the testicles during so-called spermatogenesis. In this process, the typical elongated sperm cells are formed from round germ cells. This enormous change in shape requires the fine tuned reorganization of specialized structural proteins. One of these structural proteins is ACTL7B.
To investigate the role of the structural protein in spermiogenesis, Prof. Schorle's team generated a mouse model with a mutation in the Actl7b gene using gene-editing technology. This results in a complete loss of function of ACTL7B.
Disruption in the network of proteins In this context, the Bonn researchers found that ACTL7B is required for the reorganization of the cytoskeleton of spermatids. Using mass spectrometric analyses, they identified two interaction partners of ACTL7B, DYNLL1 and DYNLL2. "We were able to show that without the structural protein, DYNLL1 and 2 are not correctly localized in the round spermatids.
This explains why the sperm of male mice with a mutated Actl7b gene is not able to develop the characteristic shape. Due to this, the animals are infertile. In addition, according to other research, there is evidence that levels of the protein ACTL7B are reduced in some fertility patients.Prof. Hubert Schorle from the Institute of Pathology at UKBJournal reference:Merges, G. E., et al.