Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.29.123851v1?rss=1 Authors: Vaughan, S. K., Barbat-Artigas, S., Myers, T., Pradham, B. S., Proszynski, T. J., Robitaille, R., Valdez, G. Abstract: Cholinergic transmission must be tightly regulated at mammalian neuromuscular junctions (NMJs) for motor neurons and skeletal muscles to properly communicate and remain viable. Here, we examined the function of Lynx1, and endogenous regulator of cholinergic transmission, at NMJs in mice. We show that Lynx1 interacts with and modulates the activity of muscle nicotinic acetylcholine receptors (nAChRs) at NMJs. We also demonstrate that deletion of Lynx1 prematurely and progressively increases the incidence of NMJs with age-related features including fragmentation, nerve sprouting, and multiple innervation. Deleterious changes at NMJs lacking Lynx1 ultimately culminate in the atrophy and de-differentiation of muscle fibers from a fast to a slow phenotype, two hallmarks of aged skeletal muscles. Additionally, we show that Lynx1 is markedly reduced at aged NMJs of control mice, further indicating that Lynx1 plays important roles in mitigating age-related changes at NMJs. These data show that Lynx1 is an attractive target for preventing aging of NMJs and skeletal muscles. Copy rights belong to original authors. Visit the link for more info