RESUMEN
ADAM29 (a disintegrin and metalloprotease domain 29) is a member of the membrane-anchored ADAM family of proteins, which is highly expressed in testis and may mediate different physiological and pathological processes. Although the functions of many ADAM family members have been well characterized, the biological relevance of ADAM29 has remained largely unknown. Here, we report the generation of an Adam29-deficient mouse model to delve deeper into the in vivo functions of this ADAM family member. We show that ADAM29 depletion does not affect mice viability, development, or fertility, but somehow impinges on metabolism and energy expenditure. We also report herein that ADAM29 deficiency leads to an accelerated wound healing process, without affecting cell reprogramming in mouse-derived fibroblasts. Collectively, our findings provide new insights into ADAM29 biological functions, highlighting the importance of non-catalytic ADAM proteases.
RESUMEN
The spindle assembly checkpoint (SAC) is an essential mechanism that ensures the accurate chromosome segregation during mitosis, thus preventing genomic instability. Deubiquitinases have emerged as key regulators of the SAC, mainly by determining the fate of proteins during cell cycle progression. Here, we identify USP49 deubiquitinase as a novel regulator of the spindle checkpoint. We show that loss of USP49 in different cancer cell lines impairs proliferation and increases aneuploidy. In addition, USP49-depleted cells overcome the arrest induced by the SAC in the presence of nocodazole. Finally, we report new binding partners of USP49, including ribophorin 1, USP44, and different centrins.
