Wdr13, a member of the WD repeat protein family, is highly conserved in vertebrates and localizes to the nucleus. It is expressed in several tissues including the pancreas, liver, uterus, and brain. It is involved in multiple cellular pathways, potentially including the PI3K/AKT signaling pathway [2]. The study of Wdr13-knockout (KO) mouse models has been crucial for understanding its in-vivo functions [2,3,4,5,6,7,8,9].

In KO mouse models, the absence of Wdr13 leads to pancreatic β-cell hyper-proliferation, higher serum insulin levels, and better glucose clearance, suggesting its role as a negative regulator of pancreatic β-cell proliferation and its potential as a drug target for diabetes [1,7,8]. Wdr13-deficient female mice develop endometrial hyperplasia, mimicking human EH-associated metabolic disorders, indicating its importance in uterine tissue [3]. In bovine skeletal muscle-derived satellite cells, Wdr13 promotes differentiation by affecting the PI3K/AKT signaling pathway [2]. Also, in mice, lack of Wdr13 gene predisposes them to a depression-like phenotype under social isolation stress and is associated with differential expression of synaptic proteins [6].

In summary, Wdr13 plays essential roles in multiple biological processes. The Wdr13 KO mouse models have been instrumental in revealing its functions in diabetes, endometrial hyperplasia, muscle cell differentiation, and stress-related mental disorders, providing potential targets for treatment in these disease areas.