ELMOD2, a GTPase-activating protein, has uniquely broad specificity for ARF family GTPases. It is involved in multiple cellular pathways, including those related to ciliogenesis, mitochondrial fusion, and cellular lipid metabolism, and is thus of great biological importance. Genetic models, such as knockout mouse models, have been crucial in understanding its functions [1,2,3,4].

In mouse embryonic fibroblasts with ELMOD2 deleted, there were changes in cilia-related processes like increased ciliation and multiciliation, along with altered ciliary morphology and signaling. These defects could be reversed by increasing ARL2 activity or overexpressing Rootletin, indicating a common pathway among ARL2, ELMOD2, and Rootletin in suppressing spurious ciliation and maintaining centrosome cohesion [1].

In oocytes, knockdown of Elmod2 by siRNA led to severe meiotic delay, abnormal chromosomal segregation, decreased oocyte maturation rate, and reduced fertilization rate, likely by regulating mitochondrial dynamics [5].

Also, in adipocytes, knockdown of ELMOD2 increased the amount of adipocyte triglyceride lipase (ATGL) in lipid droplets and decreased total cellular triglycerides, showing its role in regulating ATGL transport and cellular lipid metabolism [3].

In conclusion, ELMOD2 is essential for multiple biological processes. Its deletion in mouse models has revealed its significance in ciliogenesis, meiotic progression in oocytes, and cellular lipid metabolism. These findings contribute to understanding related disease conditions, such as potential implications in ciliopathies, reproductive disorders, and lipid-metabolism-related diseases.