Bicra, also known as GLTSCR1, encodes a subunit of the non-canonical BAF (ncBAF) chromatin remodeling complex. Chromatin remodeling is a crucial process in regulating gene expression, which impacts various biological processes and development [1]. Genetic models like zebrafish, Drosophila, and mouse are valuable for studying Bicra's function.

In zebrafish, a bicra mutation mimicking a human loss-of-function variant leads to craniofacial defects [1]. In Drosophila, loss of Bicra impairs learning and choice abilities, especially in male courtship behaviors [2]. In mice, homozygous knockout of Bicra results in small, pale pups that die within 24 hours after birth, with blood-related defects such as defective erythroblastic islands and irregular red blood cells due to a defect in fetal liver macrophages responsible for erythrocyte maturation [5].

In conclusion, Bicra plays essential roles in development, cognition-related behaviors, and blood cell maturation. The gene knockout models in different organisms have revealed its significance in neurodevelopmental phenotypes, as well as in blood-related processes, contributing to our understanding of diseases like Coffin-Siris syndrome 12 and other SWI/SNF-related intellectual disability disorders [1,3,4].