Bnc2, also known as basonuclin 2, is a gene encoding a zinc finger transcription factor. It is involved in multiple biological processes and associated pathways.

In the regulation of energy balance, Bnc2-expressing neurons in the arcuate nucleus play a key role in the neural circuit maintaining energy balance, as they can be activated by leptin to acutely suppress food intake by directly inhibiting orexigenic agouti-related protein (AGRP) neurons [1]. In fibrosis, Bnc2 is identified as a myofibroblast identity transcription factor, integrating pro-fibrotic stimuli like TGFβ and Hippo/YAP1 signaling to induce matrisome genes, and its deficiency blunts collagen deposition in fibrotic mouse livers [2].

In the context of disease, rare variants in Bnc2 are implicated in autosomal-dominant congenital lower urinary-tract obstruction (LUTO). Experimental knockdown of Bnc2 in zebrafish caused pronephric-outlet obstruction and cloacal dilatation, phenocopying human congenital LUTO [3]. Also, in high-grade serous ovarian carcinoma, Bnc2 expression levels are reduced, and its silencing increases cell survival after oxidative stress, suggesting it may be a putative tumor suppressor gene [4]. In addition, a functional SNP in Bnc2 is associated with adolescent idiopathic scoliosis, and Bnc2 overexpression produces body curvature in developing zebrafish in a gene-dosage-dependent manner [5].

In conclusion, Bnc2 is crucial in various biological processes such as energy balance regulation, fibrosis development, and is associated with multiple diseases including LUTO, high-grade serous ovarian carcinoma, and adolescent idiopathic scoliosis. The use of animal models like zebrafish and mouse models (as inferred from gene-function studies in fibrosis) has significantly contributed to understanding the role of Bnc2 in these biological processes and disease conditions.