Bnc2, also known as basonuclin 2, is a gene with diverse functions. It acts as a transcription factor involved in myofibroblastic activation in fibrosis, integrating pro-fibrotic stimuli like TGFβ and Hippo/YAP1 signaling to induce matrisome genes [2]. In the context of energy balance regulation, Bnc2-expressing neurons in the arcuate nucleus are part of the neural circuit maintaining it, as they are activated by leptin and can acutely suppress food intake by directly inhibiting orexigenic agouti-related protein (AGRP) neurons [1].

In animal models, deleting leptin receptors in Bnc2 neurons in mice led to marked hyperphagia and obesity, similar to the effect of leptin receptor knockout in AGRP neurons, highlighting its role in energy balance regulation [1]. In zebrafish, experimental knockdown of Bnc2 caused pronephric-outlet obstruction and cloacal dilatation, phenocopying human congenital lower urinary-tract obstruction (LUTO), suggesting its importance in the development of the lower urinary tract [3].

In conclusion, Bnc2 has essential functions in energy balance regulation and lower urinary tract development. The gene knockout and knockdown models in mice and zebrafish have significantly contributed to understanding its role in obesity-related energy balance disorders and congenital lower urinary-tract obstruction.