Uty, also known as KDM6C, is a gene located on the Y chromosome. It is a homologue of KDM6A (UTX) on the X chromosome. Uty encodes a histone lysine demethylase, which is involved in removing chromatin H3K27 methylation marks at genes' transcriptional start sites for activation, participating in chromatin metabolism [4]. It is associated with various biological processes, and its study via genetic models like knockout mice can reveal its functions in vivo.

Female mice with homozygous deletion of Kdm6a do not survive, but hemizygous males are viable, suggesting Uty has a compensatory function [1]. Disruption of Uty in hematopoietic cells of male mice phenocopies the profibrotic attributes of Y chromosome loss in heart failure, indicating its role in heart failure progression [2]. In addition, knockdown of Uty in gonadectomized male mice exposed to hypoxia leads to more severe pulmonary hypertension, suggesting Uty is protective against this condition [3]. Transgenic overexpression of Uty in female mice masculinizes gene expression patterns in the placenta and hypothalamus, and affects physiological outcomes like weight gain and glucose tolerance [5].

In conclusion, Uty plays crucial roles in multiple biological processes. Gene knockout mouse models have revealed its significance in diseases such as heart failure and pulmonary hypertension. Understanding Uty's functions provides insights into the mechanisms of these diseases and potential therapeutic targets.