Dchs2, a dachsous cadherin-related gene, is involved in multiple biological processes. It belongs to the FAT/DCHS family of protocadherins which have high functional redundancy. Dchs2 is important for maintaining cell adhesion and polarity as a cadherin, and is implicated in signaling pathways related to tissue development and growth regulation [2,3].

In the heart, murine DCHS2 deletion induced physiological hypertrophy and promoted cardiomyogenesis, while cardiomyocyte DCHS2 overexpression in zebrafish led to pathological hypertrophy and impaired cardiac regeneration [1]. In hypothalamic-pituitary development, analysis of Dchs2-/-mouse mutants identified anterior pituitary hypoplasia and partially penetrant infundibular defects, implicating Dchs2 in normal hypothalamic-pituitary development [2]. In craniofacial development, zebrafish embryos deficient in Dchs2 showed chondrocytes failing to stack and misregulating sox9a expression, indicating its role in coordinating cartilage differentiation and polarity [4].

In conclusion, Dchs2 plays essential roles in cardiac growth, hypothalamic-pituitary development, and craniofacial development. Gene knockout models, such as the Dchs2-/-mouse mutants, have been crucial in revealing its functions in these specific biological processes, providing insights into related disease mechanisms like heart failure, pituitary gland developmental defects, and skeletal malformations [1,2,4].