Tmem132a, a transmembrane protein, is crucial in multiple biological processes. It is involved in the Wnt/β -catenin signaling pathway, which is vital for embryonic development and adult tissue homeostasis [2,4]. Tmem132a also interacts with planar cell polarity (PCP) regulators, indicating its role in PCP-related processes [1].

In Tmem132a-null mouse models, various developmental defects were observed. These include caudal developmental defects such as skeletal, posterior neural tube closure, genitourinary tract, and hindgut defects [1]. In the hindgut, visceral endoderm fails to be excluded from the medial region in mutant embryos, leading to malformations in cloaca-derived structures and indirectly affecting the neural tube and kidney/ureter [1]. Mouse embryos lacking Tmem132a display phenotypes similar to Wnt/β-catenin mutants, like open spina bifida, caudal truncation, syndactyly, and renal defects, suggesting its key role in regulating this pathway [2]. Also, in these models, spinal neural tube closure and lateral migration of the caudal paraxial mesoderm are affected, as Tmem132a regulates integrins and downstream integrin pathway activation [3].

In conclusion, Tmem132a is a key regulator in embryonic development, especially in processes related to hindgut morphogenesis, caudal development, neural tube closure, and mesodermal migration. The study of Tmem132a knockout mouse models has provided valuable insights into its role in these processes and its association with caudal-related developmental defects [1,2,3].