Pard6b, a homolog of par-6 gene, is a component of the PAR-atypical protein kinase C (aPKC) complex. It plays a crucial role in regulating cell polarity, which is fundamental for various biological processes such as cell differentiation, tissue development, and maintenance of epithelial integrity. The PAR-aPKC complex is involved in establishing and maintaining apico-basal cell polarity in epithelial cells [1,2,3].

In Pard6b-knockdown mouse embryos, the embryos cleaved and compacted normally but failed to form the blastocyst cavity. This was due to defective intercellular junctions, abnormal distribution of actin filaments and TJP1 (ZO-1) tight junction protein, and interference with cavitation. The apical localization of PRKCZ (aPKCzeta) was absent, and the expression of CDX2, a TE-lineage transcription factor, was diminished in the outer cells, indicating that Pard6b is essential for blastocyst morphogenesis and trophectoderm formation [1]. In lung adenocarcinoma cells, silencing of the PKCζ/Pard3/Pard6 polarity complex components induced EMT, invasion, and colonization in vivo, suggesting that reduced expression of Pard6b contributes to NSCLC progression [2].

In conclusion, Pard6b is essential for processes like blastocyst morphogenesis and maintaining normal epithelial cell polarity. Its dysregulation is associated with diseases such as pancreatic cancer, lung adenocarcinoma, which may be potential disease areas for further exploration based on the role of Pard6b revealed by mouse models. The study of Pard6b through gene-knockout or knockdown models helps in understanding its functions in normal development and disease conditions. [1,2]