Mid1/Mid2 expression in craniofacial development and a literature review of X‐linked opitz syndrome

ConclusionsOur results support the hypothesis of functional redundancy of Mid1/Mid2 and their potential roles in regulating tissue remodelling in early development.

MID1 is the causative gene of X‐linked Opitz syndrome and MID2 is its homolog. We conducted expression studies on Mid1/Mid2 in mouse embryos. Our results suggested a tendency of a mutually repressive expression pattern between Mid1 and Mid2 during early development. Further investigations revealed strong expressions of Mid1 and Mid2 in the epithelium of approaching facial prominences and downregulated expressions after fusion. This study supports the hypothesis of functional redundancy of MID1/MID2.

Source: Molecular Genetics & Genomic Medicine - November 1, 2015 Category: Genetics & Stem Cells Authors: Bijun Li, Tianhong Zhou, Yi Zou Tags: Original Article Source Type: research