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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Isolation and characterisation of the chick orthologue of the Opitz syndrome gene, Mid1, supports a conserved role in vertebrate development.

The X-linked form of Opitz syndrome (OS) is caused by loss of function of the microtubule-associated MID1 protein. The phenotype of OS includes defects along the central body axis, namely hypertelorism, cleft lip and palate, hypospadias and cardiac structural anomalies. Here we describe the isolation and characterisation of full-length cDNA clones representing the chick Mid1 gene and the detailed profile of its expression in stage 7 to 28 chick embryos. Consistent with the remarkable sequence conservation of MID1 between human and chick was the good correlation of the pattern of cMid1 expression with the tissues affected in OS. In stage 10 embryos, transcripts were concentrated in the head mesenchyme which includes migratory neural crest cells. However, the incomplete overlap with a neural crest marker, Sox10, suggests that Mid1 is a marker for somitomeric mesoderm and potentially for a subset of neural crest cells. Consistent with this, cMid1 expression was also detected at later stages in neural crest-derived facial mesenchyme, in the myotome and in the condensing muscle blocks of the limb. Expression of cMid1 was observed in the neural epithelium of the forebrain beginning at stage 7 with increased signal in presumptive rhombomeres 2/3. By stage 15, expression is highest in the diencephalon. Other areas with high expression are certain facial epithelia and the midgut that will give rise to the oesophagus and trachea. These data indicate that Mid1 plays an evolutionarily conserved developmental function in vertebrates that may involve effects on cellular proliferation, tissue interactions and morphogenesis.[1]


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