Alternative polyadenylation signals and promoters act in concert to control tissue-specific expression of the Opitz Syndrome gene MID1.

ABSTRACT:

Background

Mutations in the X-linked MID1 gene are responsible for Opitz G/BBB syndrome, a malformation disorder of developing midline structures. Previous Northern blot analyses revealed the existence of at least three MID1 transcripts of differing lengths.

Results

Here we show that alternative polyadenylation generates the size differences observed in the Northern blot analyses. Analysis of EST data together with additional Northern blot analyses proved tissue-specific usage of the alternative polyadenylation sites. Bioinformatic characterization of the different 3'UTRs of MID1 revealed numerous RNA-protein interaction motifs, several of which turned out to be conserved between different species. Furthermore, our data suggest that mRNA termination at different polyadenylat

SUBMITTER: Winter J 

PROVIDER: S-EPMC2248598 | biostudies-literature | 2007 Nov

REPOSITORIES: biostudies-literature