Quaking regulates Hnrnpa1 expression through its 3' UTR in oligodendrocyte precursor cells.

ABSTRACT: In mice, Quaking (Qk) is required for myelin formation; in humans, it has been associated with psychiatric disease. QK regulates the stability, subcellular localization, and alternative splicing of several myelin-related transcripts, yet little is known about how QK governs these activities. Here, we show that QK enhances Hnrnpa1 mRNA stability by binding a conserved 3' UTR sequence with high affinity and specificity. A single nucleotide mutation in the binding site eliminates QK-dependent regulation, as does reduction of QK by RNAi. Analysis of exon expression across the transcriptome reveals that QK and hnRNP A1 regulate an overlapping subset of transcripts. Thus, a simple interpretation is that QK regulates a large set of oligodendrocyte precursor genes indirectly by increasing the intr

SUBMITTER: Zearfoss NR 

PROVIDER: S-EPMC3017110 | biostudies-literature | 2011 Jan

REPOSITORIES: biostudies-literature