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AP-2α regulates migration of GN-11 neurons via a specific genetic programme involving the Axl receptor tyrosine kinase

By Orso Francesca, Jäger Richard, Calogero Raffaele, Schorle Hubert, Sismondi Piero, De Bortoli Michele and Taverna Daniela

Abstract

<p>Abstract</p> <p>Background</p> <p>Neuronal migration is a crucial process that allows neurons to reach their correct target location to allow the nervous system to function properly. AP-2α is a transcription factor essential for neural crest cell migration and its mutation results in apoptosis within this cell population, as demonstrated by genetic models.</p> <p>Results</p> <p>We down-modulated AP-2α expression in GN-11 neurons by RNA interference and observe reduced neuron migration following the activation of a specific genetic programme including the Adhesion Related Kinase (<it>Axl</it>) gene. We prove that <it>Axl </it>is able to coordinate migration per se and by ChIP and promoter analysis we observe that its transcription is directly driven by AP-2α via the binding to one or more functional AP-2α binding sites present in its regulatory region. Analysis of migration in AP-2α null mouse embryo fibroblasts also reveals an essential role for AP-2α in cell movement via the activation of a distinct genetic programme.</p> <p>Conclusion</p> <p>We show that AP-2α plays an essential role in cell movement via the activation of cell-specific genetic programmes. Moreover, we demonstrate that the AP-2α regulated gene <it>Axl </it>is an essential player in GN-11 neuron migration.</p

Topics: Biology (General), QH301-705.5, Science, Q, DOAJ:Biology, DOAJ:Biology and Life Sciences
Publisher: BioMed Central
Year: 2009
DOI identifier: 10.1186/1741-7007-7-25
OAI identifier: oai:doaj.org/article:184886b953fe4fc5aaad8129930b566a
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