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

doi:10.1186/1741-7007-7-25

BMC Biology
Volume 7

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Orso F
Jäger R
Calogero RA
Schorle H
Sismondi P
De Bortoli M
Taverna D

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Jäger R
Calogero RA
Schorle H
Sismondi P
De Bortoli M
Taverna D
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Research article

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

Francesca Orso¹^,2^,6 , Richard Jäger³ , Raffaele Adolfo Calogero⁴^,6 , Hubert Schorle³ , Piero Sismondi⁵ , Michele De Bortoli²^,6 and Daniela Taverna¹^,2^,6

¹Molecular Biotechnology Center, University of Torino, via Nizza, 52, 10126, Torino, Italy

²Department of Oncological Sciences, University of Torino, SP142, 10060, Candiolo, Italy

³Institute of Pathology, Department of Developmental Pathology, University of Bonn Medical School, Sigmund-Freud-Strasse 25, 53127, Bonn, Germany

⁴Bioinformatics and Genomics Unit, Department of Clinical and Biological Sciences, University of Torino, Regione Gonzole 10, Orbassano, 10043, Torino, Italy

⁵Institute for Cancer Research and Treatment (IRCC), SP 142, 10060 Candiolo (To), Italy

⁶Center for Complex Systems in Molecular Biology and Medicine, University of Torino, Torino, Italy

author email corresponding author email

BMC Biology 2009, 7:25doi:10.1186/1741-7007-7-25


Published:	22 May 2009

Abstract

Background

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.

Results

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 (Axl) gene. We prove that Axl 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.

Conclusion

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 Axl is an essential player in GN-11 neuron migration.