HSPC300 and its role in neuronal connectivity

doi:10.1186/1749-8104-2-18

Neural Development

Volume 2

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Qurashi A
Sahin HB
Carrera P
Gautreau A
Schenck A
Giangrande A

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Sahin HB
Carrera P
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Giangrande A
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Research article

HSPC300 and its role in neuronal connectivity

Abrar Qurashi¹^,2 , H Bahar Sahin¹ , Pilar Carrera¹^,3 , Alexis Gautreau⁴ , Annette Schenck¹^,5 and Angela Giangrande¹

¹Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, BP 10142, 67404 Illkirch, CU de Strasbourg, France

²Department of Human Genetics, Emory University School of Medicine, Atlanta, GA 30322, USA

³Abteilung für Molekulare Entwicklungsbiologie, Institut für Molekulare Physiologie und Entwicklungsbiologie, Universität Bonn, D-53115 Bonn, Germany

⁴Laboratoire de Morphogenèse et Signalisation Cellulaires, UMR 144 CNRS/Institut Curie, 75248 Paris Cedex 05, France

⁵Department of Human Genetics (855), Nijmegen Centre for Molecular Life Science, Radboud University Nijmegen Medical Centre, Box 9101, 6500 HB Nijmegen, The Netherlands

author email corresponding author email

Neural Development 2007, 2:18doi:10.1186/1749-8104-2-18


Published:	25 September 2007

Abstract

Background

The WAVE/SCAR complex, consisting of CYFIP (PIR121 or Sra1), Kette (Nap1), Abi, SCAR (WAVE) and HSPC300, is known to regulate the actin nucleating Arp2/3 complex in a Rac1-dependent manner. While in vitro and in vivo studies have demonstrated that CYFIP, Kette, Abi and SCAR work as subunits of the complex, the role of the small protein HSPC300 remains unclear.

Results

In the present study, we identify the HSPC300 gene and characterize its interaction with the WAVE/SCAR complex in the Drosophila animal model. On the basis of several lines of evidence, we demonstrate that HSPC300 is an indispensable component of the complex controlling axonal and neuromuscular junction (NMJ) growth. First, the Drosophila HSPC300 expression profile resembles that of other members of the WAVE/SCAR complex. Second, HSPC300 mutation, as well as mutations in the other complex subunits, results in identical axonal and NMJ growth defects. Third, like with other complex subunits, defects in NMJ architecture are rescued by presynaptic expression of the respective wild-type gene. Fourth, HSPC300 genetically interacts with another subunit of the WAVE/SCAR complex. Fifth, HSPC300 physically associates with CYFIP and SCAR.

Conclusion

Present data provide the first evidence for HSPC300 playing a role in nervous system development and demonstrate in vivo that this small protein works in the context of the WAVE/SCAR complex.