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J Neurosci Methods. 2009 Mar 15;177(2):322-33. doi: 10.1016/j.jneumeth.2008.10.031. Epub 2008 Nov 6.

Loss of function genetic screens reveal MTGR1 as an intracellular repressor of beta1 integrin-dependent neurite outgrowth.

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1
Department of Anatomy, University of California San Francisco, San Francisco, CA 94158, USA. vossovskaya@biparsciences.com <vossovskaya@biparsciences.com>

Abstract

Integrins are transmembrane receptors that promote neurite growth and guidance. To identify regulators of integrin-dependent neurite outgrowth, here we used two loss of function genetic screens in SH-SY5Y neuroblastoma cells. First, we screened a genome-wide retroviral library of genetic suppressor elements (GSEs). Among the many genes identified in the GSE screen, we isolated the hematopoetic transcriptional factor MTGR1 (myeloid translocation gene-related protein-1). Treatment of SH-SY5Y cells with MTGR1 siRNA enhanced neurite outgrowth and concurrently increased expression of GAP-43, a protein linked to neurite outgrowth. Second, we transduced SH-SY5Y with a genome-wide GFP-labeled lentiviral siRNA library, which expressed 40,000 independent siRNAs targeting 8500 human genes. From this screen we isolated GFI1 (growth factor independence-1), which, like MTGR1, is a member of the myeloid translocation gene on 8q22 (MTG8)/ETO protein complex of nuclear repressor proteins. These results reveal novel contributions of MTGR1 and GFI1 to the regulation of neurite outgrowth and identify novel repressors of integrin-dependent neurite outgrowth.

PMID:
19026687
DOI:
10.1016/j.jneumeth.2008.10.031
[Indexed for MEDLINE]
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