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Resources » Paper

Laurie Earls et al. (2006) Neuronal Development, Synaptic Function, and Behavior Meeting "The Search for Targets of the Aristaless Transcription Factor in C. elegans"

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  • Comments on Laurie Earls et al. (2006) Neuronal Development, Synaptic Function, and Behavior Meeting "The Search for Targets of the Aristaless Transcription Factor in C. elegans" (0)

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00028257

    Laurie Earls, Susan Barlow, Rebecca Fox, & David Miller (2006). The Search for Targets of the Aristaless Transcription Factor in C. elegans presented in Neuronal Development, Synaptic Function, and Behavior Meeting. Unpublished information; cite only with author permission.

    Aristaless encodes an X-linked, homeodomain transcription factor conserved in eukaryotes. Mutations in the aristaless locus are a major cause of mental retardation in human males. These defects are correlated with the failure of GABA neuron differentiation and migration in the brain. The genetic programs that aristaless controls in mammalian GABA neurons are unknown. The C. elegans orthologue of aristaless, alr-1, is highly expressed in GABA neurons to control specific gene expression (Melkman & Sengupta, 2005). We have shown that process outgrowth of DD motor neurons in the ventral nerve cord is also disrupted in alr-1 mutants. To identify alr-1-regulated genes in DD motor neurons, we are using MAPCeL (Micro-Array Profiling of C. elegans Cells) to compare gene expression profiles of wildtype and alr-1 mutant DD motor neurons. Embryonic DD motor neurons labeled with the DD-specific reporter, C04G2.1::GFP, were isolated by FACS and RNA extracted for application to the C. elegans Affymetrix array. The preponderance of human homologs that we have observed in microarray profiles of C. elegans GABA neurons suggests that the alr-1-regulated genes revealed by these experiments are likely to encode aristaless target genes with comparable functions in human GABA neurons. Thus, mutant analysis of these genes in C. elegans holds the promise of revealing molecules with key functions in the etiology of neural dysfunction in the human brain.


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