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Resources » Paper

Weinberg, Peter J et al. (2013) International Worm Meeting "The SWI/SNF chromatin remodeling complex selectively affects multiple aspects of serotonergic neuron differentiation."

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  • Comments on Weinberg, Peter J et al. (2013) International Worm Meeting "The SWI/SNF chromatin remodeling complex selectively affects multiple aspects of serotonergic neuron differentiation." (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00043372

    Weinberg, Peter J, Flames, Nuria, Sawa, Hitoshi, Garriga, Gian, & Hobert, Oliver (2013). The SWI/SNF chromatin remodeling complex selectively affects multiple aspects of serotonergic neuron differentiation presented in International Worm Meeting. Unpublished information; cite only with author permission.

    Regulatory programs that control the specification of serotonergic neurons have been investigated by genetic mutant screens in the nematode Caenorhabditis elegans. Loss of a previously uncloned gene, ham-3, affects migration and serotonin antibody staining of the hermaphrodite-specific (HSN) neuron pair. We characterize these defects here in more detail, showing that the defects in serotonin antibody staining are paralleled by a loss of the transcription of all genes involved in serotonin synthesis and transport. This loss is specific to the HSN neuron class as other serotonergic neurons appear to differentiate normally in ham-3 null mutants. Besides failing to migrate appropriately, the HSN neurons also display axon pathfinding defects in ham-3 mutants. However, the HSN neurons are still generated and express a subset of their terminal differentiation features in ham-3 null mutants, demonstrating that ham-3 is a specific regulator of select features of the HSN neurons. We show that ham-3 codes for the C. elegans ortholog of human BAF60, Drosophila Bap60 and yeast Swp73, which are subunits of the yeast SWI/SNF and vertebrate BAF chromatin remodeling complex. We show that the effect of ham-3 on serotonergic fate can be explained by ham-3 regulating the expression of the Spalt/SALL-type Zn finger transcription factor sem-4, a previously identified regulator of serotonin expression in HSN and of the ham-2 Zn transcription factor, a previously identified regulator of HSN migration and axon outgrowth. Our findings provide the first evidence for the involvement of the BAF complex in the acquisition of terminal neuronal identity and constitute genetic proof by germline knockout that a BAF complex component can have cell-type specific roles during development.

    Affiliations:
    - National Institute of Genetics, Mishima, Japan
    - Department of Biochemistry and Biophysics, Howard Hughes Medical Institute, Columbia University Medical Center, New York, NY
    - Department of Molecular and Cell Biology, UC Berkeley, Berkeley, CA
    - Instituto de Biomedicina de Valencia, IBV-CSIC, Valencia, Spain
    - Department of Biological Sciences, Columbia University, New York, NY.


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