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A crucial player in neuronal differentiation

Two papers in this issue report that ZAG-1, the C. elegans homologue of the vertebrate Zn-finger homeodomain protein EF1, acts as a transcriptional repressor that regulates many crucial aspects of neuron terminal differentiation. Both groups discovered zag-1 in screens for mutant worms with defective neuronal development. These studies revealed that zag-1 mutations cause axon guidance, fasciculation and branching errors, and the misexpression of neuronal differentiation markers. The null mutant, as reported by Wacker et al. on p. 3795, also highlights the involvement of zag-1 in pharynx development as mutant larvae die from starvation, being unable to swallow food. On p. 3781, Clark and Chiu show that zag-1 is expressed in neurons and specific muscles, and directly represses its own expression, while also downregulating genes involved in neurotransmitter synthesis or reuptake. The authors expect future work on ZAG-1 targets to uncover novel and key regulators of axon guidance.

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Related articles in Development:

C. elegans ZAG-1, a Zn-finger-homeodomain protein, regulates axonal development and neuronal differentiation

Scott G. Clark and Catherine Chiu
Development 2003 130: 3781-3794. [Abstract] [Full Text]  

zag-1, a Zn-finger homeodomain transcription factor controlling neuronal differentiation and axon outgrowth in C. elegans

Irene Wacker, Valentin Schwarz, Edward M. Hedgecock, and Harald Hutter
Development 2003 130: 3795-3805. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?