The fully linked HTML version of this article has now been published.
Development ePress online publication date 3 Aug 2006
doi: 10.1242/dev.02494
Research article
An unusual Zn-finger/FH2 domain protein controls a left/right asymmetric neuronal fate decision in C. elegans
Robert J. Johnston Jr,
John W. Copeland,
Marc Fasnacht,
John F. Etchberger,
Jun Liu,
Barry Honig,
and
Oliver Hobert*
* Author for correspondence (e-mail: or38{at}columbia.edu)
Gene regulatory networks that control the terminally differentiated state of a cell are, by and large, only superficially understood. In a mutant screen aimed at identifying regulators of gene batteries that define the differentiated state of two left/right asymmetric C. elegans gustatory neurons, ASEL and ASER, we have isolated a mutant, fozi-1, with a novel mixed-fate phenotype, characterized by de-repression of ASEL fate in ASER. fozi-1 codes for a protein that functions in the nucleus of ASER to inhibit the expression of the LIM homeobox gene lim-6, neuropeptide-encoding genes and putative chemoreceptors of the GCY gene family. The FOZI-1 protein displays a highly unusual domain architecture, that combines two functionally essential C2H2 zinc-finger domains, which are probably involved in transcriptional regulation, with a formin homology 2 (FH2) domain, normally found only in cytosolic regulators of the actin cytoskeleton. We demonstrate that the FH2 domain of FOZI-1 has lost its actin polymerization function but maintains its phylogenetically ancient ability to homodimerize. fozi-1 genetically interacts with several transcription factors and micro RNAs in the context of specific regulatory network motifs. These network motifs endow the system with properties that provide insights into how cells adopt their stable terminally differentiated states.
This article has been cited by other articles:
|
|
|
|
 
S. J. Copeland, B. J. Green, S. Burchat, G. A. Papalia, D. Banner, and J. W. Copeland
The Diaphanous Inhibitory Domain/Diaphanous Autoregulatory Domain Interaction Is Able to Mediate Heterodimerization between mDia1 and mDia2
J. Biol. Chem.,
October 12, 2007;
282(41):
30120 - 30130.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Sarin, M. M. O'Meara, E. B. Flowers, C. Antonio, R. J. Poole, D. Didiano, R. J. Johnston Jr., S. Chang, S. Narula, and O. Hobert
Genetic Screens for Caenorhabditis elegans Mutants Defective in Left/Right Asymmetric Neuronal Fate Specification
Genetics,
August 1, 2007;
176(4):
2109 - 2130.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. F. Etchberger, A. Lorch, M. C. Sleumer, R. Zapf, S. J. Jones, M. A. Marra, R. A. Holt, D. G. Moerman, and O. Hobert
The molecular signature and cis-regulatory architecture of a C. elegans gustatory neuron
Genes & Dev.,
July 1, 2007;
21(13):
1653 - 1674.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. Vermeirssen, M. I. Barrasa, C. A. Hidalgo, J. A. B. Babon, R. Sequerra, L. Doucette-Stamm, A.-L. Barabasi, and A. J.M. Walhout
Transcription factor modularity in a gene-centered C. elegans core neuronal protein-DNA interaction network
Genome Res.,
July 1, 2007;
17(7):
1061 - 1071.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. M. Amin, K. Hu, D. Pruyne, D. Terzic, A. Bretscher, and J. Liu
A Zn-finger/FH2-domain containing protein, FOZI-1, acts redundantly with CeMyoD to specify striated body wall muscle fates in the Caenorhabditis elegans postembryonic mesoderm
Development,
January 1, 2007;
134(1):
19 - 29.
[Abstract]
[Full Text]
[PDF]
|
|
|
© The Company of Biologists Ltd 2006
