Worm Breeder's Gazette 15(3): 17 (June 1, 1998)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
1 | CIML, Luminy Case 906, 13288 Marseille Cedex 9, France |
2 | IBDM, Luminy Case 907, 13288 Marseille Cedex 9, France |
We are studying a C. elegans homologue of a couple of vertebrate neuron-specific transcription factors, to explore phylogenetic aspects of neuronal identity and of its transcriptional determination. Phox2a and Phox2b are two closely related homeodomain proteins of the paired-like family specifically expressed (mostly co-expressed) in specific classes of neurons in vertebrates (1,2). Careful analysis of their expression pattern has revealed a striking coherence which can be summarized by three overlapping neuroanatomical correlates: i) all noradrenergic neurons, ii) most central and peripheral neurons involved in the reflex circuits of the visceral nervous system, iii) cranial motoneurons. Published work and ongoing studies aim at reconstructing the transcriptional cascades in which Phox2a and Phox2b act and at defining which part of specific neuronal phenotypes they control (3,4). The sequencing of the C. elegans genome has unveiled a probable orthologue of Phox2a and b, D1007.1, which we call for the moment cePhox2. It is 88% identical to murine Phox2a in the homeodomain, a level of homology often associated with functional conservation among homeobox genes between vertebrates and invertebrates. We have cloned the cDNA by RT-PCR, thereby verifying the GeneFinder prediction. We have created transgenic lines harboring GFP under the control of the 1 kb upstream of CePhox2. The transgene is first expressed in early embryos. Expression continues at larval and adult stages in a few head and tail neurons, and, presumably ectopically, in the rostral and caudal part of the intestine. An antibody raised against the C-terminus of CePhox2 has confirmed its neuronal expression. Our current aim is to identify each Phox2 expressing neuron. We then plan to perform loss-of-fuction and gain-of-function studies. Our long-term hope, with the parallel mouse and worm studies, is to define what has changed and what has not throughout evolution in the "neuro-ontogenetic module" involving Phox2. Thanks to: Alan Coulson, Andy Fire and Theresa Stiernagle. (1) Tiveron et al. (1996) J. Neurosci., 16, 7649-7660. (2) Pattyn et al. (1997) Development, 124, 4065-4075. (3) Morin et al. (1997) Neuron, 18, 411-423. (4) Hirsch et al. (1998) Development, 125, 599-608.