Worm Breeder's Gazette 14(2): 85 (February 1, 1996)

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.


Regine Roubin1, Danielle Thierry-Mieg2, Daniel Birnbaum1

1 Inserm U119, 27 boulevard Lei Roure, 13009 Marseille, France
2 CRBM.CNRS, BP 5051, 34033 Montpellier, France

A putative gene coding for a heparin-binding growth factor protein and 
presenting 30 % similarity with the Fibroblast Growth Factor 5 (FGF5) has 
been identified on chromosome III of C.elegans (Wilson, R et al, Nature, 
1994, 368, 32-38, and Du, Z, unpublished data). The genomic clone CO5D11 
carries a complete copy of the gene but no cDNA has yet been identified.
In mammals, FGFs are important for embryonic development and have been 
implicated in some pathologies. Recently, Stern's group has shown that
egl-15 encodes a member of the FGF receptor family in C.elegans (DeVore,
D. l. et al, Cell, 1995, 83, 611-620). In both C.elegans and
D.melanogaster, FGF receptors are involved in cell migration.

A phylogenic study on the FGFs has been conducted in the Marseille 
laboratory (Coulier et al, submitted). It indicates that, in vertebrates,
the 10 presently identified members of the FGF family share around 30 %
sequence identity. The C.elegans FGF also presents 30 % identity with each
of the described FGFs. It was tempting to study the function of FGF in the
nematode in which only one gene may exist.

A 320 bp PCR fragment derived from the published sequence was used to 
probe a Southern blot of genomic DNA from the N2 wild type strain. A
single band was detected using standard conditions of stringency. Northern
blot analysis revealed a messenger of low abundancy at approximately 1.7
kb, predominantly expressed at the L2 and L3 larval stages. It is
transpliced to SL1. Using lacZ and GFP fusion genes, (thanks to Andy Fire
and co), we will examine the spatio-temporal expression of the FGF gene.
We also subcloned the gene and we wish to study the function of FGF in the
worm by trying to rescue candidate mutants mapping in the area (thanks to
D.Baillie's lab for many deficiencies and mutants), an alternative
approach will be to look for gain of function phenotypes, obtained for
instance by overly or ectopically expressing the FGF. 

The determination of FGF function will allow a better understanding of 
the cell interactions occuring during nematode development which, as 
compared to vertebrates, are accomplished by a limited number of growth