Worm Breeder's Gazette 13(2): 94 (February 1, 1994)
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.
At the worm meeting, the sequencing consortium reported some sequence homologies found in a YAC that was partially sequenced. One of these was to the homeobox of the Drosophila even-skipped (eve) gene. In Drosophila, eve is expressed in the embryo in stripes and in the nervous system and is required for segmentation and for the development of certain neurons. eve homologs have been identified in Xenopus, mouse, human, grasshopper, and coral. In Xenopus, mouse and grasshopper, eve is expressed in the posterior of the embryo during gastrulation (and not in stripes) and also in the developing nervous system. Experiments in Xenopus point to a role for eve in axis formation.
To determine whether any known mutations were in this eve homolog, I looked for candidates in the region corresponding to the YAC ( Y52D3 ,just left of tra-1 ).The gene vab-7 was the best candidate because vab-7 ( e1562 )animals have posterior defects and are uncoordinated (suggesting a possible nervous system defect). I sequenced the eve homeobox from vab-7 ( e1562 )and found a mutation that introduces a stop codon near the beginning of the homeobox. Further, a cosmid containing the eve gene rescues vab-7 mutants.
vab-7 RNA is expressed primarily in embryos, L1 'sand L2 's.Because vab-7 mutants have posterior defects, vab-7 RNA may be expressed in the posterior as it is in other organisms; in situs are in progress to test this. I have isolated a vab-7 cDNA from Pete Okkema's embryonic cDNA library and am sequencing it and the genomic region to complete the sequence of the gene.
To analyze the function of vab-7 ,I am first isolating more alleles. The only existing allele of vab-7 is probably not a null mutation (which is surprising given it is a nonsense mutation in the beginning of the homeobox). It is usually homozygous viable, but is sometimes lethal; mutants die with a Nob phenotype similar to that of pal-1 and nob-1 mutants. The phenotype of vab-7 ( e1562 )/ tDf2 is stronger than that of vab-7 ( e1562 )homozygotes, but they often become fertile adults. Therefore, I should be able to isolate null mutations in a noncomplementation screen. So far, I have two probable new alleles which appear to be stronger than e1562 but can be maintained as homozygotes. Because the posterior defects of vab-7 mutants are visible at hatching, vab-7 activity is probably required during embryogenesis, and a null mutant may be embryonic lethal.
In Drosophila, eve helps to regulate the genes in the homeobox clusters, and it responds to both maternal and zygotic products. In C. elegans, vab-7 may also be part of the connection between maternal products and the HOM-C genes. As a first test of this, I plan to examine the expression of lin-39 , mab-5 ,and egl-5 in vab-7 mutants.