Worm Breeder's Gazette 15(4): 44 (October 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||Dept. of Biology & Biochemistry, Univ. of Houston, TX, Dept. of Biology, College of William & Mary, VA|
|2||Dept. of Biology, College of William & Mary, VA|
Early descriptions of two C. elegans mutants, emb-27(g48ts) and emb-30(g53ts) indicated that the mutant oocytes fail to produce meiotic polar bodies and subsequently arrest at the one cell stage (1,2,3) . Later, R.Cassada and B.Fiebich reported that sperm produced by these mutants failed to support embryogenesis and arrested prior to morphogenesis (4). In an effort to better understand the nature of a gene product which if mutated gives rise to both maternal and paternal effect lethality, we pursued the phenotypic analysis of this unique class of C. elegans mutants. Early cytogenetic analysis in our lab of emb-27(g48ts) and emb-30(g53ts) demonstrated that this class of mutants share virtually identical mutant phenotypes and both play essential roles in chromosome segregation in the germline and soma of the worm. Based on a preliminary report that emb-30 encoded a novel tubulin protein (S.Siddiqui, personal communication), we initially proposed that failure to segregate chromosomes in both oocyte and sperm meiosis and germline mitosis resulted from abnormalities in microtubule spindle formation and/or organization. However, our analysis of metaphase spindles in both mutants has failed to detect any morphological abnormalities. Both chromosome condensation during prophase and chromosome-microtubule attachment during metaphase appear to be normal. In fact, the only obvious defect is a prolonged delay of chromosomes in a metaphase-like state. Thus at present, the absence of obvious spindle defects coupled with the delay in progression to anaphase indicate to us that emb-27 and emb-30 may represent an important class of C.elegans mutants that are metaphase-anaphase transition defective (MAT). We are currently considering the following two models to explain the MAT phenotype. Model 1: EMB-27 and EMB-30 are required either directly or indirectly to drive the cell through metaphase and into anaphase. Model 2: EMB-27 and EMB-30 may not actually function in the metaphase-anaphase transition, but secondary ramifications of the mutant defects (e.g. important post-translation processing of a protein required for metaphase-anaphase transition) triggers a metaphase checkpoint. Our lab is taking both a genetic and a reverse genetic approach to test our models and better understand the molecular nature of emb-27 and emb-27 related genes. David Greenstein's lab has also reported metaphase-anaphase defects in emb-30 mutants and has been very successful with similar strategies in their analysis (5,6). 1.Cassada et al. (1981) Dev Biol 84:193-205 2.Isnenghi et al. (1983) Dev Biol 98:465-480 3.Denich et al. (1984) Wilhelm Roux's Arch Dev Biol 93:164-179 4.Fiebich, B. (1989) Diplom-Thesis, Univ. of Freiberg 5.Furuta et al. (1997) International Worm Meeting Abstract 172 6.Furuta et al. (1998) Midwest Worm Meeting Abstract 17