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.

MAT Mutants: Metaphase-Anaphase Transition Defective

P. Sadler1, L. Wille2, T. Young2, G. Holt2, N. Johnson2, D. Letts2, I. Kaattari2, J. Thomas2, D. Shakes2

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
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