Worm Breeder's Gazette 14(5): 52 (February 1, 1997)
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.
Department of Biology, University of Houston, Houston, Texas, 77204-5513
In Drosophila, short term and chronic exposure of young females
to ethanol causes an approximately 10 fold rise in chromosome
nondisjunction (Rey et al., 1992). However, the question remains as to
whether this effect is caused by ethanol or its primary metabolite,
acetaldehyde (Rey et al., 1994). Caenorhabditis elegans provides a good
model for studying this effect because X chromosome nondisjunction can
be easily monitored by determination of the number of male progeny
produced following acute chemical exposure. Ethanol, in optimal
experimental conditions of 30 minute exposures of mid to late L4s to 7%
ethanol in M9 salts, caused a greater than 10 fold increase in the
production of male progeny (13.2 males/1000 worms compared to 1.03
males/1000 worms for M9 alone with approximately 10,000 F1 progeny
counted for each class). Concentrations as low as 5% generated a five
fold increase in nondisjunction than controls while 10% and 12.5%
ethanol concentrations also resulted in a 10 fold increase in
nondisjunction. Higher concentrations of ethanol proved too toxic as
noted by egg laying defects and reduced brood sizes.
Synchronous populations of N2 worms grown at 20 degrees were
tested at different developmental stages (according to age and criteria
described by Kimble and White, 1981) to determine the most sensitive
stage to 30 minute exposures of 10% ethanol in M9 salts. When L1s, L2s
and L3s were exposed to ethanol, only the normal background numbers of
males were observed. Early L4s treated with ethanol showed a slight
rise in number of males while mid to late L4s treated with ethanol
produced significantly more males than the controls. However, young
adults as well as older adults showed no increase in the number of male
progeny when treated with ethanol. The stage most sensitive to
short-term ethanol exposure correlates with the time when the majority
of sperm are produced. This suggests that ethanol induces meiotic
nondisjunction during spermatogenesis.
Surprisingly, acute exposures of mid to late L4s to acetaldehyde
concentrations ranging from 0.1% to 1.0% did not produce a higher rate
of chromosome nondisjunction compared with M9 controls, approximately
12,600 F1 progeny of 0.1% acetaldehyde treated L4s were counted
producing 1.11 males/1000 worms. Hermaphrodites treated with 0.5%
acetaldehyde had similar numbers of male progeny while 1.0% treated
hermaphrodites had such small brood sizes that no male progeny were
observed. This study suggests that ethanol in Caenorhabditis elegans
causes chromosome nondisjunction rather than its primary metabolite,
acetaldehyde.
Kimble, J.E. and White, J.G. (1981). On the Control of Germ Cell
Development in Caenorhabditis elegans. Dev. Bio. 81, 208-219.
Rey, M., Palermo, A.M. and Munoz, E.R. (1992). Nondisjunction induced by
ethanol in Drosophila melanogaster females. Mutation Research. 268,
95-104.
Rey, M., Palermo, A.M. and Munoz, E.R. (1994). Lack of effect of acute
acetaldehyde treatment on X chromosome segregation in Drosophila
melanogaster females. Mutation Research. 320, 1-7.