Worm Breeder's Gazette 10(3): 146
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.
Recent work (e.g. Cattanach and Kirk 1985, Nature 315:496) has shown that normal embryonic development in mice (and presumably other mammals) depends on correct chromosomal imprinting during gametogenesis. Thus, for example, a euploid mouse that has received both copies of chromosome 2 from its mother (MM) does not develop normally, nor does the corresponding mouse that has received both copies from its father (PP). Some regions of the mouse genome are indifferent to imprinting, some only require maternal imprinting, and some only require paternal imprinting. It is suspected that methylation of DNA at key sites provides the molecular basis of imprinting. In view of the current interest in this phenomenon, we tested for effects of this type in C. elegans. We did not expect to find any imprinting, because no phenomenon of this type has turned up during other genetic work on C. elegans, and also because there is no detectable methylated cytosine in C. elegans DNA. Also, work with nondisjunction mutants had shown that there is no imprinting of the X chromosome: both hermaphrodites and males are perfectly normal if they derive their X chromosome(s) only via oogenesis or only via spermatogenesis (Hodgkin, Horvitz & Brenner 1979). This work also demonstrated (using the generalized nondisjunction mutant, him-6(e1423) ) that at least some of the MM autosomal exceptions could be recovered. Crosses to detect the ten possible autosomal exceptions were carried out, again using him-6 to generate disomic or nullisomic gametes. In all ten crosses, several exceptional animals of the appropriate genotype were recovered and checked by progeny testing. These animals appeared to be as viable as their siblings. We conclude that there are no obvious imprinting effects at the level of individual chromosomes in this species. It remains possible that a wholly matroclinous or wholly patroclinous euploid embryo might develop abnormally. Crosses are listed below. All animals were homozygous for him-6( e1423). Other alleles bli-4(e937), ), 0), 99), 282), 91), 24).[See Figure 1]