Susceptibility of heterochromatin to aphidicolin-induced chromosomal breakage.
The distribution of aphidicolin-induced chromosomal lesions was analyzed to determine the relative breakage susceptibility of euchromatin and heterochromatin in the cactus mouse, Peromyscus eremicus. The observed breakage was tested against expected distributions corresponding to the karyotypic proportions of autosomal euchromatin, autosomal heterochromatin, X-chromosomal euchromatin, and X-chromosomal heterochromatin. The distribution of induced breakage was independent of sex but dependent on the individual. In all individuals, there was a highly significant (P < < 0.0001) deficiency in the number of breaks observed as compared to expected in autosomal heterochromatin. Sparse observations in the X chromosome and the absence of breaks in the Y chromosome precluded valid statistical tests of the sex-chromosomal distribution of induced breakage. These data indicate that the autosomal heterochromatin of Peromyscus is resistant to aphidicolin-induced chromosomal breakage and argue against a simple relationship between late replication and a general mechanism for chromosomal fragility.
Dominguez
A M
AM
Department of Biology, Texas A & M University, College Station 77843, USA.
Smith
S A
SA
Greenbaum
I F
IF
D000818:Animals; D016590:Aphidicolin / Q000633:toxicity*; D002869:Chromosome Aberrations; D005260:Female; D006570:Heterochromatin / Q000235:genetics*; D007621:Karyotyping; D008214:Lymphocytes / Q000187:drug effects / Q000648:ultrastructure; D008297:Male; D051379:Mice
D006570:Heterochromatin; D016590:Aphidicolin