title: Genetic decay of balancer chromosomes in Drosophila melanogaster.
abstract: Theoretical considerations predict that balancer chromosomes in Drosophila melanogaster should accumulate numerous deleterious mutations with time. We counted the number of recessive lethal mutations on two balancer chromosomes from the In(2LR)SM1/In(2LR)Pm strain maintained in our lab, after making the balancers heterozygous with deficiencies from second-chromosome Kyoto Deficiency kit strains. We detected 10 recessive lethal mutations in the balancer In(2LR)Pm, which is consistent with the mutation rate estimated previously. However, we detected only three mutations, a significantly smaller number, in the balancer In(2LR)SM1, although this may be an artifact. In conclusion, we observed genetic decay over an estimable timescale by using balancers with historical records. Thus, balancers of any strain may have accumulated many unidentified recessive lethal mutations.
authors: Graduate School of Life and Environmental Sciences; University of Tsukuba; Tsukuba, Japan.
authors: Quenta
authors: Q
authors: Araye
authors: Kyoichi
authors: K
authors: Sawamura
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D059006:Chromosomes, Insect; D004331:Drosophila melanogaster / Q000235:genetics*; D005260:Female; D005804:Genes, Lethal; D005808:Genes, Recessive; D008297:Male; D009154:Mutation
keywords: Drosophila melanogaster; balancer chromosomes; inversion; mutation rate; recessive lethal; recombination
references: Genetics. 1974 Feb;76(2):339-66
references: 4207116
references: Genetics. 1972 Oct;72(2):335-55
references: 4630587
references: Genetics. 1964 Jul;50:1-19
references: 14191352
references: Genetics. 1923 May;8(3):276-300
references: 17246014
references: Mutat Res. 1964 May;106:2-9
references: 14195748
references: Genetics. 1918 Sep;3(5):422-99
references: 17245914
references: Genetics. 1920 Jan;5(1):1-59
references: 17245940
references: Philos Trans R Soc Lond B Biol Sci. 2000 Nov 29;355(1403):1563-72
references: 11127901
references: Genetics. 1968 Oct;60(2):389-93
references: 5729601