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The Journal of Heredity 1982:73(1):59-63
© 1982 The American Genetic Association 73:59-63

research-article

Genetic analysis of abnormal male sexual development in Aedes aegypti and Ae. mascarensis backcross progeny

Larry R. Hilburn, and Karamjit S. Rai

Research Laboratory. USDA, SEA-AR P.O. Box 14565, Gainesville FL 3260 and the Department of Biology, University of Notre Dame Notre Dame, IN 46556

Abstract

When male hybrids of Aedes aegypti females and A. mascarensis males were backcrossed to A. aegypti females, 32.8 percent of the male progeny exhibited abnormal sexual development, including failure of the terminalia to rotate, a split sternite of the eighth abdominal segment with partially duplicated telomeres, or feminization that gives rise to sterile intersexes. Observations made on three morphological marker loci and five isozyme loci with characteristic electromorphs in the two parental species suggested that when the sex-determining M locus is derived from A. mascarensis and the chromosome regions including s, LDH, and IDH2 on chromosome 2 and bit and 6PGD on chromosome 3 are homozygous for genes from A. aegypti, the frequency of abnormal sexual development is increased. An even greater percentage of males suffer aberrant development if recombination also occurs between the M and re locus of chromosome 1. The data suggest that genes on chromosome 2 control normal development of the male terminalia, genes on chromosome 3 control sexual differentiation, and the entire process is controlled by genes on chromosome 1 that are linked to, but not identical with, the M locus.


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