A laboratory colony of Glossina morsitans morsitans Westw. which originated from puparia collected near Kariba, Rhodesia was more productive than another colony which originated from Handeni, northern Tanzania; during 1975, the former produced an average of 5 -9 puparia per female and the latter 3 -6. Although mortality in the Tanzanian colony was somewhat higher than in the Rhodesian colony, the main reason for the lower productivity of the Tanzanian colony was the much poorer fecundity of the females. This was associated with abnormalities of the reproductive system. The differences in laboratory performance between the two stocks were probably a reflection of their genetic diversity. Thus the Tanzanian Y chromosome is metacentric compared with the almost acrocentric Y chromosome of Rhodesian males, and some individuals carry small metacentric supernumerary chromosomes which are not present in Rhodesian flies. Giemsa C-banding showed band differences between the chromosome complements of the two stocks. Probably the most important difference, revealed by polytene chromosome analysis, is a large inversion in the X chromosome of Tanzanian flies, which, together with at least one band difference, is fixed in the homozygous condition. The possible evolutionary pathways of these mutations are outlined and their significance is discussed in terms of their distribution in nature and of the performance of the two strains in the laboratory.
An autosomal translocation in the tsetse fly Glossina austeni was studied genetically, cytogenetically and for its effects on viability. Flies homozygotis for the structural change could be identified by outcrossing to wild-type and demonstrating semi-sterility in all the progeny.A cytogenetical analysis of male meioses in samples of pupae which were sibs of the semi-sterile progeny showed them to be structurally heterozygous for the translocation. Matings of the translocation heterozygotes and homozygotes gave the expected progeny ratios, with the exception of a deficit of females classified as translocation homozygotes. This was due to their sterility or inviability. Those female homozygotes which did breed showed a subnormal lifetime pupal production. These deleterious recessive effects were probably due to the translocation itself although the influence of linked loci could not be ruled out. These effects would prevent the mass rearing of this particular translocation for a tesetse control project.Two other stocks which showed semi-sterility were found to carry autosomal translocations and two which currently showed holandric inheritance have F-autosome translocations. One stock with holandric inheritance of extreme sterility carries a double translocation involving two autosomes and the Y chromosome.
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