Linkage of a gene causing malaria refractoriness to Diphenol oxidase-A2 on chromosome 3 of Anopheles gambiae
| Autor: | R K Sakai, W C Black th, R W Gwadz, P Romans |
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| Rok vydání: | 1999 |
| Předmět: |
Male
Heterozygote Genotype Genetic Linkage Anopheles gambiae Population Locus (genetics) Restriction fragment Random Allocation Genetic linkage Virology Anopheles parasitic diseases Animals Allele education Gene Alleles Crosses Genetic Genetics education.field_of_study biology Homozygote biology.organism_classification Macaca mulatta Insect Vectors Malaria Infectious Diseases Multigene Family biology.protein Female Parasitology Catechol Oxidase Plasmodium cynomolgi |
| Zdroj: | The American Journal of Tropical Medicine and Hygiene. 60:22-29 |
| ISSN: | 1476-1645 0002-9637 |
| DOI: | 10.4269/ajtmh.1999.60.22 |
| Popis: | An inbred line of the African malaria vector Anopheles gambiae is refractory to development of malaria parasites. It is homozygous for a 4.3-kb Sal I restriction fragment at the Dox-A2 locus, whereas the parent population is polymorphic at this locus, and a susceptible line is homozygous for an alternate 3.85-kb fragment. The Dox-A2 locus is located in the middle of chromosome 3R, in division 33B, and is tightly linked to a cluster of genes including Dopa decarboxylase that are involved in the production of melanin. Because the refractoriness phenotype, melanotic encapsulation of ookinete/oocysts, might involve activation of or alteration in one or more of these genes, we performed genetic crosses to determine whether a previously identified Plasmodium cynomolgi Ceylon refractoriness gene, Pif-C, is linked to Dox-A2. Backcross mosquitoes fed on one infected monkey developed infections ofor = 100 oocysts. About 50% of these mosquitoes appeared phenotypically refractory, as expected for the backcross performed, but gave slight evidence of linkage between a refractoriness gene and Dox-A2. In contrast, females fed on a monkey that yielded higher infection levels, up to300 oocysts, showed clear evidence of linkage between a refractoriness gene and Dox-A2. We conclude that this Dox-A2-linked refractoriness gene is expressed under conditions particular to the higher infection levels, or that environmental factors obscured the genetic effect of this gene at lower infection levels. |
| Databáze: | OpenAIRE |
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