Genetic mapping of two loci affecting DDT resistance in the malaria vector Anopheles gambiae
Genetic mapping of two loci affecting DDT resistance in the malaria vector Anopheles gambiae
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DOI：
10.1046/j.1365-2583.2000.00214.x
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发表时间：
2000-10-01
影响因子：
2.6
通讯作者：
Collins, FH
中科院分区：
文献类型：
--
作者：
Ranson, H;Jensen, B;Collins, FH
疟疾病媒蚊子对杀虫剂滴滴涕的抗药性严重阻碍了控制这种疾病的努力，并导致近年来疟疾病例的流行率上升。每年3亿至5亿疟疾病例中有90%以上发生在非洲，那里的主要病媒是冈比亚按蚊。ZAN/U株的DDT抗性。冈比亚与杀虫剂代谢增加有关，由谷胱甘肽S-转移酶（GST）家族成员催化，但这种代谢抗性的分子机制尚不清楚。遗传杂交表明，抗性是常染色体和半显性的。我们已经使用微卫星标记，以确定两个数量性状基因座（QTL），这两个基因座共同解释了超过50%的变异，在DDT的敏感性在ZAN/U株的安。冈比亚。第一个基因座rtd 1位于3号染色体上标记H341和H88之间，具有隐性易感性。第二个位点rtd 2位于2L染色体上，靠近标记H325，具有加性遗传效应。这两个QTL侧翼的标记已被物理定位到An。冈比亚多线染色体。它们与已在该物种中克隆和定位的任何GST基因都不一致。这些QTL的特性将导致更清楚地了解代谢抗性滴滴涕的机制。
Resistance to the insecticide DDT in the mosquito vectors of malaria has severely hampered efforts to control this disease and has contributed to the increase in prevalence of malaria cases seen in recent years. Over 90% of the 300-500 million annual cases of malaria occur in Africa, where the major vector is Anopheles gambiae. DDT resistance in the ZAN/U strain of An. gambiae is associated with an increased metabolism of the insecticide, catalysed by members of the glutathione S-transferase (GST) enzyme family, but the molecular mechanism underlying this metabolic resistance is not known. Genetic crosses show that resistance is autosomal and semidominant. We have used microsatellite markers to identify two quantitative trait loci (QTL), which together explain over 50% of the variance in susceptibility to DDT in the ZAN/U strain of An. gambiae. The first locus, rtd1, is on chromosome 3 between markers H341 and H88 and has a recessive effect with respect to susceptibility. The second locus, rtd2 is on chromosome 2L, close to marker H325 and has an additive genetic effect. The markers flanking these two QTL have been physically mapped to An. gambiae polytene chromosomes. They do not coincide with any of the GST genes that have been cloned and mapped in this species. Characterization of these QTL will lead to a clearer understanding of the mechanisms of metabolic resistance to DDT.