Nrf2/Maf-binding-site-containing functional Cyp6a2 allele is associated with DDT resistance in Drosophila melanogaster
In: Pest management science, Jg. 70 (2014), Heft 7, S. 1048-1058
Online
academicJournal
- print, 56 ref
Zugriff:
BACKGROUND: Increased insecticide detoxification mediated by cytochrome P450s is a common mechanism of insecticide resistance. Although Cyp6a2 has been observed to be overexpressed in many 4,4'-dichlorodiphenyltrichloroethane (DDT)-resistant strains of Drosophila melanogaster, how Cyp6a2 is regulated and whether its overproduction confers DDT resistance remain elusive. RESULTS: Molecular analysis identified five Cyp6a2 alleles (Cyp6a2Canton-S-1, Cyp6a2Canton-S-2, Cyp6a291-c, Cyp6a291-R and Cyp6a2Wisconsin-WD) from four D. melanogaster strains, notably differing in the presence or absence of an intact Nrf2/Maf (a transcription factor) binding site in the 5'-promoter core region, a 'G1410' frameshift deletion mutation in the heme-binding region and a long terminal repeat (LTR) of transposable element 17.6 in the 3'-untranslated region (UTR). Linkage analysis confirmed that DDT resistance was genetically linked to a Nrf2/Maf-binding-site-containing, LTR-lacking functional allele of Cyp6a2 (Cyp6a291-R). The qRT-PCR results showed that overexpression of functional Cyp6a2 was consistently associated with DDT resistance. Luciferase reporter gene assays revealed that an intact Nrf2/Maf binding site in the 5'-promoter core region enhanced the constitutive transcription of Cyp6a2. CONCLUSION: The results suggest that the Nrf2/Maf binding-site-containing functional Cyp6a2 allele is associated with DDT resistance in the D. melanogaster strains under study.
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Nrf2/Maf-binding-site-containing functional Cyp6a2 allele is associated with DDT resistance in Drosophila melanogaster
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Autor/in / Beteiligte Person: | HUA, WAN ; YAN, LIU ; MEI, LI ; SHUNYI, ZHU ; XIANCHUN, LI ; PITTENDRIGH, Barry R ; XINGHUI, QIU |
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Zeitschrift: | Pest management science, Jg. 70 (2014), Heft 7, S. 1048-1058 |
Veröffentlichung: | Chichester: Wiley, 2014 |
Medientyp: | academicJournal |
Umfang: | print, 56 ref |
ISSN: | 1526-498X (print) |
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