INHERITANCE OF THE AMPLIFIED ESTERASE GENES RESPONSIBLE FOR INSECTICIDE RESISTANCE IN MYZUS-PERSICAE (HOMOPTERA, APHIDIDAE)

Citation
Rl. Blackman et al., INHERITANCE OF THE AMPLIFIED ESTERASE GENES RESPONSIBLE FOR INSECTICIDE RESISTANCE IN MYZUS-PERSICAE (HOMOPTERA, APHIDIDAE), Heredity, 77, 1996, pp. 154-167
Citations number
16
Categorie Soggetti
Genetics & Heredity
Journal title
ISSN journal
0018067X
Volume
77
Year of publication
1996
Part
2
Pages
154 - 167
Database
ISI
SICI code
0018-067X(1996)77:<154:IOTAEG>2.0.ZU;2-X
Abstract
Insecticide-resistant and susceptible clones of Myzus persicae were in duced to produce sexual morphs and crossed in the laboratory. Progeny clones were analysed for karyotype, esterase (E4, FE4 or S) gene type and activity, and amplified E4 and FE4 genes were located on their chr omosomes by fluorescence in situ hybridization (FISH). Amplified FE4 g enes of resistant parent clones (800F and French R) were inherited acc ording to expectations. Chromosomal locations of these genes (on autos omes 1 and 3 in 800F, and on 1 and 2 in French R) were confirmed by FI SH analysis of progeny that had inherited an autosome 2 marker (a diss ociation) from the susceptible parent (DS). Inheritance of amplified E 4 genes could not be studied directly as none of the available clones was able to produce mating females. Males from two clones with amplifi ed E4 genes (and with the A1,3 translocation that is common to all E4- producing genotypes) were therefore mated with females from clones wit h amplified FE4 genes at known chromosomal locations. Progeny were obt ained with both E4 and FE4 genes, a combination not yet found in natur e. Analysis of F-1 and subsequent generations confirmed that the ampli fied E4 site on autosome 3(T) is close to the translocation breakpoint , and apparently coallelic with the amplified FE4 site on the normal a utosome 3 inherited from 800F. One of the translocated parent clones ( 4156) had two additional E4 sites, unlinked to the translocation, whic h were inherited according to expectation. Esterase activities of prog eny clones, measured by immunoassay, mostly corresponded to the number of amplified sites inherited, with some discrepancies which could be attributed to copy number differences between sites, inheritance of pa rtially methylated genes from French R, or position effect variegation at the site on 3(T). Inheritance of the A1,3 translocation in two cro sses differed markedly from expectation.