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
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.