Contents - Faperta

382 Biotechnological Approaches for Pest Management and Ecological Sustainability
producing the Cry1Ab toxin were detected. Frequency of resistance alleles in France was
9.20 10 4 . In the northern U.S. Corn Belt, the frequency of the resistance allele to Bt
maize was 4.23 10 4 . The results suggested that resistance is probably rare in France
and the U.S. Corn Belt for the high-dose plus refuge strategy to delay development of
resistance to Bt maize.
Inheritance of Resistance
Resistance to Bt products or Cry toxins, in general, behaves as a completely or partially
dominant trait (Liu and Tabashnik, 1997; Tabashnik et al., 1997a, 2000b; Sayyed, Ferre, and
Wright, 2000; Sayyed et al., 2000; Liu et al., 2001). Resistance to Bt products and Cry toxins
at the LC 50 level is partially recessive, but closer to codominance than to being completely
recessive (McGaughey, 1985; McGaughey and Beeman, 1988; Gould et al., 1992, 1995;
Martinez-Ramirez et al., 1995; Chaufaux et al., 1997; Imai and Mori, 1999; Sayyed, Ferre,
and Wright, 2000; Sayyed et al., 2000). High levels of dominance have been observed in O.
nubilalis for Dipel (Huang et al., 1999), L. decemlineata for Cry3Aa (Rahardja and Whalon,
1995), P. xylostella for Cry1Ca (Liu and Tabashnik, 1997), and in H. virescens for Cry1Ab and
Cry2a (Gould et al., 1995). In general, there is a single locus or tightly linked loci associated
with resistance to Bt, and resistance is inherited as an autosomal trait. Lack of binding in
P. xylostella is inherited as an autosomal recessive trait (Martinez-Ramirez et al., 1995).
However, in a few cases, sex had a signifi cant infl uence on the survival of F 1 progeny in
P. xylostella (Martinez-Ramirez et al., 1995; Sayyed et al., 2000) and S. littoralis (Chaufaux
et al., 1997). Studies involving the progeny of crosses and backcrosses between resistant
and susceptible strains showed that resistance was autosomally inherited, incompletely
dominant, and controlled by several genetic factors (Sims and Stone, 1991). Genetic control
of resistance was unstable. An unchallenged line with an initial resistance of 69-fold
declined to 13-fold by generation 5 of nonselection.
Inheritance of resistance to the Bt toxins in transgenic crops is typically recessive,
and DNA-based screening for resistance alleles in heterozygotes is potentially much more
effi cient than detection of resistant homozygotes with bioassays (Morin et al., 2003). Using
a 37-fold resistant strain, Liang et al. (2000) reported that inheritance of resistance to Bt
transgenic cotton in H. armigera was controlled by a single autosomal incomplete recessive
allele. Daly and Olsen (2000) found that resistance in H. armigera was not always recessive,
and was probably functionally dominant under fi eld conditions at certain times. Resistance
in the Bx strains of H. armigera is completely recessive (Akhurst et al., 2003). It seems that
the dominance of resistance depends on the level of selection, as it increased with a
decrease in concentration of Cry1Ac for the pink bollworm (Tabashnik et al., 2000b, 2002a,
2002b). Populations of pink bollworm, P. gossypiella, harbored three mutant alleles of a
cadherin-encoding gene linked with resistance to Bt toxin Cry1Ac and survival on transgenic
Bt cotton. Each of the three resistance alleles has a deletion expected to eliminate at
least eight amino acids upstream of the putative toxin-binding region of the cadherin protein.
Larvae with two resistance alleles in any combination were resistant, while those
with one or no resistance allele were susceptible to Cry1Ac. Together with previous
evidence, the results suggested that cadherin gene is a leading target for DNA-based
screening of resistance to Bt crops in lepidopteran pests.
An autosomal recessive gene conferred extremely high levels of resistance in P. xylostella
to four Bt toxins (Cry1Aa, Cry1Ab, Cry1Ac, and Cry1F) (Tabashnik et al., 1997a). A recessive
autosomal gene confers resistance to at least four Bt toxins in P. xylostella and enables
survival without adverse effects on transgenic plants (Heckel et al., 1999). Allelic variants