Contents - Faperta

Development of Resistance to Transgenic Plants 377
showed low levels of resistance to Cry1Ab and Cry1Da, but no resistance to Cry1Fa (Muller-
Cohn et al., 1996).
A colony of Leptinotarsa decemlineata (Say) from fi elds sprayed with Bt formulation
containing Cry3Aa, and selection for resistance to this toxin for 29 generations resulted in
293-fold resistance (Whalon et al., 1993; Rahardja and Whalon, 1995). However, foliage
from transgenic potato lines expressing cry3Aa inhibited feeding by the grubs (Altre,
Grafi us, and Whalon, 1996). High levels of resistance have also been observed in C. scripta
under selection pressure (Ballester et al., 1999). The selected strain displayed resistance to
Cry1Ba, but not to Cyt1Aa (Federici and Bauer, 1998).
Development of Resistance under Field Conditions
The ability of insects to overcome plant resistance is always a grave risk, and ways to delay
the onset of resistance in insect populations will be an ongoing debate as transgenic crops
are deployed for cultivation on a large scale. Extensive and intensive exposure of insect
pests to Bt toxins through transgenic crop plants or other tactics may lead to development
of resistance to Bt. Development of resistance to Bt under fi eld conditions may not be a
serious issue since the Bt and the insect pests have co-evolved for millions of years under
natural conditions (Bauer, 1995; Tabashnik, 1994). Because of limited exposure and several
toxins produced by Bt, the rate of development of resistance under natural conditions may
not be high. In transgenic plants, the insects are continuously exposed to the exotic genes,
and there are possibilities of resistance development in the target insects.
Soybean looper, T. ni, collected from soybean and Bt cotton has been found to be less
susceptible to Bt formulation, Condor XL in dosage-mortality and discriminating dosage
bioassays than the reference strain (Mascarenhas et al., 1998). In some insect species, the
probability of development of resistance may be very low, for example, O. nubilalis has
been observed to develop tolerance to low levels of Cry1Ab in the artifi cial diet, but it has
not been possible to initiate or sustain the insect colonies at concentrations in the diet
closer to the actual levels expressed in the transgenic maize plants (Lang et al., 1996).
Kranthi and Kranthi (2004) estimated that when 40% of the total area under cotton in
India would be covered with Bt cotton, it would take 11 years for resistance gene frequency
to reach 0.5 in H. armigera populations if no pest control measures are adopted. If control
operations cause 90% mortality, then it would take 45 years for resistance allele frequency
to reach 0.5. Using a single locus simulation model involving ecological, biological, and
operational factors, Zhao et al. (2000b) showed that resistance allele frequency of H. armigera
to Cry1A toxin will increase from 0.001 to 0.5 after 38 generations (nine years) in a typical
cropping system in China, where corn fi elds act as a natural refuge for Bt cotton. If the whole
area in a region is cropped with Bt cotton, the expected time for fi eld failure of Bt cotton will
be only 26 generations (seven years). Similar views have been expressed for development of
resistance to H. zea, which is less susceptible to Bt cotton (Han and Caprio, 2002). Baseline
susceptibility studies and the ability of H. armigera to develop resistance to Bt have to some
extent justifi ed the fears of likelihood of development of resistance under fi eld conditions.
Mechanisms of Resistance
Ferre and Van Rie (2002) reviewed the current knowledge on the biochemical mechanisms
and genetics of resistance to Bt products and insecticidal crystal proteins. Monitoring the