Contents - Faperta

Development of Resistance to Transgenic Plants 371
broad-spectrum insecticides, which will lead to serious environmental hazards associated
with the use of synthetic insecticides. The potential for development of resistance to Bt
proteins is not only of concern to farmers, but to scientists, extension agencies, and the
transgenic plant industry. The investments made in the past would be turned useless
unless this issue is addressed on an urgent basis. Most of the transgenic plants produced
so far have Bt genes under the control of caulifl ower mosaic virus (CaMV35S) constitutive
promoter, and this system may lead to development of resistance in the target and nontarget
insect species as the toxins are expressed in all parts of the plant (Harris, 1991). Toxin
production also decreases over the crop-growing season, which may lead to development
of resistance to the toxin used because of sublethal concentrations, and to other related Bt
toxins to which the insect populations may initially be quite sensitive. Low doses of the
toxins eliminate the most sensitive individuals of a population, leaving a population in
which resistance can develop much faster. Since most Bt toxins have a similar mode of action,
resistance developed against one toxin may also lead to development of cross-resistance to
other toxins. Therefore, there is a need to take a critical look at the potential for development
of resistance to Bt transgenic crops and develop strategies to deploy different Bt toxins
alone or in combination with other novel genes and plant traits associated with resistance
to insect pests in different crops.
Factors Influencing Insect Susceptibility to Bt Toxins
Variation in Insect Populations for Susceptibility to Bt Toxins
Considerable variation has been observed in the toxicity of Dipel ® and purifi ed Cry1Ac
protein in 15 geographically diverse populations of H. zea and H. virescens collected from
several locations in the United States (Stone and Sims, 1993). The variability in susceptibility
of different populations of H. zea (16- to 52-fold) and H. virescens (17- to 71-fold) to
B. thuringiensis formulations such as Javelin WG ® , Dipel ES ® , and Condor OF ® was in contrast
to Cry1A toxins. The LC 50 ranges of Bt formulations and Cry toxins for fi eld-collected
populations were similar to those for laboratory colonies of H. virescens, but differed widely
for H. zea (Luttrell, Wan, and Knighten, 1999).
Wide variation in susceptibility of H. armigera populations collected from different
locations in India was fi rst reported by Gujar et al. (2000) by using discriminating concentrations
of B. thuringiensis var. kurstaki HD-1 strain (0.54 μg endotoxin g 1 diet) and HD-73
(1.4 μg endotoxin g 1 diet) (Figure 12.1). Chandrashekar et al. (2005) described a 16-fold
variation in susceptibility of neonates of H. armigera (LC 50 0.023 μg to 0.372 μg 1 mL). Studies
on susceptibility of H. armigera populations to Bt toxins from different parts of India indicated
that Cry1Ac was most toxic, followed by Cry1Aa, and Cry1Ab (Kranthi, Kranthi, and
Wanjari, 2001). The LC 50 values ranged from 0.07 to 0.99 μg mL 1 (14-fold) for Cry1Aa, 0.69
to 9.94 μg mL 1 (14-fold) for Cry1Ab, and 0.01 to 0.67 μg mL 1 (67-fold) of diet for Cry1Ac.
Across locations, the LC 50 values were 0.62 μg mL 1 for Cry1Aa, 4.43 μg mL 1 for Cry1Ab,
and 0.100 μg mL 1 of diet for Cry1Ac, which can be used as baseline susceptibility indices
for resistance monitoring in the future. The LC 99 values derived from cumulative data
were 515 μg mL 1 for Cry1Aa, 13,385 μg mL 1 for Cry1Ab, and 75 μg mL 1 of diet for Cry1Ac,
and these values represent the diagnostic doses for monitoring of resistance in H. armigera
to Bt toxins. The range of LC 50 values for Cry1Ac in H. armigera populations in Pakistan