Resistance disruptive selection

Resistance towards azoles has been observed in the field particularly in the case of powdery mildews. Field monitoring has shown that the development of resistance proceeds by directional rather than disruptive selection. 

Transposon integration mutagenesis can be used to allow the selection of metalloid-resistant mutants with enhanced MICs.147 Ledgham et al.148 found a transposon-disrupted gene in a mutant - with a three-fold increase in Se-resistance - that encoded a protein from a member of the DedA family of membrane proteins that was implicated in the uptake of selenite through cell membranes. This is a reasonable hypothesis for how metalloid resistance occurs in some microorganisms. 

Following initial receptor-mediated binding, toxin molecules insert into the apical membrane of columnar epidielial cells, and become resistant to proteases and monoclonal antibodies [91]. Toxin insertion subsequently induces formation of a nonspecific pore in the target membrane. Voltage-clamping studies of lipid bilayers [92 and the midgut sections [93,94 support the Actional role of toxin in pore formation. The size and selectivity of the formed pore varies with toxins and insect species, but the nature of these pores is still controversial. Alternatively, it is described as a non-specific pore that has no ion selectivity or as an ion-specific chaimel that disrupts the membrane potential [5]. 

In H. virescens, loss of expression of a cadherin-like protein was found to be associated with CiylA toxin resistance and consequently this protein plays a crucial role in B. thuringiensis toxicity in vivo [149]. In the laboratory-selected resistant H. virescens strain YHD2, a retrotransposon insertion in the cadherin gene was linked to high levels of CtylAc resistance. More recently, disruption of a cadherin gene may also be linked to the development of field resistance to CiylA toxins in the pink boUworm, Pectinophora gossypiella [150]. 

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