Genes expressing toxins, development

The third set of variables lies in the postnatal environment. These include the physical environment (outdoors and in) and the social environment (family, peers, neighborhood, socioeconomic status, education, culture, and so on). Many of these variables affect the development of emotions, learning, language skills, and the processing of information by the brain—and can also affect gene expression via stress, infection, malnutrition, and toxins in air (for example, lead), water (for example, arsenic), and food (for example, mercury). Those effects that occur during early development can be extremely critical. 

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]. 

A better approach would be to actually ignore the specifics of host range determination and instead develop a method that allows an end-run around viral-host interaction deficiencies and permits the virus to (if perhaps not carry out a full replication cycle) act as an expression vector and deliver to the host a toxin gene that will be expressed and dispatch the pest. The idea here is that the correct promoter driving the expression of a toxin gene during a weak or inapparent infection or perhaps no replication at all would nonetheless allow sufficient expression of the gene to achieve the desired result. 

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