| Abstract: | Cuticle consists of chitin microfibrils embedded in a matrix composed largely of hydrated proteins. The effect of diflubenzuron, an inhibitor of chitin synthetase, on the deposition of both these components is reviewed. The polymerisation reaction is but one step in the pathway leading to chitin microfibrils. Possibly interactions to other steps in the pathway serve to enhance the consequences of the inhibition. Such enhancement could help to explain the abrupt changes in the rate of chitin synthesis that can be observed as diflubenzuron is cleared from epidermal cells. Cuticle proteins differ widely in their ability to form a stable layer when chitin is largely absent. In the most stable regions, diflubenzuron has no effect on the amount or nature of the proteins deposited. In contrast, there are many regions where the deposition of solid cuticle is stopped, presumably because the proteins involved cannot form a coherent layer. Intermediate degrees of stability are found. There is an association between the regions of stability and those of high sclerotisation; though sclerotisation often takes place long after deposition. Even when the protein layer is fairly stable it may not be deposited in a regular manner. This statement is illustrated by electron micrographs of cuticle from the hind tibiae of adult locusts. These micrographs also show that diflubenzuron can affect epidermal cells. In normal cells the plaques are in contact with the newly secreted cuticle; they are still present but this contact is not maintained after treatment with diflubenzuron. |
