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Most of the previous studies are extensively emphasize DNA puffs induced by ecdysone, whereas a few specific DNA puff genes are studied for a better understanding of the mechanisms underlying the ecdysone response on molecular level.
We stress that our results do not depend on whether one believes that multifunctionality is a true property of genes reflected in the patterns of annotation, or some kind of artifact of how genes are studied and annotated.
When genes are studied that result in fitness effects sufficiently large to be easily quantified over short time scales, e.g. one growing season, and in experiments with low numbers of replicates, minor molecular changes resulting from the transformation procedure are unlikely to be influential, if the necessary precautions have been followed with transformation procedure.
These studies have profited enormously from genomics approaches, because only through this whole-genome approach, genes are studied in the genomic context where they evolved.
On such a tree, the small connective threads that depict LGT and discordant individual gene phylogenies can subsequently be strung as individual genes are studied.
This aspect, however, may be worthy of further investigation when clinical outcome data from our series become available and as further genes are studied.
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There is increasing evidence that the genes being studied are disease risk genes, not disease causative genes.
Gene expression of these genes was studied using online data bases including RiceXPro.
The enzymatic activity and expression of the three genes were studied.
Expression changes in major pathogenesis-related genes were studied at different time courses.
Mutations in codon 209 of GNAQ and GNA11 genes were studied by restriction-fragment length polymorphism (RFLP).
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