The detection of plasticity genes in heterogeneous environments

The molecular genetic mechanisms for phenotypic plasticity across heterogeneous macro- and microenvironments were examined using the Populus genomic map constructed by DNA-based markers. Three hypotheses have been suggested to explain genetic variation in phenotypic response to varying environments (i.e., reaction norm): Lerner's homeostasis, allelic sensitivity, and gene regulation. The homeostasis hypothesis, which predicts that heterozygotes are less sensitive to the environment than homozygotes, was supported for phenotypic plasticity to unpredictable environments (microenvironmental plasticity) at the whole-genome level, but for phenotypic plasticity to predictable environments (macroenvironmental plasticity) the hypothesis was supported only at functioning quantitative trait loci (QTLs). For all growth traits studied, gene regulation was suggested to play a prevailing role in determining the norms of reaction to environments. Indirect evidence for gene regulation is that there tend to be more QTLs with larger effects on the phenotype in optimal growing conditions than suboptimal growing conditions because the expression of these QTLs identified is mediated by regulatory genes. Direct evidence for gene regulation is the identification of some loci that differ from QTLs for trait values within environments and exert an environmentally dependent control over structural gene expression. In this study, fewer environmentally sensitive QTLs were detected that display unparalleled allelic effects across environments. For stem height, there were more regulatory loci and more structural loci (whose expression is determined by gene regulation) affecting phenotypic plasticity than for basal area. It was found that microenvironmental plasticity was likely controlled by different genetic systems than those for macroenvironmental plasticity.