Wu Rongling
Division of Ecosystem Sciences and Conservation, University of Washington, Seattle, Washington, 98195.
Evolution. 1998 Aug;52(4):967-977. doi: 10.1111/j.1558-5646.1998.tb01826.x.
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.
利用基于DNA标记构建的杨树基因组图谱，研究了在异质宏观和微观环境中表型可塑性的分子遗传机制。已提出三种假说来解释对不同环境的表型反应中的遗传变异（即反应规范）：勒纳的稳态、等位基因敏感性和基因调控。稳态假说预测杂合子比纯合子对环境的敏感性更低，在全基因组水平上，该假说得到了对不可预测环境（微环境可塑性）的表型可塑性的支持，但对于对可预测环境（宏观环境可塑性）的表型可塑性，该假说仅在功能性数量性状位点（QTL）上得到支持。对于所有研究的生长性状，基因调控在决定对环境的反应规范中起主要作用。基因调控的间接证据是，在最佳生长条件下，往往比次优生长条件下有更多对表型影响更大的QTL，因为这些已鉴定的QTL的表达是由调控基因介导的。基因调控的直接证据是鉴定出一些位点，这些位点在环境中与性状值的QTL不同，并对结构基因表达施加环境依赖性控制。在这项研究中，检测到的环境敏感QTL较少，这些QTL在不同环境中表现出无与伦比的等位基因效应。对于茎高，影响表型可塑性的调控位点和结构位点（其表达由基因调控决定）比基部面积更多。研究发现，微环境可塑性可能由与宏观环境可塑性不同的遗传系统控制。
