Control of Phenotypic Plasticity Via Regulatory Genes
Control of Phenotypic Plasticity Via Regulatory Genes
复制标题
通过调控基因控制表型可塑性
DOI：
10.1086/285543
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
M. Pigliucci
中科院分区：
文献类型：
--
作者：
C. Schlichting;M. Pigliucci
表型可塑性的遗传控制形式是什么？是否存在决定可塑性反应的特定基因座（Bradshaw 1965; Schlichting 1986; Scheiner and莱曼1989，1991），或者可塑性仅仅是在不同环境中对不同性状进行选择的附带现象（Via and Lande 1985; Via 19.87）？这个长期争论的中心问题具有根本的重要性，因为可塑性的遗传控制机制将决定反应规范演变的长期动力学、速率和约束。Via（1993）重申了她的观点，即没有必要援引单独的基因座来控制反应规范的形状：表型可塑性本身并不是一种性状，而仅仅是进化的副产品，在许多基因座上产生适当的性状手段，在不同的环境中。在没有提出新的经验证据的情况下，她观察到“目前的模型说明了表型可塑性如何演变......而不需要存在单独的“可塑性基因”“（pp. 352-353）。为了避免语义上的争论，我们将可塑性基因定义为对结构基因表达施加环境依赖性控制从而产生可塑性反应的调控位点。这样的基因座代表了一种遗传机制的塑料反应，这是不同的定量遗传模型中假设的反应规范的演变。我们对Via（1993）的观点有以下不同意见。(1)有大量的证据表明存在上述定义的可塑性基因。(2)适应性可塑性的进化涉及两个过程：（i）调整可用的数量遗传变异以接近表型最佳值;（ii）开发新的遗传机制以控制对环境的反应。(3)目前的统计模型可以解释可塑性的进化的论点避免了这样一个问题，即相似的统计结果可能是通过非常不同的遗传机制产生的。1.可塑性基因的存在。已经提出了表型可塑性的两种类型的遗传控制（Schmalhausen 1949; Smith-Gill 1983; Dragavtsev and Aver'yanova 1984）。(i)等位基因敏感性是指在不同的环境中，所有的基因座都有表达，但单个等位基因的敏感性不同，也就是说，环境对结构基因的表达有直接影响。对于等位基因敏感性，我们预期表型的逐渐变化与环境梯度成正比。(ii)调控是指并非所有基因位点都在每种环境中表达的情况，即基因表达是通过调控位点的作用介导的，这些调控位点可以控制多个结构基因的表达。对于最简单的调节控制来说，不同的表型将在环境阈值的每一侧产生。
What is the form of genetic ontrol of phenotypic plasticity? Are there specific loci determining plastic responses (Bradshaw 1965; Schlichting 1986; Scheiner and Lyman 1989, 1991), or is plasticity simply an epiphenomenon of selection for different trait means in different environments (Via and Lande 1985; Via 19.87)? This central issue in a long-standing dispute is of fundamental importance because the mechanism of genetic control of plasticity will determine the long-term dynamics, rates, and constraints on the evolution of reaction norms. Via (1993) reiterates her view that there is no need to invoke separate loci controlling the shape of reaction norms: phenotypic plasticity is not a trait itself but merely a by-product of evolution at numerous loci to produce appropriate trait means in different environments. Without presenting new empirical evidence, she observes that "current models illustrate how phenotypic plasticity can evolve ... without requiring the existence of separate 'genes for plasticity' " (pp. 352-353). To avoid semantic wrangling, we define plasticity genes as regulatory loci that exert environmentally dependent control over structural gene expression and thus produce a plastic response. Such loci represent a genetic mechanism for plastic response that is distinct from that assumed in quantitative genetic models of reaction norm evolution. We have the following disagreements with Via's (1993) viewpoint. (1) There is a wealth of evidence for the existence of plasticity genes as defined above. (2) The evolution of adaptive plasticity involves two processes: (i) adjustment of the available quantitative genetic variation to approach the phenotypic optimum and (ii) development of new genetic machinery for controlling response to the environment. (3) The argument that current statistical models can explain the evolution of plasticity avoids the issue that similar statistical results may be produced by means of very different genetic mechanisms. 1. The existence of plasticity genes.-Two types of genetic control of phenotypic plasticity have been proposed (Schmalhausen 1949; Smith-Gill 1983; Dragavtsev and Aver'yanova 1984). (i) Allelic sensitivity is the case in which in different environments all loci are expressed, but individual alleles vary in their sensitivity, that is, there are direct effects of the environment on structural gene expression. With allelic sensitivity we expect gradual changes in phenotype, proportional to the environmental gradient. (ii) Regulatory control is the scenario in which not all gene loci are expressed in each environment, that is, gene expression is mediated through the action of regulatory loci that can control the expression of multiple structural genes. For the simplest case of regulatory control, distinct phenotypes will be produced on each side of an environmental hreshold.
酵母 STE12 蛋白的信息素依赖性磷酸化与转录激活相关。
影响因子：
10.5
作者：
Song,D;Dolan,JW;Yuan,YL;Fields,S
通讯作者：
Fields,S