Constraints on utilization of the EDA-signaling pathway in threespine stickleback evolution
Constraints on utilization of the EDA-signaling pathway in threespine stickleback evolution
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DOI：
10.1111/j.1525-142x.2007.00145.x
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发表时间：
2007-03-01
影响因子：
2.9
通讯作者：
Kingsley, David M.
中科院分区：
文献类型：
--
作者：
Knecht, Anne K.;Hosemann, Kim E.;Kingsley, David M.
许多特征在相距甚远的种群中同时进化。三刺刺鱼的进化辐射为测试脊椎动物平行进化的分子基础提供了一个强大的模型。尽管海洋刺鱼完全被骨质装甲板覆盖，但大多数淡水鱼的装甲板数量急剧减少。最近的遗传学研究表明，盔甲图案的重大变化可能是由于编码分泌信号分子外典型增生蛋白（EDA）的基因的调节变化所致。在哺乳动物中，EDA 信号通路许多不同组成部分的突变会导致头发、牙齿、汗腺和真皮骨骼发生类似的变化。为了测试 EDA 途径中的其他基因是否也控制装甲板的自然变异，我们鉴定并绘制了刺鱼 EDA 受体 (EDAR)、EDAR 相关死亡域适配器、肿瘤坏死因子受体 (TNFR) 超级家族成员 19、其适配器 TNFR 相关因子 6 和下游调节核因子 kappa B 必需调节器 (NEMO)。与人类外胚层发育不良疾病表型背后的基因多样性相反，这些 EDA 途径成分均未映射到先前显示可修饰自然群体中装甲板的染色体，尽管 EDAR 对装甲板数量显示出微小但显着的影响。我们进一步研究了这些基因是否在拷贝数、靶标大小或基因组组织方面表现出差异，这些差异可能使它们不太适合进化改变的靶标。与 EDA 相比，所有这些基因都具有较小的周围非编码（假定的调控）区域，以及较少的进化保守区域。我们认为，高度模块化的顺式作用控制序列的存在可能是影响特定基因作为自然界主要表型变化基础的可能性的关键因素。
Many traits evolve in parallel in widely separated populations. The evolutionary radiation of threespine sticklebacks provides a powerful model for testing the molecular basis of parallel evolution in vertebrates. Although marine sticklebacks are completely covered with bony armor plates, most freshwater populations have dramatic reductions in plates. Recent genetic studies have shown that major changes in armor patterning are likely due to regulatory alterations in the gene encoding the secreted signaling molecule ectodysplasin (EDA). In mammals, mutations in many different components of the EDA-signaling pathway produce similar changes in hair, teeth, sweat glands, and dermal bones. To test whether other genes in the EDA pathway also control natural variation in armor plates, we identified and mapped stickleback EDA Receptor (EDAR), the EDAR-Associated Death Domain adaptor, Tumor Necrosis Factor Receptor (TNFR) SuperFamily member 19, its adaptor TNFR-Associated Factor 6, and the downstream regulator nuclear factor kappa B Essential Modulator (NEMO). In contrast to the diversity of genes underlying ectodermal dysplasia disease phenotypes in humans, none of these EDA pathway components map to chromosomes previously shown to modify armor plates in natural populations, though EDAR showed a small but significant effect on plate number. We further investigated whether these genes exhibit differences in copy number, target size, or genomic organization that might make them less suitable targets for evolutionary change. In comparison with EDA, all these genes have smaller surrounding noncoding (putative regulatory) regions, with fewer evolutionarily conserved regions. We suggest that the presence of highly modular cis-acting control sequences may be a key factor influencing the likelihood that particular genes will serve as the basis of major phenotypic changes in nature.