CTR1蛋白翻译可塑性与遗传适应的研究

在物种进化进程中，一个物种如何在保持一个稳定基因组的同时，也维持一个性状的稳定性，是物种进化与生存适应协同的一个重要问题。参与特定途径的组分，可能是单拷贝基因编码，或是多拷贝基因编码。乙烯信号的接受与转导决定植物对乙烯的响应程度;乙烯信号转导组分的复杂性，决定了特定植物物种乙烯信号转导稳定性的维持。 拟南芥乙烯信号组分CTR1由单拷贝基因编码，缺乏遗传冗余所赋予的遗传稳定性以及蛋白丰富性，CTR1一旦突变缺失，会严重影响拟南芥生存适应，甚至后代的繁衍。我们初期的研究发现，并不是所有的氨基端区域提前终止突变都能够严重影响CTR1功能。暗示拟南芥存在一个遗传补偿机制，甚至蛋白丰富机制，避免因为缺乏遗传冗余性使得CTR1和乙烯信号途径易于受到突变影响拟南芥生存适应。本项目的执行，不但解释CTR1的遗传补偿机制，也能扩展到一个普遍而重要的科学问题：遗传补偿机制对遗传冗余缺乏在物种生存适应的重要性。

Living organisms maintain biological functionality against external and internal perturbations, and the robustness is considered a fundamental property of a complex and dynamic biological system that cannot be simply explained at molecular levels by investigating individual components of a pathway. Although the underlying mechanisms are diverse, at various levels, to attain the robustness, the genome composition is an important resource that generates tools to cope against perturbations. While the genome is subject to perturbations as a driving force of evolvability, genetic robustness, which refers to phenotypic stability in the face of mutations, enables organisms to maintain fitness upon harmful mutations. Ethylene is an important gaseous plant hormone controlling plant growth and development throughout development and complexity of its signal transduction determines robustness of a plant. CTR1 is an important component in the pathway negatively regulating ethylene signaling and is encoded by a single gene in Arabidopsis. With the lack of genetic redundancy that helps stabilize robustness of the pathway for CTR1, we ask how Arabidopsis may maintain fitness in response to genetic perturbations. Our preliminary studies found that early termination mutations of CTR1 near the N-terminus do not necessarily lead to strong ctr1 mutant growth inhibition phenotype, implying a genetic compensation mechanism that may prevent impacts upon CTR1 mutations of certain types. Our study may unveil part of genetic compensations that generalizes an important biological question: how an organism cope against genetic perturbations via genetic compensations.