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NLR 基因的调控与进化:植物免疫的紧密联系。

Regulation and Evolution of NLR Genes: A Close Interconnection for Plant Immunity.

机构信息

Council for Agricultural Research and Economics-Research Centre for Cereal and Industrial Crops, s.s. 673, km 25.2, 71122 Foggia, Italy.

Council for Agricultural Research and Economics-Research Centre for Genomics and Bioinformatics, via San Protaso 302, 29017 Fiorenzuola d'Arda (PC), Italy.

出版信息

Int J Mol Sci. 2018 Jun 4;19(6):1662. doi: 10.3390/ijms19061662.

Abstract

NLR (NOD-like receptor) genes belong to one of the largest gene families in plants. Their role in plants' resistance to pathogens has been clearly described for many members of this gene family, and dysregulation or overexpression of some of these genes has been shown to induce an autoimmunity state that strongly affects plant growth and yield. For this reason, these genes have to be tightly regulated in their expression and activity, and several regulatory mechanisms are described here that tune their gene expression and protein levels. This gene family is subjected to rapid evolution, and to maintain diversity at NLRs, a plethora of genetic mechanisms have been identified as sources of variation. Interestingly, regulation of gene expression and evolution of this gene family are two strictly interconnected aspects. Indeed, some examples have been reported in which mechanisms of gene expression regulation have roles in promotion of the evolution of this gene family. Moreover, co-evolution of the gene family and other gene families devoted to their control has been recently demonstrated, as in the case of miRNAs.

摘要

NLR (NOD-like receptor) 基因属于植物中最大的基因家族之一。该基因家族的许多成员在植物对病原体的抗性中发挥作用,并且已经表明这些基因中的一些基因的失调或过表达会诱导强烈影响植物生长和产量的自身免疫状态。出于这个原因,这些基因的表达和活性必须受到严格调控,这里描述了几种调节机制来调节它们的基因表达和蛋白水平。这个基因家族经历了快速进化,为了维持 NLR 的多样性,已经确定了许多遗传机制作为变异的来源。有趣的是,基因表达调控的进化和这个基因家族的进化是两个严格相互关联的方面。事实上,已经有报道称,基因表达调控机制在促进这个基因家族的进化中发挥了作用。此外,最近还证明了这个基因家族与其他专门用于控制它们的基因家族的共同进化,例如 miRNA。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d76/6032283/9806f62efc3e/ijms-19-01662-g001.jpg

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