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ACD6中的新型等位基因变异导致拟南芥本地种群出现杂种坏死。

Novel allelic variants in ACD6 cause hybrid necrosis in local collection of Arabidopsis thaliana.

作者信息

Świadek Magdalena, Proost Sebastian, Sieh Daniela, Yu Jing, Todesco Marco, Jorzig Christian, Rodriguez Cubillos Andrés Eduardo, Plötner Björn, Nikoloski Zoran, Chae Eunyoung, Giavalisco Patrick, Fischer Axel, Schröder Florian, Kim Sang-Tae, Weigel Detlef, Laitinen Roosa A E

机构信息

Max Planck Institute of Molecular Plant Physiology, Potsdam, 14476, Germany.

University of Potsdam, Potsdam, 14476, Germany.

出版信息

New Phytol. 2017 Jan;213(2):900-915. doi: 10.1111/nph.14155. Epub 2016 Sep 2.

DOI:10.1111/nph.14155
PMID:27588563
Abstract

Hybrid necrosis is a common type of hybrid incompatibility in plants. This phenomenon is caused by deleterious epistatic interactions, resulting in spontaneous activation of plant defenses associated with leaf necrosis, stunted growth and reduced fertility in hybrids. Specific combinations of alleles of ACCELERATED CELL DEATH 6 (ACD6) have been shown to be a common cause of hybrid necrosis in Arabidopsis thaliana. Increased ACD6 activity confers broad-spectrum resistance against biotrophic pathogens but reduces biomass production. We generated 996 crosses among individuals derived from a single collection area around Tübingen (Germany) and screened them for hybrid necrosis. Necrotic hybrids were further investigated by genetic linkage, amiRNA silencing, genomic complementation and metabolic profiling. Restriction site associated DNA (RAD)-sequencing was used to understand genetic diversity in the collection sites containing necrosis-inducing alleles. Novel combinations of ACD6 alleles found in neighbouring stands were found to activate the A. thaliana immune system. In contrast to what we observed in controlled conditions, necrotic hybrids did not show reduced fitness in the field. Metabolic profiling revealed changes associated with the activation of the immune system in ACD6-dependent hybrid necrosis. This study expands our current understanding of the active role of ACD6 in mediating trade-offs between defense responses and growth in A.  thaliana.

摘要

杂种坏死是植物中一种常见的杂种不亲和类型。这种现象是由有害的上位性相互作用引起的,导致与叶片坏死、生长发育迟缓以及杂种育性降低相关的植物防御反应自发激活。在拟南芥中,加速细胞死亡6(ACD6)等位基因的特定组合已被证明是杂种坏死的常见原因。ACD6活性增加赋予了对活体营养型病原体的广谱抗性,但降低了生物量的产生。我们在源自德国图宾根附近一个单一采集区域的个体之间进行了996次杂交,并对它们进行杂种坏死筛选。对坏死杂种进一步进行了遗传连锁、amiRNA沉默、基因组互补和代谢谱分析。利用限制性位点相关DNA(RAD)测序来了解含有坏死诱导等位基因的采集位点的遗传多样性。在相邻植株中发现的ACD6等位基因的新组合被发现激活了拟南芥的免疫系统。与我们在受控条件下观察到的情况相反,坏死杂种在田间并未表现出适应性降低。代谢谱分析揭示了与ACD6依赖性杂种坏死中免疫系统激活相关的变化。这项研究扩展了我们目前对ACD6在介导拟南芥防御反应和生长之间权衡中所起积极作用的理解。

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