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大麦中数量和定性的茎锈病抗性因素与防御调控因子的转录抑制有关。

Quantitative and qualitative stem rust resistance factors in barley are associated with transcriptional suppression of defense regulons.

机构信息

Bioinformatics and Computational Biology Graduate Program, Iowa State University, Ames, Iowa, United States of America.

出版信息

PLoS Genet. 2011 Jul;7(7):e1002208. doi: 10.1371/journal.pgen.1002208. Epub 2011 Jul 28.

DOI:10.1371/journal.pgen.1002208
PMID:21829384
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3145622/
Abstract

Stem rust (Puccinia graminis f. sp. tritici; Pgt) is a devastating fungal disease of wheat and barley. Pgt race TTKSK (isolate Ug99) is a serious threat to these Triticeae grain crops because resistance is rare. In barley, the complex Rpg-TTKSK locus on chromosome 5H is presently the only known source of qualitative resistance to this aggressive Pgt race. Segregation for resistance observed on seedlings of the Q21861 × SM89010 (QSM) doubled-haploid (DH) population was found to be predominantly qualitative, with little of the remaining variance explained by loci other than Rpg-TTKSK. In contrast, analysis of adult QSM DH plants infected by field inoculum of Pgt race TTKSK in Njoro, Kenya, revealed several additional quantitative trait loci that contribute to resistance. To molecularly characterize these loci, Barley1 GeneChips were used to measure the expression of 22,792 genes in the QSM population after inoculation with Pgt race TTKSK or mock-inoculation. Comparison of expression Quantitative Trait Loci (eQTL) between treatments revealed an inoculation-dependent expression polymorphism implicating Actin depolymerizing factor3 (within the Rpg-TTKSK locus) as a candidate susceptibility gene. In parallel, we identified a chromosome 2H trans-eQTL hotspot that co-segregates with an enhancer of Rpg-TTKSK-mediated, adult plant resistance discovered through the Njoro field trials. Our genome-wide eQTL studies demonstrate that transcript accumulation of 25% of barley genes is altered following challenge by Pgt race TTKSK, but that few of these genes are regulated by the qualitative Rpg-TTKSK on chromosome 5H. It is instead the chromosome 2H trans-eQTL hotspot that orchestrates the largest inoculation-specific responses, where enhanced resistance is associated with transcriptional suppression of hundreds of genes scattered throughout the genome. Hence, the present study associates the early suppression of genes expressed in this host-pathogen interaction with enhancement of R-gene mediated resistance.

摘要

茎锈病(Puccinia graminis f. sp. tritici;Pgt)是一种毁灭性的小麦和大麦真菌病。Pgt 菌株 TTKSK(分离株 Ug99)是这些禾本科谷物作物的严重威胁,因为很少有抗性。在大麦中,5H 染色体上的复杂 Rpg-TTKSK 基因座是目前唯一已知的对这种侵袭性 Pgt 菌株具有定性抗性的来源。在 Q21861×SM89010(QSM)加倍单倍体(DH)群体的幼苗上观察到的抗性分离主要是定性的,除了 Rpg-TTKSK 以外的其他基因座解释的剩余方差很小。相比之下,在肯尼亚 Njoro 用 Pgt 菌株 TTKSK 田间接种物感染的成年 QSM DH 植物的分析显示,有几个额外的数量性状基因座有助于抗性。为了对这些基因座进行分子表征,使用 Barley1 GeneChips 测量了 QSM 群体在接种 Pgt 菌株 TTKSK 或模拟接种后的 22792 个基因的表达。处理之间表达数量性状基因座(eQTL)的比较表明,一种肌动蛋白解聚因子 3(在 Rpg-TTKSK 基因座内)的接种依赖性表达多态性暗示其为候选易感性基因。同时,我们发现了一个 2H 染色体的反式 eQTL 热点,该热点与通过 Njoro 田间试验发现的增强 Rpg-TTKSK 介导的成年植物抗性的增强子共分离。我们的全基因组 eQTL 研究表明,在受到 Pgt 菌株 TTKSK 挑战后,25%的大麦基因的转录积累发生改变,但这些基因中很少有被 5H 染色体上的定性 Rpg-TTKSK 调节。相反,2H 染色体的反式 eQTL 热点协调了最大的接种特异性反应,其中增强的抗性与基因组中散布的数百个基因的转录抑制相关。因此,本研究将宿主-病原体相互作用中表达基因的早期抑制与 R 基因介导的抗性增强联系起来。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/2984b1766689/pgen.1002208.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/80730aa737a5/pgen.1002208.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/fa8b016315e5/pgen.1002208.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/2947c85b3397/pgen.1002208.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/0f5bf14d6b08/pgen.1002208.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/03ec44d2a0d7/pgen.1002208.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/ec0b455b8239/pgen.1002208.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/b181acc0e070/pgen.1002208.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/5696817df087/pgen.1002208.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/2984b1766689/pgen.1002208.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/80730aa737a5/pgen.1002208.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/fa8b016315e5/pgen.1002208.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/2947c85b3397/pgen.1002208.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/0f5bf14d6b08/pgen.1002208.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/03ec44d2a0d7/pgen.1002208.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/ec0b455b8239/pgen.1002208.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/b181acc0e070/pgen.1002208.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/5696817df087/pgen.1002208.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e0/3145622/2984b1766689/pgen.1002208.g009.jpg

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