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拟南芥基因座与细菌效应基因之间的遗传互作是对感染的定量抗病性自然变异的基础。

Genetic Interaction between Arabidopsis Locus and Bacterial Effector Gene Underlies Natural Variation in Quantitative Disease Resistance to Infection.

作者信息

Luo Qi, Liu Wei-Wei, Pan Ke-Di, Peng You-Liang, Fan Jun

机构信息

Ministry of Agriculture Key Laboratory of Plant Pathology, College of Plant Protection, China Agricultural UniversityBeijing, China.

State Key Laboratory of Agrobiotechnology, China Agricultural UniversityBeijing, China.

出版信息

Front Plant Sci. 2017 May 4;8:695. doi: 10.3389/fpls.2017.00695. eCollection 2017.

DOI:10.3389/fpls.2017.00695
PMID:28523008
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5415610/
Abstract

Wide quantitative variation in plant disease resistance across Arabidopsis wild populations has been documented and the underlying mechanisms remain largely unknown. To investigate the genetic and molecular basis of this variation, Arabidopsis recombinant inbred lines (RILs) derived from Aa-0 × Col-0 and Gie-0 × Col-0 crosses were constructed and used for inoculation with pathovars ES4326 (ES4326) and DC3000 (DC3000). Bacterial growth assays revealed continuous distribution across the large differences between the most and the least susceptible lines in the RILs. Quantitative trait locus (QTL) mapping analyses identified a number of QTLs underpinning the variance in disease resistance, among which , a major QTL on chromosome III from both Aa-0 and Gie-0 accessions, preferentially restricted the growth of ES4326. A genetic screen for the ES4326 gene selectively leading to bacterial growth inhibition on accession Aa-0 uncovered the effector gene . Further QTL analysis of disease in RILs inoculated with DC3000 carrying showed that the genetic interaction between and determined Arabidopsis resistance to bacterial infection. These findings illustrate the complexity of Arabidopsis- interaction and highlight the importance of pathogen effectors in delineating genetic architectures of quantitative variation in plant disease resistance.

摘要

拟南芥野生群体中植物抗病性存在广泛的数量变异，但其潜在机制仍 largely 未知。为了研究这种变异的遗传和分子基础，构建了源自 Aa-0×Col-0 和 Gie-0×Col-0 杂交的拟南芥重组自交系（RILs），并用于接种致病型 ES4326（ES4326）和 DC3000（DC3000）。细菌生长测定揭示了 RILs 中最易感和最不易感品系之间巨大差异的连续分布。数量性状位点（QTL）定位分析确定了许多支撑抗病性变异的 QTL，其中，来自 Aa-0 和 Gie-0 种质的位于第三条染色体上的一个主要 QTL 优先限制了 ES4326 的生长。对导致 Aa-0 种质上细菌生长抑制的 ES4326 基因进行遗传筛选，发现了效应基因。对接种携带的 DC3000 的 RILs 中的病害进行进一步的 QTL 分析表明，和之间的遗传相互作用决定了拟南芥对细菌感染的抗性。这些发现说明了拟南芥 - 相互作用的复杂性，并强调了病原体效应基因在描绘植物抗病性数量变异的遗传结构中的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/013676da6c0a/fpls-08-00695-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/fa94d39303d6/fpls-08-00695-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/0e76ffb2660c/fpls-08-00695-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/f1446ed77224/fpls-08-00695-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/ca3e2995626a/fpls-08-00695-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/c6695d573e79/fpls-08-00695-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/82f98a1a25f8/fpls-08-00695-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/013676da6c0a/fpls-08-00695-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/fa94d39303d6/fpls-08-00695-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/0e76ffb2660c/fpls-08-00695-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/f1446ed77224/fpls-08-00695-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/ca3e2995626a/fpls-08-00695-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/c6695d573e79/fpls-08-00695-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/82f98a1a25f8/fpls-08-00695-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bced/5415610/013676da6c0a/fpls-08-00695-g007.jpg

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