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乙烯和脱落酸信号通路对番茄抵抗白粉病和盐胁迫复合胁迫的影响存在差异。

Ethylene and Abscisic Acid Signaling Pathways Differentially Influence Tomato Resistance to Combined Powdery Mildew and Salt Stress.

作者信息

Kissoudis Christos, Seifi Alireza, Yan Zhe, Islam A T M Tanjimul, van der Schoot Hanneke, van de Wiel Clemens C M, Visser Richard G F, van der Linden C G, Bai Yuling

机构信息

Plant Breeding, Wageningen University & Research Wageningen, Netherlands.

Biotechnology and Plant Breeding Department, Faculty of Agriculture, Ferdowsi University of Mashhad Mashhad, Iran.

出版信息

Front Plant Sci. 2017 Jan 9;7:2009. doi: 10.3389/fpls.2016.02009. eCollection 2016.

DOI:10.3389/fpls.2016.02009
PMID:28119708
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5220069/
Abstract

There is currently limited knowledge on the role of hormones in plants responses to combinations of abiotic and pathogen stress factors. This study focused on the response of tomato near-isogenic lines (NILs) that carry the , and loci, conferring resistance to tomato powdery mildew (PM) caused by , to combined PM and salt stress. These NILs were crossed with the (ABA-deficient), (JA-deficient), and (ET overproducer) tomato mutants to investigate possible roles of hormone signaling in response to combined stresses. In the NILs, marker genes for hormonal pathways showed differential expression patterns upon PM infection. The mutation resulted in breakdown of resistance in NIL-Ol-1 and NIL-ol-2. This was accompanied by reduced callose deposition, and was more pronounced under combined salt stress. The mutation resulted in HO overproduction and reduced susceptibility to PM in NIL-Ol-1 under combined stress, but lead to higher plant growth reduction under salinity and combined stress. Resistance in NIL-ol-2 was compromised by the mutation, which was potentially caused by reduction of callose deposition. Under combined stress the compromised resistance in NIL-ol-2 was restored. PM resistance in NIL-Ol-4 remained robust across all mutant and treatment combinations. Hormone signaling is critical to the response to combined stress and PM, in terms of resistance and plant fitness. ABA appears to be at the crossroads of disease susceptibility/senescence and plant performance under combined stress These gained insights can aid in narrowing down targets for improving crop performance under stress combinations.

摘要

目前,关于激素在植物对非生物胁迫和病原体胁迫因素组合的反应中的作用,人们了解有限。本研究聚焦于携带 、 和 位点的番茄近等基因系(NILs)对番茄白粉病(PM)和盐胁迫组合的反应,这些位点赋予了对由 引起的番茄白粉病的抗性。将这些NILs与 (脱落酸缺陷型)、 (茉莉酸缺陷型)和 (乙烯过量产生型)番茄突变体杂交,以研究激素信号在对复合胁迫反应中的可能作用。在NILs中,激素途径的标记基因在PM感染后表现出不同的表达模式。 突变导致NIL-Ol-1和NIL-ol-2中的抗性丧失。这伴随着胼胝质沉积减少,在复合盐胁迫下更为明显。 突变导致在复合胁迫下NIL-Ol-1中HO过量产生且对PM的敏感性降低,但在盐胁迫和复合胁迫下导致更高的植物生长抑制。 突变损害了NIL-ol-2中的抗性,这可能是由胼胝质沉积减少引起的。在复合胁迫下,NIL-ol-2中受损的抗性得以恢复。NIL-Ol-4中的PM抗性在所有突变体和处理组合中都保持强劲。就抗性和植物适应性而言,激素信号对于对复合胁迫和PM的反应至关重要。脱落酸似乎处于复合胁迫下疾病易感性/衰老和植物性能的交叉点。这些新获得的见解有助于缩小在胁迫组合下提高作物性能的目标范围。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/3ce4699560a7/fpls-07-02009-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/e0aeaf251c69/fpls-07-02009-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/42290f06d666/fpls-07-02009-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/04281c1d0f1c/fpls-07-02009-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/cb2a33977fbb/fpls-07-02009-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/17c65d5d099f/fpls-07-02009-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/756e45480edc/fpls-07-02009-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/3ce4699560a7/fpls-07-02009-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/e0aeaf251c69/fpls-07-02009-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/42290f06d666/fpls-07-02009-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/04281c1d0f1c/fpls-07-02009-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/cb2a33977fbb/fpls-07-02009-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/17c65d5d099f/fpls-07-02009-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/756e45480edc/fpls-07-02009-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/646f/5220069/3ce4699560a7/fpls-07-02009-g007.jpg

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