scholarly journals Salicylic acid biosynthesis is enhanced and contributes to increased biotrophic pathogen resistance in Arabidopsis hybrids

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Li Yang ◽  
Bosheng Li ◽  
Xiao-yu Zheng ◽  
Jigang Li ◽  
Mei Yang ◽  
...  

Abstract Heterosis, the phenotypic superiority of a hybrid over its parents, has been demonstrated for many traits in Arabidopsis thaliana, but its effect on defence remains largely unexplored. Here, we show that hybrids between some A. thaliana accessions show increased resistance to the biotrophic bacterial pathogen Pseudomonas syringae pv. tomato (Pst) DC3000. Comparisons of transcriptomes between these hybrids and their parents after inoculation reveal that several key salicylic acid (SA) biosynthesis genes are significantly upregulated in hybrids. Moreover, SA levels are higher in hybrids than in either parent. Increased resistance to Pst DC3000 is significantly compromised in hybrids of pad4 mutants in which the SA biosynthesis pathway is blocked. Finally, increased histone H3 acetylation of key SA biosynthesis genes correlates with their upregulation in infected hybrids. Our data demonstrate that enhanced activation of SA biosynthesis in A. thaliana hybrids may contribute to their increased resistance to a biotrophic bacterial pathogen.

2019 ◽  
Vol 374 (1767) ◽  
pp. 20180314 ◽  
Author(s):  
Na Cui ◽  
Hong Lu ◽  
Tianzuo Wang ◽  
Wenhao Zhang ◽  
Le Kang ◽  
...  

Effector proteins present in aphid saliva are thought to modulate aphid–plant interactions. Armet, an effector protein, is found in the phloem sap of pea-aphid-infested plants and is indispensable for the survival of aphids on plants. However, its function in plants has not been investigated. Here, we explored the functions of Armet after delivery into plants. Examination of the transcriptomes of Nicotiana benthamiana and Medicago truncatula following transgenic expression of Armet or infiltration of the protein showed that Armet activated pathways associated with plant–pathogen interactions, mitogen-activated protein kinase and salicylic acid (SA). Armet induced a fourfold increase in SA accumulation by regulating the expression of SAMT and SABP2 , two genes associated with SA metabolism, in Armet-infiltrated tobacco. The increase in SA enhanced the plants' resistance to bacterial pathogen Pseudomonas syringae but had no detectable adverse effects on aphid survival or reproduction. Similar molecular responses and a chlorosis phenotype were induced in tobacco by Armet from two aphid species but not by locust Armet, suggesting that the effector function of Armet may be specific for aphids. The results suggest that Armet causes plants to make a pathogen-resistance decision and reflect a novel tripartite insect–plant–pathogen interaction. This article is part of the theme issue ‘Biotic signalling sheds light on smart pest management’.


2010 ◽  
Vol 23 (3) ◽  
pp. 340-351 ◽  
Author(s):  
Madhumati Mukherjee ◽  
Katherine E. Larrimore ◽  
Naushin J. Ahmed ◽  
Tyler S. Bedick ◽  
Nadia T. Barghouthi ◽  
...  

The ascorbic acid (AA)-deficient Arabidopsis thaliana vtc1-1 mutant exhibits increased resistance to the virulent bacterial pathogen Pseudomonas syringae. This response correlates with heightened levels of salicylic acid (SA), which induces antimicrobial pathogenesis-related (PR) proteins. To determine if SA-mediated, enhanced disease resistance is a general phenomenon of AA deficiency, to elucidate the signal that stimulates SA synthesis, and to identify the biosynthetic pathway through which SA accumulates, we studied the four AA-deficient vtc1-1, vtc2-1, vtc3-1, and vtc4-1 mutants. We also studied double mutants defective in the AA-biosynthetic gene VTC1 and the SA signaling pathway genes PAD4, EDS5, and NPR1, respectively. All vtc mutants were more resistant to P. syringae than the wild type. With the exception of vtc4-1, this correlated with constitutively upregulated H2O2, SA, and messenger RNA levels of PR genes. Double mutants exhibited decreased SA levels and enhanced susceptibility to P. syringae compared with the wild type, suggesting that vtc1-1 requires functional PAD4, EDS5, and NPR1 for SA biosynthesis and pathogen resistance. We suggest that AA deficiency causes constitutive priming through a buildup of H2O2 that stimulates SA accumulation, conferring enhanced disease resistance in vtc1-1, vtc2-1, and vtc3-1, whereas vtc4-1 might be sensitized to H2O2 and SA production after infection.


2010 ◽  
Vol 23 (12) ◽  
pp. 1584-1591 ◽  
Author(s):  
Gudrun Schmitz ◽  
Thomas Reinhold ◽  
Cornelia Göbel ◽  
Ivo Feussner ◽  
H. Ekkehard Neuhaus ◽  
...  

When grown under short-day conditions at low light, leaves of an Arabidopsis thaliana (accession Col-0) mutant with defects in the two genes encoding plastid ATP/ADP antiporters (so-called ntt1-2 null mutants) display a variety of physiological changes. These include the formation of necrotic lesions and the accumulation of hydrogen peroxide in the leaves. Here, we show that, under short-day conditions, leaves of the ntt1-2 mutant display enhanced resistance to Hyaloperonospora arabidopsidis, Botrytis cinerea, and Pseudomonas syringae pv. tomato DC3000. Resistance to these pathogens was associated with constitutively elevated levels of the plant hormone salicylic acid and, eventually, jasmonic acid, and constitutive or primed activation after pathogen attack of various defense genes that are dependent on these hormones. In addition, the antagonistic crosstalk between the salicylic acid and jasmonic acid signaling pathways seems to be affected in ntt1-2. Because the enhanced resistance of ntt1-2 to H. arabidopsidis was not seen when the mutant was grown under long-day conditions, our findings argue that nocturnal ATP import into chloroplasts is crucial to keep A. thaliana from runaway activation of pathogen resistance.


Development ◽  
2020 ◽  
Vol 147 (16) ◽  
pp. dev189647
Author(s):  
Yiqiao Wang ◽  
Xing Cui ◽  
Bo Yang ◽  
Shutao Xu ◽  
Xiangyan Wei ◽  
...  

ABSTRACTReactive oxygen species (ROS) and salicylic acid (SA) are two factors regulating leaf senescence and defense against pathogens. However, how a single gene integrates both ROS and SA pathways remains poorly understood. Here, we show that Arabidopsis WRKY55 transcription factor positively regulates ROS and SA accumulation, and thus leaf senescence and resistance against the bacterial pathogen Pseudomonas syringae. WRKY55 is predominantly expressed in senescent leaves and encodes a transcriptional activator localized to nuclei. Both inducible and constitutive overexpression of WRKY55 accelerates leaf senescence, whereas mutants delay it. Transcriptomic sequencing identified 1448 differentially expressed genes, of which 1157 genes are upregulated by WRKY55 expression. Accordingly, the ROS and SA contents in WRKY55-overexpressing plants are higher than those in control plants, whereas the opposite occurs in mutants. Moreover, WRKY55 positively regulates defense against P. syringae. Finally, we show that WRKY55 activates the expression of RbohD, ICS1, PBS3 and SAG13 by binding directly to the W-box-containing fragments. Taken together, our work has identified a new WRKY transcription factor that integrates both ROS and SA pathways to regulate leaf senescence and pathogen resistance.


2007 ◽  
Vol 64 (1-2) ◽  
pp. 1-15 ◽  
Author(s):  
Yeon Jong Koo ◽  
Myeong Ae Kim ◽  
Eun Hye Kim ◽  
Jong Tae Song ◽  
Choonkyun Jung ◽  
...  

2018 ◽  
Vol 19 (12) ◽  
pp. 4071 ◽  
Author(s):  
Mei-Chi Chang ◽  
Yunn-Jy Chen ◽  
Yun-Chia Lian ◽  
Bei-En Chang ◽  
Chih-Chia Huang ◽  
...  

Butyric acid as a histone deacetylase (HDAC) inhibitor is produced by a number of periodontal and root canal microorganisms (such as Porphyromonas, Fusobacterium, etc.). Butyric acid may affect the biological activities of periodontal/periapical cells such as osteoblasts, periodontal ligament cells, etc., and thus affect periodontal/periapical tissue destruction and healing. The purposes of this study were to study the toxic effects of butyrate on the matrix and mineralization marker expression in MG-63 osteoblasts. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Cellular apoptosis and necrosis were analyzed by propidium iodide/annexin V flow cytometry. The protein and mRNA expression of osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-B ligand (RANKL) were analyzed by Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR). OPG, soluble RANKL (sRANKL), 8-isoprostane, pro-collagen I, matrix metalloproteinase-2 (MMP-2), osteonectin (SPARC), osteocalcin and osteopontin (OPN) secretion into culture medium were measured by enzyme-linked immunosorbant assay. Alkaline phosphatase (ALP) activity was checked by ALP staining. Histone H3 acetylation levels were evaluated by immunofluorescent staining (IF) and Western blot. We found that butyrate activated the histone H3 acetylation of MG-63 cells. Exposure of MG-63 cells to butyrate partly decreased cell viability with no marked increase in apoptosis and necrosis. Twenty-four hours of exposure to butyrate stimulated RANKL protein expression, whereas it inhibited OPG protein expression. Butyrate also inhibited the secretion of OPG in MG-63 cells, whereas the sRANKL level was below the detection limit. However, 3 days of exposure to butyrate (1 to 8 mM) or other HDAC inhibitors such as phenylbutyrate, valproic acid and trichostatin stimulated OPG secretion. Butyrate stimulated 8-isoprostane, MMP-2 and OPN secretion, but not procollagen I, or osteocalcin in MG-63 cells. Exposure to butyrate (2–4 mM) for 3 days markedly stimulated osteonectin secretion and ALP activity. In conclusion, higher concentrations of butyric acid generated by periodontal and root canal microorganisms may potentially induce bone destruction and impair bone repair by the alteration of OPG/RANKL expression/secretion, 8-isoprostane, MMP-2 and OPN secretion, and affect cell viability. However, lower concentrations of butyrate (1–4 mM) may stimulate ALP, osteonectin and OPG. These effects are possibly related to increased histone acetylation. These events are important in the pathogenesis and repair of periodontal and periapical destruction.


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