MPK3/MPK6-mediated ERF72 Phosphorylation Positively Regulates Resistance to Botrytis cinerea Through Directly and Indirectly Activating the Transcription of Camalexin-biosynthesis Enzymes

2021 ◽  
Author(s):  
Yihao Li ◽  
Kun Liu ◽  
Ganlu Tong ◽  
Chao Xi ◽  
Jin Liu ◽  
...  
Keyword(s):  
Immune Responses ◽  
Botrytis Cinerea ◽  
Target Genes ◽  
Plant Immunity ◽  
Ethylene Response Factor ◽  
Wild Type ◽  
Abiotic Stress Response ◽  
Necrotrophic Pathogen ◽  
Ethylene Response

Abstract Ethylene response factor (ERF) Group VII members generally function in regulating plant growth and development, abiotic stress response, and plant immunity in Arabidopsis. However, the detail regulatory mechanism by which Group VII ERFs mediate plant immune responses remains elusive. Here, we characterised ERF72, a member of the Group VII ERFs, as a positive regulator mediating resistance to the necrotrophic pathogen Botrytis cinerea. Compared with wild type (WT), erf72 mutant showed the lower camalexin contents and more susceptible to B. cinerea, while complementation of ERF72 in erf72 rescued susceptibility phenotypes. Moreover, overexpression of ERF72 in WT promoted camalexin biosynthesis and resistance to B. cinerea. Then, we identified camalexin biosynthesis genes PAD3 and CYP71A13, and transcription factor WRKY33 as target genes of ERF72. Furthermore, MPK3 and MPK6 phosphorylate ERF72 at Ser151 to improve its transactivation activity, camalexin contents and resistance to B. cinerea. These findings highlight the role of ERF72 in coordinating the camalexin biosynthesis via directly regulating the expression of camalexin biosynthetic genes and indirectly by targeting WRKK33 in plant immunity.

scholarly journals Diversified Regulation of Cytokinin Levels and Signaling During Botrytis cinerea Infection in Arabidopsis

2021 ◽  
Vol 12 ◽  
Author(s):  
Beibei Li ◽  
Ruolin Wang ◽  
Shiya Wang ◽  
Jiang Zhang ◽  
Ling Chang
Keyword(s):  
Botrytis Cinerea ◽  
Response Regulator ◽  
Plant Immunity ◽  
Defense Responses ◽  
Cytokinin Oxidase ◽  
Plant Defense Responses ◽  
Necrotrophic Pathogen ◽  
Transcriptional Changes ◽  
Complex Regulation

Cytokinins (CKs) can modulate plant immunity to various pathogens, but how CKs are involved in plant defense responses to the necrotrophic pathogen Botrytis cinerea is still unknown. Here, we found that B. cinerea infection induced transcriptional changes in multiple genes involved in the biosynthesis, degradation, and signaling of CKs, as well as their contents, in pathogen-infected Arabidopsis leaves. Among the CKs, the gene expression of CYTOKININ OXIDASE/DEHYDROGENASE 5 (CKX5) was remarkably induced in the local infected leaves and the distant leaves of the same plant without pathogen inoculation. Cis-zeatin (cZ) and its riboside (cZR) accumulated considerably in infected leaves, suggesting an important role of the cis-zeatin type of CKs in the plant response to B. cinerea. Cytokinin double-receptor mutants were more susceptible to B. cinerea infection, whereas an exogenous CK treatment enhanced the expression levels of defense-related genes and of jasmonic acid (JA) and ethylene (ET), but not salicylic acid (SA), resulting in higher resistance of Arabidopsis to B. cinerea. Investigation of CK responses to B. cinerea infection in the JA biosynthesis mutant, jar1-1, and ET-insensitive mutant, ein2-1, showed that CK signaling and levels of CKs, namely, those of isopentenyladenine (iP), isopentenyladenine riboside (iPR), and trans-zeatin (tZ), were enhanced in jar1-1-infected leaves. By contrast, reductions in iP, iPR, tZ, and tZ riboside (tZR) as well as cZR contents occurred in ein2-1-infected leaves, whose transcript levels of CK signaling genes were likewise differentially regulated. The Arabidopsis Response Regulator 5 (ARR5) gene was upregulated in infected leaves of ein2-1 whereas another type-A response regulator, ARR16, was significantly downregulated, suggesting the existence of a complex regulation of CK signaling via the ET pathway. Accumulation of the cis-zeatin type of CKs in B. cinerea-infected leaves depended on ET but not JA pathways. Collectively, our findings provide evidence that CK responds to B. cinerea infection in a variety of ways that are differently modulated by JA and ET pathways in Arabidopsis.

scholarly journals Tomato wall-associated kinase SlWak1 acts in an Fls2- and Fls3-dependent manner to promote apoplastic immune responses to Pseudomonas syringae

2020 ◽  
Author(s):  
Ning Zhang ◽  
Marina A Pombo ◽  
Hernan G Rosli ◽  
Gregory B Martin
Keyword(s):  
Gene Expression ◽  
Immune Responses ◽  
Pseudomonas Syringae ◽  
Molecular Mechanisms ◽  
Plant Immunity ◽  
Transcript Abundance ◽  
Dependent Manner ◽  
Wild Type ◽  
Disease Symptoms

Wall-associated kinases (Waks) are known to be important components of plant immunity against various pathogens including Pseudomonas syringae pv. tomato (Pst) although their molecular mechanisms are largely unknown. In tomato, SlWak1 has been implicated in immunity because its transcript abundance increases significantly in leaves after treatment with the flagellin-derived peptides flg22 and flgII-28, which activate the receptors Fls2 and Fls3, respectively. We generated two SlWak1 tomato mutants (Δwak1) using CRISPR/Cas9 and investigated the role of SlWak1 in tomato-Pst interactions. PTI activated in the apoplast by flg22 or flgII-28 was compromised in Δwak1 plants but PTI at the leaf surface was unaffected. The Δwak1 plants developed fewer callose deposits than wild-type plants but retained the ability to generate reactive oxygen species and activate MAPKs in response to flg22 and flgII-28. The induction of Wak1 gene expression by flg22 and flgII-28 was greatly reduced in a tomato mutant lacking Fls2 and Fls3 but induction of Fls3 gene expression by flgII-28 was unaffected in Δwak1 plants. After Pst inoculation, Δwak1 plants developed disease symptoms more slowly than Δfls2.1/fls2.2/fls3 mutant plants, although both plants ultimately were similarly susceptible. SlWak1 co-immunoprecipitated with both Fls2 and Fls3 independently of flg22/flgII-28 or Bak1. These observations suggest that SlWak1 acts in a complex with Fls2/Fls3 and plays an important role at later stages of the PTI in the apoplast.

scholarly journals Role of ethylene and the APETALA 2/ethylene response factor superfamily in rice under various abiotic and biotic stress conditions

2017 ◽  
Vol 134 ◽  
pp. 33-44 ◽  
Author(s):  
Rambod Abiri ◽  
Noor Azmi Shaharuddin ◽  
Mahmood Maziah ◽  
Zetty Norhana Balia Yusof ◽  
Narges Atabaki ◽  
...  
Keyword(s):  
Biotic Stress ◽  
Stress Conditions ◽  
Ethylene Response Factor ◽  
Response Factor ◽  
Abiotic And Biotic Stress ◽  
Ethylene Response ◽  
Apetala 2

scholarly journals The Role of Vitamin D and Vitamin D Receptor in Immunity toLeishmania majorInfection

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
James P. Whitcomb ◽  
Mary DeAgostino ◽  
Mark Ballentine ◽  
Jun Fu ◽  
Martin Tenniswood ◽  
...  
Keyword(s):  
Vitamin D ◽  
Immune Responses ◽  
Vitamin D Receptor ◽  
Leishmania Major ◽  
Active Form ◽  
Wild Type ◽  
Vitamin D Signaling ◽  
Deficient Mice ◽  
Th 1

Vitamin D signaling modulates a variety of immune responses. Here, we assessed the role of vitamin D in immunity to experimental leishmaniasis infection in vitamin D receptor-deficient mice (VDRKO). We observed that VDRKO mice on a genetically resistant background have decreasedLeishmania major-induced lesion development compared to wild-type (WT) mice; additionally, parasite loads in infected dermis were significantly lower at the height of infection. Enzymatic depletion of the active form of vitamin D mimics the ablation of VDR resulting in an increased resistance toL. major. Conversely, VDRKO or vitamin D-deficient mice on the susceptible Th2-biased background had no change in susceptibility. These studies indicate vitamin D deficiency, either through the ablation of VDR or elimination of its ligand, 1,25D3, leads to an increase resistance toL. majorinfection but only in a host that is predisposed for Th-1 immune responses.

Role of the Hypoxia-Inducible Factor Pathway in Normal and Osteoarthritic Meniscus and in Mice after Destabilization of the Medial Meniscus

Cartilage ◽  
2020 ◽  
pp. 194760352095814
Author(s):  
Austin V. Stone ◽  
Richard F. Loeser ◽  
Michael F. Callahan ◽  
Margaret A. McNulty ◽  
David L. Long ◽  
...  
Keyword(s):  
Gene Expression ◽  
Target Genes ◽  
Medial Meniscus ◽  
Transforming Growth Factor ◽  
Hypoxia Inducible Factor ◽  
Early Time ◽  
Wild Type ◽  
Inflammatory Stimuli ◽  
Hif Pathway

Objective Meniscus injury and the hypoxia-inducible factor (HIF) pathway are independently linked to osteoarthritis pathogenesis, but the role of the meniscus HIF pathway remains unclear. We sought to identify and evaluate HIF pathway response in normal and osteoarthritic meniscus and to examine the effects of Epas1 (HIF-2α) insufficiency in mice on early osteoarthritis development. Methods Normal and osteoarthritic human meniscus specimens were obtained and used for immunohistochemical evaluation and cell culture studies for the HIF pathway. Meniscus cells were treated with pro-inflammatory stimuli, including interleukins (IL)-1β, IL-6, transforming growth factor (TGF)-α, and fibronectin fragments (FnF). Target genes were also evaluated with HIF-1α and HIF-2α (Epas1) overexpression and knockdown. Wild-type ( n = 36) and Epas1+/− ( n = 30) heterozygous mice underwent destabilization of the medial meniscus (DMM) surgery and were evaluated at 2 and 4 weeks postoperatively for osteoarthritis development using histology. Results HIF-1α and HIF-2α immunostaining and gene expression did not differ between normal and osteoarthritic meniscus. While pro-inflammatory stimulation significantly increased both catabolic and anabolic gene expression in the meniscus, HIF-1α and Epas1 expression levels were not significantly altered. Epas1 overexpression significantly increased Col2a1 expression. Both wild-type and Epas1+/− mice developed osteoarthritis following DMM surgery. There were no significant differences between genotypes at either time point. Conclusion The HIF pathway is likely not responsible for osteoarthritic changes in the human meniscus. Additionally, Epas1 insufficiency does not protect against osteoarthritis development in the mouse at early time points after DMM surgery. The HIF pathway may be more important for protection against catabolic stress.

scholarly journals NADPH Oxidases Are Involved in Differentiation and Pathogenicity in Botrytis cinerea

2008 ◽  
Vol 21 (6) ◽  
pp. 808-819 ◽  
Author(s):  
Nadja Segmüller ◽  
Leonie Kokkelink ◽  
Sabine Giesbert ◽  
Daniela Odinius ◽  
Jan van Kan ◽  
...  
Keyword(s):  
Botrytis Cinerea ◽  
Nicotinamide Adenine Dinucleotide ◽  
Amino Acid Sequences ◽  
Host Tissue ◽  
Regulatory Subunit ◽  
Phytopathogenic Fungus ◽  
Wild Type ◽  
Nadph Oxidases ◽  
Knock Out

Nicotinamide adenine dinucleotide (NADPH) oxidases have been shown to be involved in various differentiation processes in fungi. We investigated the role of two NADPH oxidases in the necrotrophic phytopathogenic fungus, Botrytis cinerea. The genes bcnoxA and bcnoxB were cloned and characterized; their deduced amino acid sequences show high homology to fungal NADPH oxidases. Analyses of single and double knock-out mutants of both NADPH oxidase genes showed that both bcnoxA and bcnoxB are involved in formation of sclerotia. Both genes have a great impact on pathogenicity: whereas bcnoxB mutants showed a retarded formation of primary lesions, probably due to an impaired formation of penetration structures, bcnoxA mutants were able to penetrate host tissue in the same way as the wild type but were much slower in colonizing the host tissue. Double mutants showed an additive effect: they were aberrant in penetration and colonization of plant tissue and, therefore, almost nonpathogenic. To study the structure of the fungal Nox complex in more detail, bcnoxR (encoding a homolog of the mammalian p67phox, a regulatory subunit of the Nox complex) was functionally characterized. The phenotype of ΔbcnoxR mutants is identical to that of ΔbcnoxAB double mutants, providing evidence that BcnoxR is involved in activation of both Bcnox enzymes.

scholarly journals Indoleamine 2,3-Dioxygenase 2 Deficiency Exacerbates Imiquimod-Induced Psoriasis-Like Skin Inflammation

2020 ◽  
Vol 21 (15) ◽  
pp. 5515
Author(s):  
Kento Fujii ◽  
Yasuko Yamamoto ◽  
Yoko Mizutani ◽  
Kuniaki Saito ◽  
Mariko Seishima
Keyword(s):  
Immune Responses ◽  
Immune Cells ◽  
Skin Inflammation ◽  
Kynurenine Pathway ◽  
Immune Functions ◽  
Wild Type ◽  
Indoleamine 2,3 Dioxygenase ◽  
Tnf Α ◽  
In The Wild

Indoleamine 2,3-dioxygenase 1 (IDO1) is an enzyme known to suppress immune responses, and several reports have showed that it is associated with psoriasis. IDO2 is an isoform of IDO1, recently identified as a catalytic enzyme in the tryptophan-kynurenine pathway, which is expressed in dendritic cells and monocytes. The expression of IDO2 in immune cells suggests that IDO2 may contribute to immune functions. However, the role of IDO2 in the pathogenesis of psoriasis remains unclear. In this study, to elucidate the role of IDO2 in psoriasis, we assessed imiquimod (IMQ)-induced psoriasis-like dermatitis in IDO2 knockout (KO) mice. Skin inflammation, evaluated by scoring erythema, scaling, and ear thickness, was significantly worse in the IDO2 KO mice than in the wild-type (WT) mice. The mRNA expression levels of TNF-α, IL-23p19, and IL-17A, key cytokines involved in the development of psoriasis, were also increased in the IDO2 KO mice. Furthermore, immunohistochemistry revealed that the number of Ki67-positive cells in the epidermis and CD4-, CD8-, and IL-17-positive lymphocytes infiltrating the dermis were significantly increased in the IDO2 KO mice. These results suggest that IDO2 might decrease IL-17 expression, thereby resulting in the suppression of skin inflammation in IMQ-induced psoriasis-like dermatitis.

scholarly journals B-1a B Cells that Link the Innate and Adaptive Immune Responses Are Lacking in the Absence of the Spleen

2002 ◽  
Vol 195 (6) ◽  
pp. 771-780 ◽  
Author(s):  
Hedda Wardemann ◽  
Thomas Boehm ◽  
Neil Dear ◽  
Rita Carsetti
Keyword(s):  
B Cells ◽  
Immune Responses ◽  
B Cell ◽  
Innate Immune ◽  
Streptococcal Infections ◽  
Wild Type ◽  
Adaptive Immune ◽  
Encapsulated Bacteria ◽  
Increased Susceptibility

Splenectomized individuals are prone to overwhelming infections with encapsulated bacteria and splenectomy of mice increases susceptibility to streptococcal infections, yet the exact mechanism by which the spleen protects against such infections is unknown. Using congenitally asplenic mice as a model, we show that the spleen is essential for the generation of B-1a cells, a B cell population that cooperates with the innate immune system to control early bacterial and viral growth. Splenectomy of wild-type mice further demonstrated that the spleen is also important for the survival of B-1a cells. Transfer experiments demonstrate that lack of these cells, as opposed to the absence of the spleen per se, is associated with an inability to mount a rapid immune response against streptococcal polysaccharides. Thus, absence of the spleen and the associated increased susceptibility to streptococcal infections is correlated with lack of B-1a B cells. These findings reveal a hitherto unknown role of the spleen in generating and maintaining the B-1a B cell pool.

scholarly journals Toll-Like Receptor 9 Modulates Immune Responses to Aspergillus fumigatus Conidia in Immunodeficient and Allergic Mice

2008 ◽  
Vol 77 (1) ◽  
pp. 108-119 ◽  
Author(s):  
Hemanth Ramaprakash ◽  
Toshihiro Ito ◽  
Theodore J. Standiford ◽  
Steven L. Kunkel ◽  
Cory M. Hogaboam
Keyword(s):  
Immune Responses ◽  
Aspergillus Fumigatus ◽  
Inflammatory Responses ◽  
Fungal Growth ◽  
Lower Airway ◽  
Interleukin 17 ◽  
Toll Like Receptor ◽  
Wild Type ◽  
Immunodeficient Mice

ABSTRACT The role of Toll-like receptor 9 (TLR9) in antifungal responses in the immunodeficient and allergic host is unclear. We investigated the role of TLR9 in murine models of invasive aspergillosis and fungal asthma. Neutrophil-depleted TLR9 wild-type (TLR9+/+) and TLR9-deficient (TLR9−/−) mice were challenged with resting or swollen Aspergillus fumigatus conidia and monitored for survival and lung inflammatory responses. The absence of TLR9 delayed, but did not prevent, mortality in immunodeficient mice challenged with resting or swollen conidia compared to TLR9+/+ mice. In a fungal asthma model, TLR9+/+ and TLR9−/− mice were sensitized to soluble A. fumigatus antigens and challenged with resting or swollen A. fumigatus conidia, and both groups of mice were analyzed prior to and at days 7, 14, and 28 after the conidium challenge. When challenged with resting conidia, TLR9−/− mice exhibited significantly lower airway hyper-responsiveness compared to the TLR9+/+ groups. In contrast, A. fumigatus-sensitized TLR9−/− mice exhibited pulmonary fungal growth at days 14 and 28 after challenge with swollen conidia, a finding never observed in their allergic wild-type counterparts. Increased fungal growth in allergic TLR9−/− mice correlated with markedly decreased dectin-1 expression in whole lung samples and isolated dendritic cell populations. Further, whole lung levels of interleukin-17 were lower in allergic TLR9−/− mice compared to similar TLR9+/+ mice. Together, these data suggest that TLR9 modulates pulmonary antifungal immune responses to swollen conidia, possibly through the regulation of dectin-1 expression.

scholarly journals The Ethylene Response factor SmERF1 Improves Salinity Tolerance and Impacts Seed Size in Tobacco

2020 ◽  
Author(s):  
Wenping Hua ◽  
Chen Chen ◽  
Weiwei Kong ◽  
Zhezhi Wang
Keyword(s):  
Transgenic Tobacco ◽  
Seed Size ◽  
Plant Resistance ◽  
Seedling Stage ◽  
Ethylene Response Factor ◽  
Response Factor ◽  
Wild Type ◽  
Tobacco Plants ◽  
Ethylene Response ◽  
Significant Difference

Abstract Background Ethylene response factor (ERF) proteins play vital roles in plant resistance and plant development. However, little is known about the ERF transcription factors of Salvia miltiorrhiza, which is a famous Chinese herb with good resistance to stress. Result Screened from our previous transcriptome data, SmERF1, an ERF transcript factor, was isolated from S. miltiorrhiza. SmERF1 had a single AP domain and was classified in the ERF E3 subfamily. SmERF1-expressing tobacco plants showed slower growth, less biomass and a decrease in chlorophyll only at the seedling stage, and there was no significant difference in other growth stages. In addition, seeds of tobacco plants with SmERF1 expression were smaller and lighter than those of wild plants, similar to some AP2 TFs. Under NaCl treatment, transgenic tobacco lines showed better tolerance to salinity, and the proline content, SOD and POD activities of transgenic lines were higher than those of wild-type plants, while MDA content was lower than that of wild-type plants. Furthermore, we determined the phytohormones related to plant resistance and showed that transgenic tobacco plants had higher ABA levels and lower GA levels than wild tobacco. The expression of SmERF1 regulated the expression of key enzyme genes related to plant hormone biosynthesis, such as NtSDR, NtGA20ox, NtACO and NtACS. Conclusions The SmERF1-expression in tobacco affect plant growth at seedling stage, and increase plant tolerance to salt. And the expression of SmERF1 cause tobacco seeds smaller and lighter. Our study suggested that SmERF1 enhanced tobacco tolerance to salt and impacted seed size through an ABA-dependent pathway.

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