scholarly journals Sumoylation E3 Ligase SIZ1 Modulates Plant Immunity Partly through the Immune Receptor Gene SNC1 in Arabidopsis

2017 ◽  
Vol 30 (4) ◽  
pp. 334-342 ◽  
Author(s):  
Mingyue Gou ◽  
Quansheng Huang ◽  
Weiqiang Qian ◽  
Zemin Zhang ◽  
Zhenhua Jia ◽  
...  
Keyword(s):  
Plant Immunity ◽  
Receptor Gene ◽  
E3 Ligase ◽  
Transcript Level ◽  
Defense Responses ◽  
Fine Tuning ◽  
Loss Of Function ◽  
In Planta ◽  
Immune Receptor ◽  
Mutant Phenotypes

The small ubiqutin-like modifier E3 ligase SIZ1 regulates multiple processes in Arabidopsis, including salicylic-acid-dependent immune responses. However, the targets of SIZ1 in plant immunity are not known. Here, we provide evidence that the plant immune receptor nucleotide-binding leucine-rich repeat gene SNC1 partially mediates the regulation of plant immunity by SIZ1. The siz1 loss-of-function mutant has an autoimmune phenotype that is dependent on SNC1 and temperature. Overexpression of SIZ1 partially rescues autoimmune mutant phenotypes induced by activation or overaccumulation of SNC1, and the SNC1 protein amount is attenuated by SIZ1 overexpression. In addition, overexpression of the F-box protein CPR1 that degrades the SNC1 protein inhibits the growth defects and disease resistance of the siz1 mutant. Furthermore, we found that the SNC1 protein is sumoylated in planta. Although it remains to be determined whether SIZ1 primarily modulates the SNC1 protein via sumoylation or affects SNC1 transcript level, our data indicate that SNC1 is a major mediator of defense response modulated by SIZ1 and that SNC1 is a crucial target for fine-tuning plant defense responses.

scholarly journals A Role of Cytokinin Transporter in Arabidopsis Immunity

2017 ◽  
Vol 30 (4) ◽  
pp. 325-333 ◽  
Author(s):  
Shuai Wang ◽  
Shu Wang ◽  
Qi Sun ◽  
Leiyun Yang ◽  
Ying Zhu ◽  
...  
Keyword(s):  
Disease Resistance ◽  
Induced Defense ◽  
Plant Immunity ◽  
Receptor Gene ◽  
Defense Responses ◽  
Plant Growth And Development ◽  
Immune Receptor ◽  
Receptor Mutant ◽  
Induced Defense Responses

The phytohormone cytokinin (CK) is not only essential for plant growth and development but also impacts plant immunity. A mutant screen in a constitutively active plant immune receptor mutant snc1 (suppressor of npr1, constitutive1) identified a suppressor mutation of SNC1-induced defense responses in an ABC transporter coding gene ABCG14. ABCG14 transports CK from roots to the shoots, and the suppression of the SNC1-mediated defense response by the loss of ABCG14 is due to a deficiency of trans-zeatin (tZ)-type CK in the shoot. In addition, exogenous application of the tZ-type CK enhances disease resistance associated with increased expression of the plant immune receptor gene SNC1. Taken together, this study further established the role of tZ-type CK in disease resistance and suggests a new intersection of CKs with plant immunity at the expression regulation of a plant immune receptor gene.

scholarly journals Arabidopsis CALMODULIN-BINDING PROTEIN 60b plays dual roles in plant immunity

2021 ◽  
Author(s):  
Weijie Huang ◽  
Zhongshou Wu ◽  
Hainan Tian ◽  
Xin Li ◽  
Yuelin Zhang
Keyword(s):  
Systemic Acquired Resistance ◽  
Binding Protein ◽  
Plant Immunity ◽  
Interleukin 1 ◽  
Constitutive Expression ◽  
Defense Responses ◽  
Negative Regulator ◽  
Loss Of Function ◽  
Constitutive Defense ◽  
Calmodulin Binding

AbstractArabidopsis SYSTEMIC ACQUIRED RESISTANCE DEFICIENT 1 (SARD1) and CALMODULIN-BINDING PROTEIN 60g (CBP60g) are two master transcription factors that regulate many defense-related genes in plant immunity. They are required for immunity downstream of the receptor-like protein SUPPRESSOR OF NPR1-1, CONSTITUTIVE 2 (SNC2). Constitutive defense responses in the gain-of-function autoimmune snc2-1D mutant are modestly affected by either sard1 or cbp60g single mutants, but completely suppressed by the sard1 cbp60g double mutant. Here we report that CBP60b, another member of the CBP60 family, also functions as a positive regulator of SNC2-mediated immunity. Loss-of-function mutations of CBP60b suppress the constitutive expression of SARD1 and enhanced disease resistance in cbp60g-1 snc2-1D, whereas over-expression of CBP60b leads to elevated SARD1 expression and constitutive defense responses. In addition, transient expression of CBP60b in Nicotiana benthamiana activates the expression of the pSARD1::luciferase reporter gene. Chromatin immunoprecipitation assay further showed that CBP60b is recruited to the promoter region of SARD1, suggesting that it directly regulates SARD1 expression. Interestingly, knocking out CBP60b in the wild type background leads to ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1)-dependent autoimmunity, suggesting that CBP60b is required for the expression of a guardee/decoy or a negative regulator in immunity mediated by receptors carrying an N-terminal TIR (Toll-interleukin-1 receptor-like) domain.Significance statementArabidopsis SARD1 serves as a master transcription factor in plant immunity. In this study, we showed that CBP60b positively regulates SARD1 expression, and TIR signaling is activated when CBP60b is inactivated.

scholarly journals Arabidopsis JASMONATE-INDUCED OXYGENASES down-regulate plant immunity by hydroxylation and inactivation of the hormone jasmonic acid

2017 ◽  
Author(s):  
Lotte Caarls ◽  
Joyce Elberse ◽  
Mo Awwanah ◽  
Nora R. Ludwig ◽  
Michel de Vries ◽  
...  
Keyword(s):  
Gene Expression ◽  
Jasmonic Acid ◽  
Plant Immunity ◽  
Defense Responses ◽  
Mamestra Brassicae ◽  
Loss Of Function ◽  
Defense Gene Expression ◽  
Quadruple Mutant ◽  
Arabidopsis Mutant

ABSTRACTThe phytohormone jasmonic acid (JA) is vital in plant defense and development. Although biosynthesis of JA and activation of JA-responsive gene expression by the bioactive form JA-isoleucine (JA-Ile) have been well-studied, knowledge on JA metabolism is incomplete. In particular, the enzyme that hydroxylates JA to 12-OH-JA, an inactive form of JA that accumulates after wounding and pathogen attack, is unknown. Here, we report the identification of four paralogous 2-oxoglutarate/Fe(II)-dependent oxygenases in Arabidopsis thaliana as JA hydroxylases and show that they down-regulate JA-dependent responses. As they are induced by JA we named them JASMONATE-INDUCED OXYGENASEs (JOXs). Concurrent mutation of the four genes in a quadruple Arabidopsis mutant resulted in increased defense gene expression and increased resistance to the necrotrophic fungus Botrytis cinerea and the caterpillar Mamestra brassicae. In addition, root and shoot growth of the plants was inhibited. Metabolite analysis of leaves showed that loss of function of the four JOX enzymes resulted in over-accumulation of JA and in reduced turnover of JA into 12-OH-JA. Transformation of the quadruple mutant with each JOX gene strongly reduced JA levels, demonstrating that all four JOXs inactivate JA in plants. The in vitro catalysis of 12-OH-JA from JA by recombinant enzyme could be confirmed for three JOXs. The identification of the enzymes responsible for hydroxylation of JA reveals a missing step in JA metabolism, which is important for the inactivation of the hormone and subsequent down-regulation of JA-dependent defenses.SIGNIFICANCE STATEMENTIn plants, the hormone jasmonic acid (JA) is synthesized in response to attack by pathogens and herbivores, leading to activation of defense responses. Rapidly following JA accumulation, the hormone is metabolized, presumably to prevent inhibitive effects of high JA levels on growth and development. The enzymes that directly inactivate JA were so far unknown. Here, we identify four jasmonate-induced oxygenases (JOXs) in Arabidopsis that hydroxylate jasmonic acid to form inactive 12-OH-JA. A mutant that no longer produces the four enzymes hyperaccumulates JA, exhibits reduced growth, and is highly resistant to attackers that are sensitive to JA-dependent defense. The JOX enzymes thus play an important role in determining the amplitude and duration of JA responses to balance the growth-defense tradeoff.

scholarly journals The Flower-Infecting Fungus Ustilaginoidea virens Subverts Plant Immunity by Secreting a Chitin-Binding Protein

2021 ◽  
Vol 12 ◽  
Author(s):  
Guo-Bang Li ◽  
Jing Fan ◽  
Jin-Long Wu ◽  
Jia-Xue He ◽  
Jie Liu ◽  
...  
Keyword(s):  
Induced Defense ◽  
Plant Immunity ◽  
Floral Organ ◽  
Defense Responses ◽  
High Yield ◽  
In Planta ◽  
Callose Deposition ◽  
Ustilaginoidea Virens ◽  
Chitin Binding Protein

Ustilaginoidea virens is a biotrophic fungal pathogen specifically colonizing rice floral organ and causes false smut disease of rice. This disease has emerged as a serious problem that hinders the application of high-yield rice cultivars, by reducing grain yield and quality as well as introducing mycotoxins. However, the pathogenic mechanisms of U. virens are still enigmatic. Here we demonstrate that U. virens employs a secreted protein UvCBP1 to manipulate plant immunity. In planta expression of UvCBP1 led to compromised chitin-induced defense responses in Arabidopsis and rice, including burst of reactive oxygen species (ROS), callose deposition, and expression of defense-related genes. In vitro-purified UvCBP1 protein competes with rice chitin receptor OsCEBiP to bind to free chitin, thus impairing chitin-triggered rice immunity. Moreover, UvCBP1 could significantly promote infection of U. virens in rice flowers. Our results uncover a mechanism of a floral fungus suppressing plant immunity and pinpoint a universal role of chitin-battlefield during plant–fungi interactions.

scholarly journals Identification of Susceptibility Genes in Castanea sativa and Their Transcription Dynamics following Pathogen Infection

Plants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 913
Author(s):  
Vera Pavese ◽  
Andrea Moglia ◽  
Paolo Gonthier ◽  
Daniela Torello Marinoni ◽  
Emile Cavalet-Giorsa ◽  
...  
Keyword(s):  
Phylogenetic Analyses ◽  
Castanea Sativa ◽  
Transcript Level ◽  
Cryphonectria Parasitica ◽  
Plant Responses ◽  
Functional Domain ◽  
Loss Of Function ◽  
Pathogen Infection ◽  
Domain Identification ◽  
S Genes

Castanea sativa is one of the main multipurpose tree species valued for its timber and nuts. This species is susceptible to two major diseases, ink disease and chestnut blight, caused by Phytophthora spp. and Cryphonectria parasitica, respectively. The loss-of-function mutations of genes required for the onset of pathogenesis, referred to as plant susceptibility (S) genes, are one mechanism of plant resistance against pathogens. On the basis of sequence homology, functional domain identification, and phylogenetic analyses, we report for the first time on the identification of S-genes (mlo1, dmr6, dnd1, and pmr4) in the Castanea genus. The expression dynamics of S-genes were assessed in C. sativa and C. crenata plants inoculated with P. cinnamomi and C. parasitica. Our results highlighted the upregulation of pmr4 and dmr6 in response to pathogen infection. Pmr4 was strongly expressed at early infection phases of both pathogens in C. sativa, whereas in C. crenata, no significant upregulation was observed. The infection of P. cinnamomi led to a higher increase in the transcript level of dmr6 in C. sativa compared to C. crenata-infected samples. For a better understanding of plant responses, the transcript levels of defense genes gluB and chi3 were also analyzed.

scholarly journals A peroxisomal β-oxidative pathway contributes to the formation of C6–C1 aromatic volatiles in poplar

2021 ◽  
Author(s):  
Nathalie D Lackus ◽  
Axel Schmidt ◽  
Jonathan Gershenzon ◽  
Tobias G Köllner
Keyword(s):  
Cinnamic Acid ◽  
Aromatic Compounds ◽  
Populus Trichocarpa ◽  
Alternative Pathway ◽  
Gene Families ◽  
Defense Responses ◽  
In Planta ◽  
Black Cottonwood ◽  
Oxidative Pathway

AbstractBenzenoids (C6–C1 aromatic compounds) play important roles in plant defense and are often produced upon herbivory. Black cottonwood (Populus trichocarpa) produces a variety of volatile and nonvolatile benzenoids involved in various defense responses. However, their biosynthesis in poplar is mainly unresolved. We showed feeding of the poplar leaf beetle (Chrysomela populi) on P. trichocarpa leaves led to increased emission of the benzenoid volatiles benzaldehyde, benzylalcohol, and benzyl benzoate. The accumulation of salicinoids, a group of nonvolatile phenolic defense glycosides composed in part of benzenoid units, was hardly affected by beetle herbivory. In planta labeling experiments revealed that volatile and nonvolatile poplar benzenoids are produced from cinnamic acid (C6–C3). The biosynthesis of C6–C1 aromatic compounds from cinnamic acid has been described in petunia (Petunia hybrida) flowers where the pathway includes a peroxisomal-localized chain shortening sequence, involving cinnamate-CoA ligase (CNL), cinnamoyl-CoA hydratase/dehydrogenase (CHD), and 3-ketoacyl-CoA thiolase (KAT). Sequence and phylogenetic analysis enabled the identification of small CNL, CHD, and KAT gene families in P. trichocarpa. Heterologous expression of the candidate genes in Escherichia coli and characterization of purified proteins in vitro revealed enzymatic activities similar to those described in petunia flowers. RNA interference-mediated knockdown of the CNL subfamily in gray poplar (Populus x canescens) resulted in decreased emission of C6–C1 aromatic volatiles upon herbivory, while constitutively accumulating salicinoids were not affected. This indicates the peroxisomal β-oxidative pathway participates in the formation of volatile benzenoids. The chain shortening steps for salicinoids, however, likely employ an alternative pathway.

scholarly journals Method for the Production and Purification of Plant Immuno-Active Xylanase from Trichoderma

2021 ◽  
Vol 22 (8) ◽  
pp. 4214
Author(s):  
Gautam Anand ◽  
Meirav Leibman-Markus ◽  
Dorin Elkabetz ◽  
Maya Bar
Keyword(s):  
Immune System ◽  
Plant Defense ◽  
Plant Immunity ◽  
Xylanase Activity ◽  
Hydrolytic Enzymes ◽  
Adaptive Immune System ◽  
Defense Responses ◽  
Plant Defense Responses ◽  
Xylanase Production ◽  
Ideal System

Plants lack a circulating adaptive immune system to protect themselves against pathogens. Therefore, they have evolved an innate immune system based upon complicated and efficient defense mechanisms, either constitutive or inducible. Plant defense responses are triggered by elicitors such as microbe-associated molecular patterns (MAMPs). These components are recognized by pattern recognition receptors (PRRs) which include plant cell surface receptors. Upon recognition, PRRs trigger pattern-triggered immunity (PTI). Ethylene Inducing Xylanase (EIX) is a fungal MAMP protein from the plant-growth-promoting fungi (PGPF)–Trichoderma. It elicits plant defense responses in tobacco (Nicotiana tabacum) and tomato (Solanum lycopersicum), making it an excellent tool in the studies of plant immunity. Xylanases such as EIX are hydrolytic enzymes that act on xylan in hemicellulose. There are two types of xylanases: the endo-1, 4-β-xylanases that hydrolyze within the xylan structure, and the β-d-xylosidases that hydrolyze the ends of the xylan chain. Xylanases are mainly synthesized by fungi and bacteria. Filamentous fungi produce xylanases in high amounts and secrete them in liquid cultures, making them an ideal system for xylanase purification. Here, we describe a method for cost- and yield-effective xylanase production from Trichoderma using wheat bran as a growth substrate. Xylanase produced by this method possessed xylanase activity and immunogenic activity, effectively inducing a hypersensitive response, ethylene biosynthesis, and ROS burst.

scholarly journals The Effect of Fusarium verticillioides Fumonisins on Fatty Acids, Sphingolipids, and Oxylipins in Maize Germlings

2021 ◽  
Vol 22 (5) ◽  
pp. 2435
Author(s):  
Marzia Beccaccioli ◽  
Manuel Salustri ◽  
Valeria Scala ◽  
Matteo Ludovici ◽  
Andrea Cacciotti ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fusarium Verticillioides ◽  
Fungal Growth ◽  
Defense Responses ◽  
Ceramide Synthase ◽  
Ear Rot ◽  
In Planta ◽  
Disease Symptoms ◽  
The Impact

Fusarium verticillioides causes multiple diseases of Zea mays (maize) including ear and seedling rots, contaminates seeds and seed products worldwide with toxic chemicals called fumonisins. The role of fumonisins in disease is unclear because, although they are not required for ear rot, they are required for seedling diseases. Disease symptoms may be due to the ability of fumonisins to inhibit ceramide synthase activity, the expected cause of lipids (fatty acids, oxylipins, and sphingolipids) alteration in infected plants. In this study, we explored the impact of fumonisins on fatty acid, oxylipin, and sphingolipid levels in planta and how these changes affect F. verticillioides growth in maize. The identity and levels of principal fatty acids, oxylipins, and over 50 sphingolipids were evaluated by chromatography followed by mass spectrometry in maize infected with an F. verticillioides fumonisin-producing wild-type strain and a fumonisin-deficient mutant, after different periods of growth. Plant hormones associated with defense responses, i.e., salicylic and jasmonic acid, were also evaluated. We suggest that fumonisins produced by F. verticillioides alter maize lipid metabolism, which help switch fungal growth from a relatively harmless endophyte to a destructive necrotroph.

scholarly journals Crosstalk of CREB and Fos/Jun on a single cis-element: transcriptional repression of the steroidogenic acute regulatory protein gene

2007 ◽  
Vol 39 (4) ◽  
pp. 261-277 ◽  
Author(s):  
Pulak R Manna ◽  
Douglas M Stocco
Keyword(s):  
Transcriptional Repression ◽  
Protein Gene ◽  
Binding Protein ◽  
Regulatory Protein ◽  
Ectopic Expression ◽  
Fine Tuning ◽  
Creb Binding Protein ◽  
Loss Of Function ◽  
Cis Element ◽  
Steroidogenic Acute Regulatory

AbstractTranscriptional regulation of the steroidogenic acute regulatory (StAR) protein gene by cAMP-dependent mechanisms occurs in the absence of a consensus cAMP-response element (CRE; TGACGTCA) and is mediated by several sequence-specific transcription factors. We previously identified three CRE-like sites (within the −151/−1 bp cAMP-responsive region of the mouse StAR gene), of which the CRE2 site overlaps with an activator protein-1 (AP-1) motif (TGACTGA, designated as CRE2/AP-1) that can bind both CRE and AP-1 DNA-binding proteins. The present studies were aimed at exploring the functional crosstalk between CREB (CRE-binding protein) and cFos/cJun (AP-1 family members) on the CRE2/AP-1 element and its role in regulating transcription of the StAR gene. Using MA-10 mouse Leydig tumor cells, we demonstrate that the CRE and AP-1 families of proteins interact with the CRE2/AP-1 sequence. CREB, cFos, and cJun proteins were found to bind to the CRE2/AP-1 motif but not the CRE1 and CRE3 sites. Treatment with the cAMP analog (Bu)2cAMP augmented phosphorylation of CREB (Ser133), cFos (Thr325), and cJun (ser73). Chromatin immunoprecipitation studies revealed that the induction of CREB, cFos, and cJun by (Bu)2cAMP was correlated with protein–DNA interactions and recruitment of the coactivator CREB-binding protein (CBP) to the StAR promoter. EMSA studies employing CREB and cFos/cJun proteins demonstrated competition between these factors for binding to the CRE2/AP-1 motif. Transfection of cells containing the −151/−1 StAR reporter with CREB and cFos/cJun resulted in trans-repression of the StAR gene, an event tightly associated with CBP, demonstrating that both CREB and Fos/Jun compete with each other for binding with limited amounts of intracellular CBP. Overexpression of adenovirus E1A, which binds and inactivates CBP, markedly suppressed StAR gene expression. Ectopic expression of CBP eliminated the repression of the StAR gene by E1A and potentiated the activity of CREB and cFos/cJun on StAR promoter responsiveness. These findings identify molecular events involved in crosstalk between CREB and cFos/cJun, which confer both gain and loss of function on a single cis-element in fine-tuning of the regulatory events involved in transcription of the StAR gene.

scholarly journals Goα Regulates Volatile Anesthetic Action in Caenorhabditis elegans

Genetics ◽  
2001 ◽  
Vol 158 (2) ◽  
pp. 643-655 ◽  
Author(s):  
Bruno van Swinderen ◽  
Laura B Metz ◽  
Laynie D Shebester ◽  
Jane E Mendel ◽  
Paul W Sternberg ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Novel Mutation ◽  
Volatile Anesthetic ◽  
Loss Of Function ◽  
Wild Type ◽  
Α Subunit ◽  
C Elegans ◽  
Missense Mutant ◽  
Anesthetic Action ◽  
Mutant Phenotypes

Abstract To identify genes controlling volatile anesthetic (VA) action, we have screened through existing Caenorhabditis elegans mutants and found that strains with a reduction in Go signaling are VA resistant. Loss-of-function mutants of the gene goa-1, which codes for the α-subunit of Go, have EC50s for the VA isoflurane of 1.7- to 2.4-fold that of wild type. Strains overexpressing egl-10, which codes for an RGS protein negatively regulating goa-1, are also isoflurane resistant. However, sensitivity to halothane, a structurally distinct VA, is differentially affected by Go pathway mutants. The RGS overexpressing strains, a goa-1 missense mutant found to carry a novel mutation near the GTP-binding domain, and eat-16(rf) mutants, which suppress goa-1(gf) mutations, are all halothane resistant; goa-1(null) mutants have wild-type sensitivities. Double mutant strains carrying mutations in both goa-1 and unc-64, which codes for a neuronal syntaxin previously found to regulate VA sensitivity, show that the syntaxin mutant phenotypes depend in part on goa-1 expression. Pharmacological assays using the cholinesterase inhibitor aldicarb suggest that VAs and GOA-1 similarly downregulate cholinergic neurotransmitter release in C. elegans. Thus, the mechanism of action of VAs in C. elegans is regulated by Goα, and presynaptic Goα-effectors are candidate VA molecular targets.

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