HOS15 is a transcriptional corepressor of NPR1-mediated gene activation of plant immunity

Transcriptional regulation is a complex and pivotal process in living cells. HOS15 is a transcriptional corepressor. Although transcriptional repressors generally have been associated with inactive genes, increasing evidence indicates that, through poorly understood mechanisms, transcriptional corepressors also associate with actively transcribed genes. Here, we show that HOS15 is the substrate receptor for an SCF/CUL1 E3 ubiquitin ligase complex (SCFHOS15) that negatively regulates plant immunity by destabilizing transcriptional activation complexes containing NPR1 and associated transcriptional activators. In unchallenged conditions, HOS15 continuously eliminates NPR1 to prevent inappropriate defense gene expression. Upon defense activation, HOS15 preferentially associates with phosphorylated NPR1 to stimulate rapid degradation of transcriptionally active NPR1 and thus limit the extent of defense gene expression. Our findings indicate that HOS15-mediated ubiquitination and elimination of NPR1 produce effects contrary to those of CUL3-containing ubiquitin ligase that coactivate defense gene expression. Thus, HOS15 plays a key role in the dynamic regulation of pre- and postactivation host defense.

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Induction of Plant Defense Gene Expression by Plant Activators and Pseudomonas syringae pv. tomato in Greenhouse-Grown Tomatoes

Phytopathology ◽

10.1094/phyto-98-11-1226 ◽

2008 ◽

Vol 98 (11) ◽

pp. 1226-1232 ◽

Cited By ~ 35

Author(s):

M. A. B. Herman ◽

J. K. Davidson ◽

C. D. Smart

Keyword(s):

Gene Expression ◽

Plant Defense ◽

Pseudomonas Syringae ◽

Systemic Acquired Resistance ◽

Marker Gene ◽

Gene Activation ◽

Systemic Resistance ◽

Defense Gene Expression ◽

Defense Gene ◽

Bacterial Speck

Plant activators provide an appealing management option for bacterial diseases of greenhouse-grown tomatoes. Two types of plant activators, one that induces systemic acquired resistance (SAR) and a second that activates induced systemic resistance (ISR), were evaluated for control of Pseudomonas syringae pv. tomato and effect on plant defense gene activation. Benzothiadiazole (BTH, SAR-inducing compound) effectively reduced bacterial speck incidence and severity, both alone and in combination with the ISR-inducing product. Application of BTH also led to elevated activation of salicylic acid and ethylene-mediated responses, based on real-time polymerase chain reaction analysis of marker gene expression levels. In contrast, the ISR-inducing product (made up of plant growth-promoting rhizobacteria) inconsistently modified defense gene expression and did not provide disease control to the same level as did BTH. No antagonism was observed by combining the two activators as control of bacterial speck was similar to or better than BTH alone.

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Overexpression of Pti5 in Tomato Potentiates Pathogen-Induced Defense Gene Expression and Enhances Disease Resistance to Pseudomonas syringae pv. tomato

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi.2001.14.12.1453 ◽

2001 ◽

Vol 14 (12) ◽

pp. 1453-1457 ◽

Cited By ~ 60

Author(s):

Ping He ◽

Randall F. Warren ◽

Tiehan Zhao ◽

Libo Shan ◽

Lihuang Zhu ◽

...

Keyword(s):

Gene Expression ◽

Disease Resistance ◽

Pseudomonas Syringae ◽

Transcriptional Activation ◽

Induced Defense ◽

Constitutive Expression ◽

Disease Resistance Gene ◽

Defense Gene Expression ◽

Positive Role ◽

Defense Gene

The tomato Pti5 gene encodes a pathogen-inducible ethylene response element-binding protein-like transcription factor that interacts with the disease resistance gene product Pto. Overexpression of Pti5 or Pti5-VP16, a translational fusion with a constitutive transcriptional activation domain, in tomato enhanced resistance to Pseudomonas syringae pv. tomato. Constitutive expression of Pti5 or Pti5-VP16 did not affect the basal level of pathogenesis-related gene expression, but it accelerated pathogen-induced expression of GluB and Catalase. The results demonstrate a positive role of Pti5 in defense gene regulation and disease resistance and suggest that a pathogen-activated posttran-scriptional regulatory step is necessary for the pathogen induction of the defense gene expression.

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

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1701101114 ◽

2017 ◽

Vol 114 (24) ◽

pp. 6388-6393 ◽

Cited By ~ 55

Author(s):

Lotte Caarls ◽

Joyce Elberse ◽

Mo Awwanah ◽

Nora R. Ludwig ◽

Michel de Vries ◽

...

Keyword(s):

Gene Expression ◽

Jasmonic Acid ◽

Plant Immunity ◽

Mamestra Brassicae ◽

Loss Of Function ◽

Defense Gene Expression ◽

Defense Gene ◽

Inactive Form ◽

Quadruple Mutant

The 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 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. Because 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 overaccumulation 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.

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Jasmonate and salicylate as global signals for defense gene expression

Current Opinion in Plant Biology ◽

10.1016/s1369-5266(98)80264-1 ◽

1998 ◽

Vol 1 (5) ◽

pp. 404-411 ◽

Cited By ~ 605

Author(s):

Philippe Reymond ◽

Edward E. Farmer

Keyword(s):

Gene Expression ◽

Defense Gene Expression ◽

Defense Gene

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Evaluation of the Use of the TobaccoPR-1aPromoter to Monitor Defense Gene Expression by the Luciferase Bioluminescence Reporter System

Bioscience Biotechnology and Biochemistry ◽

10.1271/bbb.110326 ◽

2011 ◽

Vol 75 (9) ◽

pp. 1796-1800 ◽

Cited By ~ 8

Author(s):

Sachiko ONO ◽

Masahiro KUSAMA ◽

Rieko OGURA ◽

Kazuyuki HIRATSUKA

Keyword(s):

Gene Expression ◽

Reporter System ◽

Defense Gene Expression ◽

Defense Gene

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The Arabidopsis Mediator complex subunits MED14/SWP and MED16/SFR6/IEN1 differentially regulate defense gene expression in plant immune responses

The Plant Journal ◽

10.1111/tpj.12216 ◽

2013 ◽

Vol 75 (3) ◽

pp. 484-497 ◽

Cited By ~ 45

Author(s):

Xudong Zhang ◽

Jin Yao ◽

Yanping Zhang ◽

Yijun Sun ◽

Zhonglin Mou

Keyword(s):

Gene Expression ◽

Immune Responses ◽

Mediator Complex ◽

Defense Gene Expression ◽

Defense Gene

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Characterization of a Diffusible Signal Capable of Inducing Defense Gene Expression in Tobacco

PLANT PHYSIOLOGY ◽

10.1104/pp.113.2.621 ◽

1997 ◽

Vol 113 (2) ◽

pp. 621-629 ◽

Cited By ~ 18

Author(s):

J. Chappell ◽

A. Levine ◽

R. Tenhaken ◽

M. Lusso ◽

C. Lamb

Keyword(s):

Gene Expression ◽

Defense Gene Expression ◽

Defense Gene

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Gene activation precedes DNA demethylation in response to infection in human dendritic cells

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1814700116 ◽

2019 ◽

Vol 116 (14) ◽

pp. 6938-6943 ◽

Cited By ~ 39

Author(s):

Alain Pacis ◽

Florence Mailhot-Léonard ◽

Ludovic Tailleux ◽

Haley E. Randolph ◽

Vania Yotova ◽

...

Keyword(s):

Gene Expression ◽

Dna Methylation ◽

Dendritic Cells ◽

Transcriptional Activation ◽

Time Course ◽

Gene Activation ◽

Dna Demethylation ◽

Epigenetic Mark ◽

Distal Enhancer ◽

Human Dendritic Cells

DNA methylation is considered to be a relatively stable epigenetic mark. However, a growing body of evidence indicates that DNA methylation levels can change rapidly; for example, in innate immune cells facing an infectious agent. Nevertheless, the causal relationship between changes in DNA methylation and gene expression during infection remains to be elucidated. Here, we generated time-course data on DNA methylation, gene expression, and chromatin accessibility patterns during infection of human dendritic cells withMycobacterium tuberculosis. We found that the immune response to infection is accompanied by active demethylation of thousands of CpG sites overlapping distal enhancer elements. However, virtually all changes in gene expression in response to infection occur before detectable changes in DNA methylation, indicating that the observed losses in methylation are a downstream consequence of transcriptional activation. Footprinting analysis revealed that immune-related transcription factors (TFs), such as NF-κB/Rel, are recruited to enhancer elements before the observed losses in methylation, suggesting that DNA demethylation is mediated by TF binding to cis-acting elements. Collectively, our results show that DNA demethylation plays a limited role to the establishment of the core regulatory program engaged upon infection.

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