UV RESISTANCE LOCUS8 mediates ultraviolet-B-induced stomatal closure in an ethylene-dependent manner

A critical component of plant immunity against invading pathogens is the rapid transcriptional reprogramming of the attacked cell to minimize virulence. Many adapted plant bacterial pathogens use type III effector (T3E) proteins to interfere with plant defense responses, including the induction of immunity genes. The elucidation of effector function is essential to understanding bacterial pathogenesis. Here, we show that XopS, a T3E of Xanthomonas campestris pv. vesicatoria (Xcv), interacts with and inhibits the proteasomal degradation of the transcriptional regulator of defense gene expression WRKY40. Virus-induced gene silencing of WRKY40 in pepper enhanced plant tolerance towards Xcv infection, indicating it represses immunity. Stabilization of WRKY40 by XopS reduces the expression of its targets including salicylic acid (SA)-responsive genes and the jasmonic acid (JA) signaling repressor JAZ8. Xcv bacteria lacking XopS display significantly reduced virulence when surface inoculated onto susceptible pepper leaves. XopS delivery by Xcv, as well as ectopic expression of XopS in Arabidopsis or Nicotiana benthamiana prevented stomatal closure in response to bacteria and biotic elicitors in a WRKY40 dependent manner. This suggests that XopS interferes with preinvasion as well as with apoplastic defense by manipulating WRKY40 stability and gene expression eventually altering phytohormone crosstalk to promote pathogen proliferation.

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Rapid Reversion from Monomer to Dimer Regenerates the Ultraviolet-B Photoreceptor UV RESISTANCE LOCUS8 in Intact Arabidopsis Plants

PLANT PHYSIOLOGY ◽

10.1104/pp.112.206805 ◽

2012 ◽

Vol 161 (1) ◽

pp. 547-555 ◽

Cited By ~ 41

Author(s):

Monika Heilmann ◽

Gareth I. Jenkins

Keyword(s):

Ultraviolet B ◽

Uv Resistance

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Ultraviolet B radiation induction of ornithine decarboxylase gene expression in mouse epidermis

Biochemical Journal ◽

10.1042/bj2700565 ◽

1990 ◽

Vol 270 (3) ◽

pp. 565-568 ◽

Cited By ~ 8

Author(s):

C F Rosen ◽

D Gajic ◽

Q Jia ◽

D J Drucker

Keyword(s):

Gene Expression ◽

Ornithine Decarboxylase ◽

Hairless Mouse ◽

Ultraviolet B ◽

Dependent Manner ◽

Mouse Epidermis ◽

Cellular Effects ◽

Mrna Transcripts ◽

Maximal Induction

The cellular effects of u.v. radiation have been studied by using a hairless-mouse model in vivo. U.v. B radiation (u.v.B) induced the activity of the enzyme ornithine decarboxylase (ODC) in mouse epidermis. Maximal induction was noted after radiation with 90 mJ/cm2, and increased ODC activity was first detected 2 h after u.v.B exposure. U.v.B. also induced the expression of the ODC gene in a time- and dose-dependent manner, but did not induce the levels of actin mRNA transcripts. Cycloheximide treatment did not alter basal levels of ODC mRNA transcripts and had no effect on the u.v.B induction of ODC-gene expression. The results of these experiments demonstrate that u.v.B radiation induces both the expression of the ODC gene and the activity of the enzyme, and provides a useful ‘in vivo’ paradigm for the analysis of the molecular effects of u.v.B radiation.

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Single-stranded oligodeoxynucleotides induce plant defence in Arabidopsis thaliana

Annals of Botany ◽

10.1093/aob/mcaa061 ◽

2020 ◽

Vol 126 (3) ◽

pp. 413-422

Author(s):

Laila Toum ◽

Gabriela Conti ◽

Francesca Coppola Guerriero ◽

Valeria P Conforte ◽

Franco A Garolla ◽

...

Keyword(s):

Arabidopsis Thaliana ◽

Nadph Oxidase ◽

Pseudomonas Syringae ◽

Plant Immunity ◽

Stomatal Closure ◽

Plant Defence ◽

Oxidase Inhibitor ◽

Bacterial Toxin ◽

Dependent Manner ◽

Concentration Dependent Manner

Abstract Background and Aims Single-stranded DNA oligodeoxynucleotides (ssODNs) have been shown to elicit immune responses in mammals. In plants, RNA and genomic DNA can activate immunity, although the exact mechanism through which they are sensed is not clear. The aim of this work was to study the possible effect of ssODNs on plant immunity. Key Results The ssODNs IMT504 and 2006 increased protection against the pathogens Pseudomonas syringae pv. tomato DC3000 and Botrytis cinerea but not against tobacco mosaic virus-Cg when infiltrated in Arabidopsis thaliana. In addition, ssODNs inhibited root growth and promoted stomatal closure in a concentration-dependent manner, with half-maximal effective concentrations between 0.79 and 2.06 µm. Promotion of stomatal closure by ssODNs was reduced by DNase I treatment. It was also diminished by the NADPH oxidase inhibitor diphenyleneiodonium and by coronatine, a bacterial toxin that inhibits NADPH oxidase-dependent reactive oxygen species (ROS) synthesis in guard cells. In addition it was found that ssODN-mediated stomatal closure was impaired in bak1-5, bak1-5/bkk1, mpk3 and npr1-3 mutants. ssODNs also induced early expression of MPK3, WRKY33, PROPEP1 and FRK1 genes involved in plant defence, an effect that was reduced in bak1-5 and bak1-5/bkk1 mutants. Conclusions ssODNs are capable of inducing protection against pathogens through the activation of defence genes and promotion of stomatal closure through a mechanism similar to that of other elicitors of plant immunity, which involves the BAK1 co-receptor, and ROS synthesis.

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Protection against UVB-Induced Photoaging by Nypa fruticans via Inhibition of MAPK/AP-1/MMP-1 Signaling

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/2905362 ◽

2020 ◽

Vol 2020 ◽

pp. 1-14

Author(s):

Hee-Jeong Choi ◽

Md Badrul Alam ◽

Mi-Eun Baek ◽

Yoon-Gyung Kwon ◽

Ji-Young Lim ◽

...

Keyword(s):

Radical Scavenging Activity ◽

Radical Scavenging ◽

Reactive Oxygen Species Generation ◽

Skin Aging ◽

Current Data ◽

Collagen Degradation ◽

Ultraviolet B ◽

Skin Thickness ◽

Dependent Manner ◽

Nypa Fruticans

Ultraviolet B (UVB) irradiation is major causative factor in skin aging. The aim of the present study was to investigate the protective effect of a 50% ethanol extract from Nypa fruticans (NF50E) against UVB-induced skin aging. The results indicated that NF50E exerted potent antioxidant activity (IC50 = 17.55 ± 1.63 and 10.78 ± 0.63 μg/mL for DPPH and ABTS-radical scavenging activity, respectively) in a dose-dependent manner. High-performance liquid chromatography revealed that pengxianencin A, protocatechuic acid, catechin, chlorogenic acid, epicatechin, and kaempferol were components of the extract. In addition, the extract exhibited elastase inhibitory activity (IC50 = 17.96 ± 0.39 μg/mL). NF50E protected against UVB-induced HaCaT cell death and strongly suppressed UVB-stimulated cellular reactive oxygen species generation without cellular toxicity. Moreover, topical application of NF50E mitigated UVB-induced photoaging lesions including skin erythema and skin thickness in BALB/C mice. NF50E treatment inhibited UVB-induced collagen degradation as well as MMP-1 and IL-1β expressions and significantly stimulated SIRT1 expression. Furthermore, the extract treatment markedly suppressed the activation of NF-κB and AP-1 (p-c-Jun) by deactivating the p38 and JNK proteins. Taken together, current data suggest that NF50E exhibits potent antioxidant potential and protection against photoaging by attenuating MMP-1 activity and collagen degradation possibly through the downregulation of MAPK/NF-κB/AP-1 signaling and SIRT1 activation.

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Honokiol, a chemopreventive agent against skin cancer, induces cell cycle arrest and apoptosis in human epidermoid A431 cells

Experimental Biology and Medicine ◽

10.1258/ebm.2011.011030 ◽

2011 ◽

Vol 236 (11) ◽

pp. 1351-1359 ◽

Cited By ~ 22

Author(s):

Chandeshwari Chilampalli ◽

Ruth Guillermo ◽

Radhey S Kaushik ◽

Alan Young ◽

Gudiseva Chandrasekher ◽

...

Keyword(s):

Cell Cycle ◽

Skin Cancer ◽

Cell Cycle Arrest ◽

Squamous Carcinoma ◽

Ultraviolet B ◽

Dependent Manner ◽

A431 Cells ◽

Squamous Carcinoma Cells ◽

Cycle Arrest ◽

M Phase

Honokiol is a plant lignan isolated from bark and seed cones of Magnolia officinalis. Recent studies from our laboratory indicated that honokiol pretreatment decreased ultraviolet B-induced skin cancer development in SKH-1 mice. The aim of the present investigation was to study the effects of honokiol on human epidermoid squamous carcinoma A431 cells and to elucidate possible mechanisms involved in preventing skin cancer. A431 cells were pretreated with different concentrations of honokiol for a specific time period and investigated for effects on apoptosis and cell cycle analysis. Treatment with honokiol significantly decreased cell viability and cell proliferation in a concentration- and time-dependent manner. Honokiol pretreatment at 50 μmol/L concentration induced G0/G1 cell cycle arrest significantly ( P < 0.05) and decreased the percentage of cells in the S and G2/M phase. Honokiol down-regulated the expression of cyclin D1, cyclin D2, Cdk2, Cdk4 and Cdk6 proteins and up-regulated the expression of Cdk's inhibitor proteins p21 and p27. Pretreatment of A431 cells with honokiol leads to induction of apoptosis and DNA fragmentation. These findings indicate that honokiol provides its effects in squamous carcinoma cells by inducing cell cycle arrest at G0/G1 phase and apoptosis.

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NFκB-dependent Down-regulation of Tumor Necrosis Factor Receptor-associated Proteins Contributes to Interleukin-1-mediated Enhancement of Ultraviolet B-induced Apoptosis

Journal of Biological Chemistry ◽

10.1074/jbc.m413006200 ◽

2005 ◽

Vol 280 (16) ◽

pp. 15635-15643 ◽

Cited By ~ 40

Author(s):

Birgit Pöppelmann ◽

Kerstin Klimmek ◽

Elwira Strozyk ◽

Reinhard Voss ◽

Thomas Schwarz ◽

...

Keyword(s):

Tumor Necrosis ◽

Molecular Mechanisms ◽

Interleukin 1 ◽

Tumor Necrosis Factor Receptor ◽

Ultraviolet B ◽

Dependent Manner ◽

Tnf Receptor ◽

Inhibitory Protein ◽

Down Regulation ◽

Induced Apoptosis

Activation of the transcription factor nuclear factor-κB (NFκB) by inflammatory cytokines like tumor necrosis (TNF) factor and interleukin-1 (IL-1) is generally associated with the induction of antiapoptotic pathways. Therefore, NFκB inhibits both intrinsically and extrinsically induced apoptosis and thus is regarded to act universally in an antiapoptotic fashion. Accordingly, activation of NFκB by IL-1 was shown to result in reduction of death ligand-induced apoptosis via up-regulation of antiapoptotic inhibitor of apoptosis proteins (IAPs). In contrast, apoptosis induced by ultraviolet-B radiation (UVB) was shown to be enhanced in an NFκB-dependent manner, indicating that NFκB can also act in a proapoptotic fashion. This study investigates the molecular mechanisms underlying IL-1-mediated enhancement of UVB-induced apoptosis. We show that NFκB activation in costimulation with UVB treatment results in repression of antiapoptotic genes and consequently in down-regulation of the respective proteins, like c-IAP, FLICE-inhibitory protein (FLIP), and some members of the TNF receptor-associated (TRAF)2 protein family. In parallel, TNFα is released, leading to activation of signaling pathways mediated by TNF receptor-1 (TNF-R1). Although TNF is well known to induce both proapoptotic and antiapoptotic effects, the down-regulated levels of TRAF-1, -2, and -6 proteins by IL-1 plus UVB action leads to a shift toward promotion of the proapoptotic pathway. In concert with the down-regulation of IAPs and FLIP, TNF-R1 activation as an additional proapoptotic stimulus now results in significant enhancement of UVB-induced apoptosis. Taken together, elucidation of the molecular mechanisms underlying IL-1-mediated enhancement of UVB-induced apoptosis revealed that NFκB does not exclusively act in an antiapoptotic fashion but may also mediate proapoptotic effects.

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Inhibition of light-induced stomatal opening by allyl isothiocyanate does not require guard cell cytosolic Ca2+ signaling

Journal of Experimental Botany ◽

10.1093/jxb/eraa073 ◽

2020 ◽

Vol 71 (10) ◽

pp. 2922-2932 ◽

Cited By ~ 2

Author(s):

Wenxiu Ye ◽

Eigo Ando ◽

Mohammad Saidur Rhaman ◽

Md Tahjib-Ul-Arif ◽

Eiji Okuma ◽

...

Keyword(s):

Plasma Membrane ◽

Stomatal Closure ◽

Allyl Isothiocyanate ◽

Stomatal Opening ◽

Cation Channels ◽

Dependent Manner ◽

Defense System ◽

Independent Manner ◽

Dose Dependent

Abstract The glucosinolate–myrosinase system is a well-known defense system that has been shown to induce stomatal closure in Brassicales. Isothiocyanates are highly reactive hydrolysates of glucosinolates, and an isothiocyanate, allyl isothiocyanate (AITC), induces stomatal closure accompanied by elevation of free cytosolic Ca2+ concentration ([Ca2+]cyt) in Arabidopsis. It remains unknown whether AITC inhibits light-induced stomatal opening. This study investigated the role of Ca2+ in AITC-induced stomatal closure and inhibition of light-induced stomatal opening. AITC induced stomatal closure and inhibited light-induced stomatal opening in a dose-dependent manner. A Ca2+ channel inhibitor, La3+, a Ca2+chelator, EGTA, and an inhibitor of Ca2+ release from internal stores, nicotinamide, inhibited AITC-induced [Ca2+]cyt elevation and stomatal closure, but did not affect inhibition of light-induced stomatal opening. AITC activated non-selective Ca2+-permeable cation channels and inhibited inward-rectifying K+ (K+in) channels in a Ca2+-independent manner. AITC also inhibited stomatal opening induced by fusicoccin, a plasma membrane H+-ATPase activator, but had no significant effect on fusicoccin-induced phosphorylation of the penultimate threonine of H+-ATPase. Taken together, these results suggest that AITC induces Ca2+ influx and Ca2+ release to elevate [Ca2+]cyt, which is essential for AITC-induced stomatal closure but not for inhibition of K+in channels and light-induced stomatal opening.

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