Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The involvement of phosphorylation/dephosphorylation in the salicylic acid (SA) signal transduction pathway leading to pathogenesis-related gene induction has previously been demonstrated using kinase and phosphatase inhibitors. Here, we show that in tobacco suspension cells, SA induced a rapid and transient activation of a 48-kD kinase that uses myelin basic protein as a substrate. This kinase is called the p48 SIP kinase (for SA-Induced Protein kinase). Biologically active analogs of SA, which induce pathogenesis-related genes and enhanced resistance, also activated this kinase, whereas inactive analogs did not. Phosphorylation of a tyrosine residue(s) in the SIP kinase was associated with its activation. The SIP kinase was purified to homogeneity from SA-treated tobacco suspension culture cells. The purified SIP kinase is strongly phosphorylated on a tyrosine residue(s), and treatment with either protein tyrosine or serine/threonine phosphatases abolished its activity. Using primers corresponding to the sequences of internal tryptic peptides, we cloned the SIP kinase gene. Analysis of the SIP kinase sequence indicates that it belongs to the MAP kinase family and that it is distinct from the other plant MAP kinases previously implicated in stress responses, suggesting that different members of the MAP kinase family are activated by different stresses.
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PMID:Salicylic acid activates a 48-kD MAP kinase in tobacco. 916 55

Hypoosmotic stress activates a phosphorylation-dependent oxidative burst. In-gel kinase assays were performed to characterize the protein kinases that could be implicated in osmoregulation and in the activation of the oxidative burst. Hypoosmotic stress activated several kinases among which 50 and 46 kDa proteins displayed mitogen-activated protein kinase (MAP kinase) properties. They phosphorylated myelin basic protein in the absence of calcium, were recognized by antibodies directed against human MAP kinases, and were phosphorylated on tyrosine. Immunoprecipitation with an antibody directed against the tobacco MAP kinase Ntf4 showed that at least one of the activated kinases would be Ntf4-like. Apigenin, a MAP kinase and cyclin-dependent kinase inhibitor which prevents the hypoosmotically induced oxidative burst (Cazale et al. 1998; Plant Physiol. 116, 659-669), inhibited these kinases in vitro suggesting that they may play a role in the activation of the oxidative burst. Like the oxidative response, activation of the kinases depended on extracellular calcium influx and protein kinases sensitive to staurosporine and 6-DMAP. However, kinase activation did not depend on effluxes through anion channels or on the oxidative burst. Two-dimensional in-gel kinase assays revealed the presence of three protein kinases with an apparent molecular mass of 50 kDa and one of 46 kDa, all four being activated by hypoosmotic stress. The same kinases were also activated by oligogalacturonides and salicylic acid, underlying the importance of these MAP kinases as common components of different signaling pathways triggered by different extracellular stimuli.
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PMID:MAP kinase activation by hypoosmotic stress of tobacco cell suspensions: towards the oxidative burst response? 1047 77

Arabidopsis contains 20 MAP kinase genes, but their roles in plant physiology have remained largely unknown because of a lack of mutants. Recent papers from two groups have shed new light on the function of two different MAP kinases. The Arabidopsis MPK4 gene appears to negatively regulate salicylic acid-mediated defense responses and positively regulate jasmonic acid-induced responses. The tobacco SIPK gene (orthologous to Arabidopsis MPK6) appears to positively regulate programmed cell death.
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PMID:Mapping out the roles of MAP kinases in plant defense. 1154 9

A wheat line, Bai Nong 3217 x Mardler BC5F4 with resistance to powdery mildew was used in the study. A suppression subtractive hybridization cDNA library was constructed from wheat leaves challenged by Erysiphe graminis DC at primary stage. Seven hundred and sixty ESTs were acquired, and the ESTs similarity analysis based on BLASTx software was finished by comparing sequences in nr database of GenBank. Two hundred and seventy one ESTs' functions were identified in the total ESTs. The results showed that GTP-binding proteins associated signal pathway, salicylic acid pathway, MAP pathway etc were supposed to involved in the disease resistance reaction. SAR genes were rich not only in varieties but also in quantity, including five kinds of phyogenesis-related proteins, induced defence-resistance genes, heat shock proteins and genes induced by abiotic-stresses etc. There are lots of evidence to testify PAL pathway, cell wall modification, cell survive system serving in the disease resistance. In the function unknown ESTs, many homologous ESTs were found from other biotic and abiotic-stresses selected cDNA libraries after BLASTn analysis, the stresses included pathogen, salt, drought, cold, high temperature etc. The novel ESTs was 16.6% in total ESTs.
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PMID:[ESTs analysis of resistance to powdery mildew in wheat at primary infected stage]. 1209 31

The Arabidopsis ssi4 mutant, which exhibits spontaneous lesion formation, constitutive expression of pathogenesis-related (PR) genes and enhanced resistance to virulent bacterial and oomycete pathogens, contains a gain-of-function mutation in a TIR-NBS-LRR type R gene. Epistatic analyses revealed that both PR gene expression and disease resistance are activated via a salicylic acid (SA)- and EDS1-dependent, but NPR1- and NDR1-independent signaling pathway. In this study, we demonstrate that in moderate relative humidity (RH; 60%), the ssi4 mutant accumulates H(2)O(2) and SA prior to lesion formation and displays constitutive activation of the MAP kinases AtMPK6 and AtMPK3. It also constitutively expresses a variety of defense-associated genes, including those encoding the WRKY transcription factors AtWRKY29 and AtWRKY6, the MAP kinases AtMPK6 and AtMPK3, the powdery mildew R proteins RPW8.1 and RPW8.2, EDS1 and PR proteins. All of these ssi4-induced responses, as well as the chlorotic, stunted morphology and enhanced disease resistance phenotype, are suppressed by high RH (95%) growth conditions. Thus, a humidity sensitive factor (HSF) appears to function at an early point in the ssi4 signaling pathway. All ssi4 phenotypes, except for MAP kinase activation, also were suppressed by the eds1-1 mutation. Thus, ssi4-induced MAP kinase activation occurs downstream of the HSF but either upstream of EDS1 or on a separate branch of the ssi4 signaling pathway. SA is a critical signaling component in ssi4-mediated defense responses. However, exogenously supplied SA failed to restore lesion formation in high RH-grown ssi4 plants, although it induced defense gene expression. Thus, additional signals also are involved.
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PMID:High humidity suppresses ssi4-mediated cell death and disease resistance upstream of MAP kinase activation, H2O2 production and defense gene expression. 1534 34

Several lines of evidences show that reactive oxygen species (ROS), taking H(2)O(2) considered, and the protein kinase, especially mitogen-activated protein kinase (MAP kinase), jointly regulated plant stress signaling. In plant cells, a number of MAP kinases were specifically involved in oxidative burst (OXB) or hypersensitive response (HR) in response to biotic stresses, besides salicylic acid (SA) induced MAP kinase (SIPK) and ROS play the crucial roles in the processes of systemic acquired resistance (SAR) being established. The reciprocal relationship between SIPK and ROS could be essential in response to abiotic stresses in plant cells, because it was indicated that ozone, wounding, or osmotic stimuli activated SIPK. Together, these primary results showed that MAP kinases were required for ROS signaling in response to stress in plant cells, and more studies are in demand in this area.
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PMID:[Regulation role of reactive oxygen species and mitogen-activated protein kinases in plant stress signaling]. 1569 72

The Arabidopsis mitogen-activated protein kinase (MAPK) kinase 2 (MKK2) was shown to mediate cold and salt stress responses through activation of the two MAP kinases MPK4 and MPK6. Transcriptome analysis of plants expressing constitutively active MKK2 (MKK2-EE plants) showed altered expression of genes induced by abiotic stresses but also a significant number of genes involved in defense responses. Both MPK4 and MPK6 became rapidly activated upon Pseudomonas syringae pv. tomato DC3000 infection and MKK2-EE plants showed enhanced levels of MPK4 activation. Although MKK2-EE plants shared enhanced expression of genes encoding enzymes of ethylene (ET) and jasmonic acid (JA) synthesis, ET, JA, and salicylic acid (SA) levels did not differ dramatically from those of wild-type or mkk2-null plants under ambient growth conditions. Upon P. syringae pv. tomato DC3000 infection, however, MKK2-EE plants showed reduced increases of JA and SA levels. These results indicate that MKK2 is involved in regulating hormone levels in response to pathogens. MKK2-EE plants were more resistant to infection by P. syringae pv. tomato DC3000 and Erwinia carotovora subsp. carotovora, but showed enhanced sensitivity to the fungal necrotroph Alternaria brassicicola. Our data indicate that MKK2 plays a role in abiotic stress tolerance and plant disease resistance.
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PMID:The MAP kinase kinase MKK2 affects disease resistance in Arabidopsis. 1750 36

Programmed cell death (PCD) is a crucial process for plant innate immunity and development. In plant innate immunity, PCD is believed to prevent the spread of pathogens from the infection site. Although proper control of PCD is important for plant fitness, we have limited understanding of the molecular mechanisms regulating plant PCD. Plant innate immunity triggered by recognition of effectors (effector-triggered immunity, ETI) is often associated with PCD. However pattern-triggered immunity (PTI), which is triggered by recognition of elicitors called microbe-associated molecular patterns (MAMPs), is not. Therefore we hypothesized that PTI might suppress PCD. Here we report that PCD triggered by the mycotoxin fumonisin B1 (FB1) can be suppressed by PTI in Arabidopsis. FB1-triggered cell death was suppressed by treatment with the MAMPs flg22 (a part of bacterial flagellin) or elf18 (a part of the bacterial elongation factor EF-Tu) but not chitin (a component of fungal cell walls). Although plant hormone signaling is associated with PCD and PTI, both FB1-triggered cell death and suppression of cell death by flg22 treatment were still observed in mutants deficient in jasmonic acid (JA), ethylene (ET) and salicylic acid (SA) signaling. The MAP kinases MPK3 and MPK6 are transiently activated and inactivated within one hour during PTI. We found that FB1 activated MPK3 and MPK6 about 36-48 hours after treatment. Interestingly, this late activation was attenuated by flg22 treatment. These results suggest that PTI suppression of FB1-triggered cell death may involve suppression of MPK3/MPK6 signaling but does not require JA/ET/SA signaling.
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PMID:Pattern-triggered immunity suppresses programmed cell death triggered by fumonisin b1. 2356 Jan 4

In higher eukaryotes, induced resistance associates with acquisition of a priming state of the cells for a more effective activation of innate immunity; however, the nature of the components for mounting this type of immunological memory is not well known. We identified an extracellular subtilase from Arabidopsis, SBT3.3, the overexpression of which enhances innate immune responses while the loss of function compromises them. SBT3.3 expression initiates a durable autoinduction mechanism that promotes chromatin remodeling and activates a salicylic acid(SA)-dependent mechanism of priming of defense genes for amplified response. Moreover, SBT3.3 expression-sensitized plants for enhanced expression of the OXI1 kinase gene and activation of MAP kinases following pathogen attack, providing additional clues for the regulation of immune priming by SBT3.3. Conversely, in sbt3.3 mutant plants pathogen-mediated induction of SA-related defense gene expression is drastically reduced and activation of MAP kinases inhibited. Moreover, chromatin remodeling of defense-related genes normally associated with activation of an immune priming response appear inhibited in sbt3.3 plants, further indicating the importance of the extracellular SBT3.3 subtilase in the establishment of immune priming. Our results also point to an epigenetic control in the regulation of plant immunity, since SBT3.3 is up-regulated and priming activated when epigenetic control is impeded. SBT3.3 represents a new regulator of primed immunity.
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PMID:An extracellular subtilase switch for immune priming in Arabidopsis. 2780 16

Among the various abiotic stresses, low temperature is one of the major environmental constraints that limit the plant development and crop productivity. Plants are able to adapt to low-temperature stress through the changes in membrane composition and activation of reactive oxygen scavenging systems. The genetic pathway induced due to temperature downshift is based on C-repeat-binding factors (CBF) which activate promoters through the C-repeat (CRT) cis-element. Calcium entry is a major signalling event occurring immediately after a downshift in temperature. The increase in the level of cytosolic calcium activates many enzymes, such as phospholipases and calcium dependent-protein kinases. MAP-kinase module has been shown to be involved in the cold response. Ultimately, the activation of these signalling pathways leads to changes in the transcriptome. Several phytohormones, such as abscisic acid, brassinosteroids, auxin, salicylic acid, gibberellic acid, cytokinins and jasmonic acid, have been shown to play key roles in regulating the plant development under low-temperature stress. These phytohormones modulate important events involved in tolerance to low-temperature stress in plants. Better understanding of these events and genes controlling these could open new strategies for improving tolerance mediated by phytohormones.
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PMID:Low-temperature stress: is phytohormones application a remedy? 2883 64


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