scholarly journals The Liriodendron chinense MKK2 Gene Enhances Arabidopsis thaliana Salt Resistance

Forests ◽  
2020 ◽  
Vol 11 (11) ◽  
pp. 1160
Author(s):  
Xinying Chen ◽  
Pengkai Wang ◽  
Fangfang Zhao ◽  
Lu Lu ◽  
Xiaofei Long ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Mechanical Damage ◽  
Salt Resistance ◽  
Stress Conditions ◽  
Mitogen Activated Protein Kinase ◽  
Biotic And Abiotic Stress ◽  
Regulatory Pathways ◽  
Mitogen Activated Protein ◽  
Liriodendron Chinense ◽  
Related Stress

To adapt and sense environmental perturbations, including a variety of biotic and abiotic stress conditions, plants have developed disparate regulatory pathways. Mitogen-activated protein kinase (MAPK or MPK) signaling cascades are found widespread across the eukaryotic kingdoms of life. In plants, they may regulate signaling pathways aimed at resisting the stressful effects of low temperature, salt damage, drought, touch, and mechanical damage. To date, no conclusive studies into Liriodendron chinense (Hemsl.) Sarg MPK-related stress resistance signaling have been performed. In our study, we cloned three homologous L. chinense MAP kinase kinase family genes: LcMKK2, LcMKK4, and LcMKK6. LcMKK2 and LcMKK6 have their highest expression level in the root, while LcMKK4 is highly expressed in the stem. LcMKK2 showed upregulation in response to salt and cold stress conditions in L. chinense. To further analyze its gene function, we overexpressed LcMKK2 in wild-type Arabidopsis thaliana (L.) Heynh. and obtained transgenic plants. Overexpression of LcMKK2 caused a significant reduction in plant mortality (from 96% to 70%) in response to a 7-day 200 mM NaCl treatment. Therefore, we conclude that LcMKK2 is involved in a signaling response to salt stress, and it could thus prove an effective target gene for breeding strategies to improve Liriodendron salt tolerance.

Mitogen-activated protein kinase 6 integrates phosphate and iron responses for indeterminate root growth in Arabidopsis thaliana

Planta ◽  
2019 ◽  
Vol 250 (4) ◽  
pp. 1177-1189 ◽  
Author(s):  
Jesús Salvador López-Bucio ◽  
Guadalupe Jessica Salmerón-Barrera ◽  
Gustavo Ravelo-Ortega ◽  
Javier Raya-González ◽  
Patricia León ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Protein Kinase ◽  
Root Growth ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein

Diverse Responses Are Involved in the Defence of Arabidopsis thaliana against Turnip Crinkle Virus

2013 ◽  
Vol 68 (3-4) ◽  
pp. 148-154 ◽  
Author(s):  
Hui Yang ◽  
Shu Yuan ◽  
Yi Luo ◽  
Ji Huang ◽  
Yang-Er Chen ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Plant Hormones ◽  
Plant Defence ◽  
Mitogen Activated Protein Kinase ◽  
Turnip Crinkle Virus ◽  
Wild Type ◽  
Antagonistic Action ◽  
Pathogenesis Related ◽  
Mitogen Activated Protein ◽  
Plant Pathogen Interactions

Plant hormones play pivotal roles as signals of plant-pathogen interactions. Here, we report that exogenous application of salicylic acid (SA), jasmonic acid (JA), ethephon (ETH), and abscisic acid (ABA) can reduce Turnip crinkle virus (TCV) accumulation in systemic leaves of Arabidopsis thaliana during early infection. SA and ABA are more efficient and confer a longer-lasting resistance against TCV than JA and ETH, and the plant hormones interact in effecting the plant defence. Synergistic actions of SA and JA, and SA and ET, and an antagonistic action of SA and ABA have been observed in the Arabidopsis-TCV interaction. ABA can down-regulate the expression of the pathogenesis-related genes PR1 and PDF1.2, and compared to the wild type, it drastically reduces TCV accumulation in NahG transgenic plants and the eds5-p1 mutant, both of which do not accumulate SA. This indicates that SA signaling negatively regulates the ABA-mediated defence. ABA-induced resistance against TCV is independent of SA. We also found that mitogen-activated protein kinase 5 (MPK5) may be involved in ABA-mediated defence. These results indicate that Arabidopsis can activate distinct signals to inhibit virus accumulation. Cooperative or antagonistic crosstalk between them is pivotal for establishing disease resistance. These results show potential to enhance the plant defence against viruses by manipulating diverse hormones.

Adaptation of uterine artery thick- and thin-filament regulatory pathways to pregnancy

2005 ◽  
Vol 288 (1) ◽  
pp. H142-H148 ◽  
Author(s):  
DaLiao Xiao ◽  
Lubo Zhang
Keyword(s):  
Uterine Artery ◽  
Thin Filament ◽  
Kinase Inhibitor ◽  
Isometric Tension ◽  
Mitogen Activated Protein Kinase ◽  
Regulatory Pathways ◽  
Uterine Arteries ◽  
Pregnant Sheep ◽  
Mitogen Activated Protein ◽  
Near Term

Little is known about the adaptation of uterine artery smooth muscle contractile mechanisms to pregnancy. The present study tested the hypothesis that pregnancy differentially regulates thick- and thin-filament regulatory pathways in uterine arteries. Isometric tension, intracellular free Ca2+ concentration, and phosphorylation of 20-kDa myosin light chain (MLC20) were measured simultaneously in uterine arteries isolated from nonpregnant and near-term (140 days gestation) pregnant sheep. Phenylephrine-mediated intracellular free Ca2+ concentration, MLC20 phosphorylation, and contraction tension were significantly increased in uterine arteries of pregnant compared with nonpregnant animals. In contrast, phenylephrine-mediated Ca2+ sensitivity of MLC20 phosphorylation was decreased in the uterine arteries of pregnant sheep. Simultaneous measurement of phenylephrine-stimulated tension and MLC20 phosphorylation in the same tissue indicated a decrease in MLC20 phosphorylation-independent contractions in the uterine arteries of pregnant sheep. In addition, activation of PKC produced significantly lower sustained contractions in uterine arteries of pregnant compared with nonpregnant animals in the absence of changes in MLC20 phosphorylation levels in either vessels. In uterine arteries of nonpregnant sheep, the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase inhibitor PD-098059 significantly increased phenylephrine-mediated, MLC20 phosphorylation-independent contractions. The results suggest that in uterine arteries, pregnancy upregulates α1-adrenoceptor-mediated Ca2+ mobilization and MLC20 phosphorylation. In contrast, pregnancy downregulates the Ca2+ sensitivity of myofilaments, which is mediated by both thick- and thin-filament pathways.

scholarly journals The Absence of Caveolin-1 Increases Proliferation and Anchorage- Independent Growth by a Rac-Dependent, Erk-Independent Mechanism

2009 ◽  
Vol 29 (18) ◽  
pp. 5046-5059 ◽  
Author(s):  
Ana Cerezo ◽  
Marta C. Guadamillas ◽  
Jacky G. Goetz ◽  
Sara Sánchez-Perales ◽  
Eric Klein ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cyclin D1 ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Mitogen Activated Protein Kinase ◽  
Serum Starvation ◽  
Regulatory Pathways ◽  
Anchorage Independent Growth ◽  
Caveolin 1 ◽  
Mitogen Activated Protein

ABSTRACT Anchorage-independent growth (AIG) of cancer cells requires escape from integrin-mediated signals. A protein frequently downregulated in cancer, caveolin-1 (Cav1), mediates integrin control of several growth-regulatory pathways. We report that loss of Cav1 results in faster exit from quiescence and progress through the cell cycle, proliferation without anchorage to substrate, and absence of cyclin D1 downregulation upon serum deprivation or detachment. Surprisingly, this proliferative advantage is independent of Erk-mitogen-activated protein kinase signaling; instead, cyclin expression and cell cycle progression in the absence of Cav1 are driven by increased membrane order and Rac targeting. AIG was induced in Cav1-expressing cells by forced membrane targeting of Rac1 or by inhibiting Cav1-mediated internalization of plasma membrane ordered domains at which Rac1 accumulates. Restoring Rho activity, which is downregulated after loss of Cav1, antagonizes Rac1 and prevents cyclin D1 accumulation after serum starvation or loss of adhesion. Anchorage independence and increased proliferation in Cav1-deficient tumoral and null cells are thus due to an increased fraction of active Rac1 at membrane ordered domains. These results provide insight into the mechanisms regulating growth of cancer cells, which frequently lose Cav1 function.

scholarly journals A novel positive feedback mechanism of ABI5 phosphorylation by mitogen activated protein kinase-3 regulates ABA signaling in Arabidopsis

2021 ◽  
Author(s):  
Prakash Kumar Bhagat ◽  
Deepanjali Verma ◽  
Neetu Verma ◽  
Alok Krishna Sinha
Keyword(s):  
Seed Germination ◽  
Map Kinases ◽  
Feedback Mechanism ◽  
Floral Transition ◽  
Mitogen Activated Protein Kinase ◽  
Aba Signaling ◽  
Regulatory Pathways ◽  
Mitogen Activated Protein ◽  
Kinase Cascade ◽  
Positive Feedback Mechanism

AbstractSeed germination is the crucial physiological process regulated by both environmental and endogenous phytohormones. ABA negatively regulates seed germination, post-germination growth and floral transition, however, the cross talk between multiple regulatory pathways are still unclear. Here, we show that ABA activates two MAP kinases, AtMPK3/AtMPK6 and selectively regulates the transcript of AtMPK3 through ABI5, a master regulator of ABA signaling. As a feedback loop, AtMPK3 interacts and phosphorylates ABI5 at the serine-314 position. ABI5 phosphorylation by MAP kinases positively regulates ABI5 nuclear localization and negatively regulates its dimerization. Subcellular localization of ABI5 phospho-null protein further suggests the role of phosphorylation in regulation of its cytoplasmic stability and its nuclear dimerization. Overexpression of phosphor-null ABI5 in abi5-8 mutant restored the ABA sensitivity during seed germination and delayed the floral transition as compared to phospho-mimic ABI5. Additionally, overexpression of constitutive phosphorylated ABI5 in abi5-8 mutants suggest that phosphorylation makes ABI5 partially inactive. Furthermore, phospho-null ABI5 plants showed drought sensitive phenotype whereas, mpk3, mkk4, mkk5, abi5-8 and phosphor-mimic plants showed drought tolerant phenotype. Our findings present a new insight between MAP kinase cascade and ABA signaling which collectively regulates the ABA response through ABI5 phosphorylation.

scholarly journals Transcriptome analysis of Rhizopus oryzae seed pellet formation using triethanolamine

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Na Wu ◽  
Jiahui Zhang ◽  
Wen Ou ◽  
Yaru Chen ◽  
Ru Wang ◽  
...  
Keyword(s):  
Rhizopus Oryzae ◽  
Mitogen Activated Protein Kinase ◽  
Acid Fermentation ◽  
Regulatory Pathways ◽  
Seed Culture ◽  
Pellet Formation ◽  
Pellet Morphology ◽  
Mitogen Activated Protein ◽  
Protein Kinase Signaling ◽  
Product Output

AbstractRhizopus oryzae (R. oryzae) can effectively produce organic acids, and its pellet formation in seed cultures has been shown to significantly enhance subsequent fermentation processes. Despite advances in strain development, simple and effective methods for inducing pellet morphology and a basic understanding of the mechanisms controlling this process could facilitate substantial increases in efficiency and product output. Here, we report that 1.5% triethanolamine (TEOA) in seed culture medium can activate the growth of R. oryzae spores in compact and uniform pellets which is optimal for fermentation conditions. Analysis of fermentation kinetics showed that the production of fumaric and L-malic acid increases 293% and 177%, respectively. Transcriptomic analysis revealed that exposure of R. oryzae to 1.5% TEOA during the seed culture activated the phosphatidylinositol and mitogen-activated protein kinase signaling pathways. Theses pathways subsequently stimulated the downstream carbohydrate-active synthases and hydrolases that required for cell wall component synthesis and reconstruction. Our results thus provide insight into the regulatory pathways controlling pellet morphology germane to the viability of seed cultures, and provide valuable reference data for subsequent optimization of organic acid fermentation by R. oryzae.

scholarly journals The monothiol glutaredoxin Grx4 influences thermotolerance, cell wall integrity, and Mpk1 signaling in Cryptococcus neoformans

2021 ◽  
Author(s):  
Guanggan Hu ◽  
Linda Horianopoulos ◽  
Eddy Sánchez-León ◽  
Mélissa Caza ◽  
Wonhee Jung ◽  
...  
Keyword(s):  
Cell Wall ◽  
Cryptococcus Neoformans ◽  
Iron Homeostasis ◽  
Elevated Temperatures ◽  
Stress Conditions ◽  
Cell Wall Integrity ◽  
Mitogen Activated Protein Kinase ◽  
Calcofluor White ◽  
Mitogen Activated Protein ◽  
Increased Sensitivity

Abstract Monothiol glutaredoxins are important regulators of iron homeostasis that play conserved roles in the sensing and trafficking of iron-sulfur clusters. We previously characterized the role of the monothiol glutaredoxin Grx4 in iron homeostasis, the interaction with the iron regulator Cir1, and virulence in Cryptococcus neoformans. This important fungal pathogen causes cryptococcal meningoencephalitis in immunocompromised individuals worldwide. Here, we demonstrate that Grx4 is required for proliferation at elevated temperatures (both 37°C and 39°C) and under stress conditions. In particular, the grx4Δ mutant was hypersensitive to SDS, calcofluor white (CFW), and caffeine, suggesting that Grx4 is required for membrane and cell wall integrity (CWI). In this context, we found that Grx4 regulated the phosphorylation of the Mpk1 mitogen-activated protein kinase (MAPK) of the CWI pathway in cells grown at elevated temperature or upon treatment with CFW, caffeine, or SDS. The grx4Δ mutant also displayed increased sensitivity to FK506 and cyclosporin A, two inhibitors of the calcineurin pathway, indicating that Grx4 may influence growth at higher temperatures in parallel with calcineurin signaling. Upon thermal stress or calcium treatment, loss of Grx4 also caused partial mis-localization of Crz1, the transcription factor that is a calcineurin substrate. The phenotypes of the grx4Δ, crz1Δ, and cna1Δ (calcineurin) mutants suggest shared contributions to the regulation of temperature, cell wall, and other stresses. In summary, we show that Grx4 is also a key regulator of the responses to a variety of stress conditions in addition to its roles in iron homeostasis in C. neoformans.

scholarly journals Nitration-induced ubiquitination and degradation control quality of ERK1

2019 ◽  
Vol 476 (13) ◽  
pp. 1911-1926 ◽  
Author(s):  
Yuanya Zhang ◽  
Xiahe Huang ◽  
Jinlong Wang ◽  
Xiaorong Wang ◽  
Xiaofei Liu ◽  
...  
Keyword(s):  
Quality Control ◽  
Wide Spectrum ◽  
Control Program ◽  
Stress Conditions ◽  
Mitogen Activated Protein Kinase ◽  
General Mechanism ◽  
Quality Control Program ◽  
Interacting Protein ◽  
Spatiotemporal Regulation ◽  
Mitogen Activated Protein

Abstract The mitogen-activated protein kinase ERK1/2 (ERKs, extracellular-regulated protein kinases) plays important roles in a wide spectrum of cellular processes and have been implicated in many disease states. The spatiotemporal regulation of ERK activity has been extensively studied. However, scarce information has been available regarding the quality control of the kinases to scavenge malfunctioning ERKs. Using site-specific mutagenesis and mass spectrometry, we found that the disruption of the conserved H-bond between Y210 and E237 of ERK1 through point mutation at or naturally occurring nitration on Y210 initiates a quality control program dependent on chaperon systems and CHIP (C-terminal of Hsp70-interacting protein)-mediated ubiquitination and degradation. The H-bond is also important for the quality control of ERK2, but through a distinct mechanism. These findings clearly demonstrate how malfunctioning ERKs are eliminated when cells are in certain stress conditions or unhealthy states, and could represent a general mechanism for scavenging malfunctioning kinases in stress conditions.

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