AIK1, A Mitogen-Activated Protein Kinase, Modulates Abscisic Acid Responses through the MKK5-MPK6 Kinase Cascade

Li, Kun; Yang, Fengbo; Zhang, Guozeng; Song, Shufei; Li, Yuan; Ren, Dongtao; Miao, Yuchen; Song, Chun‐Peng

doi:10.1104/pp.16.01386

Cited by 103 publications

(87 citation statements)

References 94 publications

(133 reference statements)

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“…In the present study, we also found that the smxl6,7,8 mutant plants were hypersensitive to ABA in both cotyledon opening and growth inhibition assays (Figure 4), which is in agreement with the positive roles of SLs and SL signaling in regulating ABA responsiveness [16,[19][20][21]. An increase in ABA responsiveness may lead to activation of downstream signaling components, such as mitogen-activated protein kinase cascade module [60,61] and ABA-RESPONSIVE ELEMENT BINDING PROTEIN 1 pathway [62], resulting in enhanced drought resistance both dependently [61] and independently [62] of the status of stomatal closure.…”

Section: Discussionsupporting

confidence: 90%

Negative Roles of Strigolactone-Related SMXL6, 7 and 8 Proteins in Drought Resistance in Arabidopsis

Nguyen

Tran

et al. 2020

Biomolecules

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Previous investigations have shown that the SUPPRESSORS OF MAX2 1-LIKE6, 7 and 8 (SMXL6, 7 and 8) proteins redundantly repress strigolactone (SL) signaling in plant growth and development. Recently, a growing body of evidence indicated that SLs positively regulate plant drought resistance through functional analyses of genes involved in SL biosynthesis and positive regulation of SL signaling. However, the functions of the SL-signaling negative regulators SMXL6, 7 and 8 in drought resistance and the associated mechanisms remain elusive. To reveal the functions of these SMXL proteins, we analyzed the drought-resistant phenotype of the triple smxl6,7,8 mutant plants and studied several drought resistance-related traits. Our results showed that the smxl6,7,8 mutant plants were more resistant to drought than wild-type plants. Physiological investigations indicated that the smxl6,7,8 mutant plants exhibited higher leaf surface temperature, reduced cuticle permeability, as well as decreases in drought-induced water loss and cell membrane damage in comparison with wild-type plants. Additionally, smxl6,7,8 mutant plants displayed an increase in anthocyanin biosynthesis during drought, enhanced detoxification capacity and increased sensitivity to abscisic acid in cotyledon opening and growth inhibition assays. A good correlation between the expression levels of some relevant genes and the examined physiological and biochemical traits was observed. Our findings together indicate that the SMXL6, 7 and 8 act as negative regulators of drought resistance, and that disruption of these SMXL genes in crops may provide a novel way to improve their drought resistance.

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Section: Discussionsupporting

confidence: 90%

Negative Roles of Strigolactone-Related SMXL6, 7 and 8 Proteins in Drought Resistance in Arabidopsis

Nguyen

Tran

et al. 2020

Biomolecules

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“…The DEGs with KEGG annotation were assigned to 28 classes, mainly related to signal transduction (221), carbohydrate metabolism (212), biosynthesis of other secondary metabolites (166), and metabolism of terpenoids and polyketides (69) (Additional file 5: Figure S5). KEGG enrichment analyses also indicated the DEGs were significantly enriched in the main pathways of phenylpropanoid biosynthesis (ko00940), of starch and sucrose metabolism (ko00500), and in the plant MAPK signaling pathway (ko04016, their responses to wounding and their roles in the biosynthesis of secondary metabolism have been illustrated previously [23][24][25] (Fig. 4).…”

Section: Functional Classification and Enrichment Analysis Of Degsmentioning

confidence: 60%

Transcriptome analysis reveals key genes involved in the regulation of nicotine biosynthesis at early time points after topping in tobacco (Nicotiana tabacum L.)

Qin

Bai

et al. 2020

BMC Plant Biol

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Background: Nicotiana tabacum is an important economic crop. Topping, a common agricultural practice employed with flue-cured tobacco, is designed to increase leaf nicotine contents by increasing nicotine biosynthesis in roots. Many genes are found to be differentially expressed in response to topping, particularly genes involved in nicotine biosynthesis, but comprehensive analyses of early transcriptional responses induced by topping are not yet available. To develop a detailed understanding of the mechanisms regulating nicotine biosynthesis after topping, we have sequenced the transcriptomes of Nicotiana tabacum roots at seven time points following topping.Results: Differential expression analysis revealed that 4830 genes responded to topping across all time points. Amongst these, nine gene families involved in nicotine biosynthesis and two gene families involved in nicotine transport showed significant changes during the immediate 24 h period following topping. No obvious preference to the parental species was detected in the differentially expressed genes (DEGs). Significant changes in transcript levels of nine genes involved in nicotine biosynthesis and phytohormone signal transduction were validated by qRT-PCR assays. 549 genes encoding transcription factors (TFs), found to exhibit significant changes in gene expression after topping, formed 15 clusters based on similarities of their transcript level time-course profiles. 336 DEGs involved in phytohormone signal transduction, including genes functionally related to the phytohormones jasmonic acid, abscisic acid, auxin, ethylene, and gibberellin, were identified at the earliest time point after topping. Conclusions:Our research provides the first detailed analysis of the early transcriptional responses to topping in N. tabacum, and identifies excellent candidates for further detailed studies concerning the regulation of nicotine biosynthesis in tobacco roots.

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“…Based on self-healing ability, immunotherapy has been great expectation against distinct types of cancer. [32][33][34][35][36][37] Current immunotherapies targeting different cellular checkpoint controllers emerged as having either innate or acquired resistance due to the immunosuppressive tumor environment, guiding the direction of developing cancer immunotherapy. [38] The object of cancer immunotherapy is to stimulate a long-lasting immunosurveillance, maintaining the antitumor immunity.…”

Section: Discussionmentioning

confidence: 99%

Melatonin Maintains Macrophage M1 Phenotype to Reverse LPS-stimulated Tumor Immune Tolerance

Lin

Zhang

Zhou

et al. 2020

Preprint

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Background: Lipopolysaccharide (LPS) is a potent trigger of macrophage-mediated inflammation and its repeated stimulation results in immune tolerance. This study is to explore the cellular mechanisms of LPS-mediated tumor immune tolerance and to investigate whether melatonin can reverse this tolerance. Methods: The effect of melatonin and LPS on macrophages was assessed by cell proliferation, morphological changes, phagocytosis and autophagy in vitro. The tumor-preventing effect of melatonin and LPS were evaluated in the urethane-induced lung carcinoma model and in the H22 liver cancer allograft model. Immunofluorescence, immunohistochemistry and ELISA were used to examine protein expression. The related targets and pathways of melatonin were predicted by comprehensive bioinformatics, and the clinical association of bacterial infections and survival was evaluated in cancer patients by meta-analysis.Results: In vitro，Raw264.7 macrophages were polarized toward the M1 phenotype by single LPS administration but toward the M2 phenotype by repeated LPS administration. Interestingly, combination treatment with repeated LPS and 10 µM melatonin prevented macrophage polarization toward the M2-like phenotype and exerted lasting antitumor efficacy. In the urethane-induced lung carcinoma model, repeated LPS administration stimulated macrophage polarization toward the M2 phenotype and promoted lung carcinogenesis, which was abrogated by macrophage depletion, while melatonin alone or in combination with repeated LPS challenge restored M1-like macrophages and prevented carcinogenesis. In the H22 liver cancer allograft model, melatonin maintained the macrophage phenotype and promoted the tumor-suppressing effect of repeated LPS challenge. Furthermore, we found that macrophages repeatedly stimulated with LPS had a high level of surface lipid rafts that mediated PI3K/AKT and JAK2/STAT3 signaling and prevented both LPS sensitivity and immune response by self-expression of PD-L1 and surface expression of PD-1 receptor on NK cells, whereas melatonin decreased surface lipid rafts and PI3K/AKT and JAK2/STAT3 signaling. Finally, we conducted a comprehensive bioinformatics analysis of melatonin-relevant targets and pathways involved in M2 macrophage polarization and evaluated the clinical associations of bacterial infections and survival in cancer patients. Conclusions: This study suggests a function of melatonin in regulating macrophage polarization to maintain LPS-stimulated tumor immune surveillance.

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AIK1, A Mitogen-Activated Protein Kinase, Modulates Abscisic Acid Responses through the MKK5-MPK6 Kinase Cascade

Cited by 103 publications

References 94 publications

Negative Roles of Strigolactone-Related SMXL6, 7 and 8 Proteins in Drought Resistance in Arabidopsis

Negative Roles of Strigolactone-Related SMXL6, 7 and 8 Proteins in Drought Resistance in Arabidopsis

Transcriptome analysis reveals key genes involved in the regulation of nicotine biosynthesis at early time points after topping in tobacco (Nicotiana tabacum L.)

Melatonin Maintains Macrophage M1 Phenotype to Reverse LPS-stimulated Tumor Immune Tolerance

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