1. XYLEM CYSTEINE PEPTIDASE 1 and its inhibitor CYSTATIN 6 regulate pattern-triggered immunity by modulating the stability of the NADPH oxidase RESPIRATORY BURST OXIDASE HOMOLOG D.
期刊:The Plant cell
日期:2024-01-30
DOI :10.1093/plcell/koad262
Plants produce a burst of reactive oxygen species (ROS) after pathogen infection to successfully activate immune responses. During pattern-triggered immunity (PTI), ROS are primarily generated by the NADPH oxidase RESPIRATORY BURST OXIDASE HOMOLOG D (RBOHD). RBOHD is degraded in the resting state to avoid inappropriate ROS production; however, the enzyme mediating RBOHD degradation and how to prevent RBOHD degradation after pathogen infection is unclear. In this study, we identified an Arabidopsis (Arabidopsis thaliana) vacuole-localized papain-like cysteine protease, XYLEM CYSTEINE PEPTIDASE 1 (XCP1), and its inhibitor CYSTATIN 6 (CYS6). Pathogen-associated molecular pattern-induced ROS burst and resistance were enhanced in the xcp1 mutant but were compromised in the cys6 mutant, indicating that XCP1 and CYS6 oppositely regulate PTI responses. Genetic and biochemical analyses revealed that CYS6 interacts with XCP1 and depends on XCP1 to enhance PTI. Further experiments showed that XCP1 interacts with RBOHD and accelerates RBOHD degradation in a vacuole-mediated manner. CYS6 inhibited the protease activity of XCP1 toward RBOHD, which is critical for RBOHD accumulation upon pathogen infection. As CYS6, XCP1, and RBOHD are conserved in all plant species tested, our findings suggest the existence of a conserved strategy to precisely regulate ROS production under different conditions by modulating the stability of RBOHD.
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2区Q1影响因子: 5.7
英汉
2. An Arabidopsis mutant disrupted in ASN2 encoding asparagine synthetase 2 exhibits low salt stress tolerance.
Salt tolerance of Arabidopsis knockout mutant with T-DNA insertion in ASN2 gene encoding asparagine synthetase (AS, EC 6.3.5.4) (asn2-1) was investigated. Wild-type Arabidopsis Col0 and asn2-1 mutant were grown for one month by hydroponic culture and subjected to 100 mM NaCl stress for a short time from 6 to 24 h. The salt treatment decreased chlorophyll and soluble protein contents, and increased ammonium level in the asn2-1 leaves. The salinity induced ASN1 mRNA level in the wild-type and asn2-1 leaves. By contrast, the salt treatment inhibited the transcript and protein levels of chloroplastic glutamine synthetase 2 (GS2, EC 6.3.1.2) in the wild-type and asn2-1 leaves. Increase in asparagine and proline contents in response to the salt treatment provides evidence for the role of asparagine as a prevailing stress responding amino acid. Glutamate dehydrogenase (NADH-GDH, EC 1.4.1.2) exhibited a slight increase in the α-subunit and β-subunit in the wild-type line and the asn2-1 line, respectively under the salinity, whereas its in vitro aminating activity in the wild-type leaves was not affected. The results indicate that the asn2-1 mutant was impaired in nitrogen assimilation and translocation under salt treatment.
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3区Q1影响因子: 3.9
英汉
3. Comparative proteomic analysis of the Arabidopsis cbl1 mutant in response to salt stress.
作者:Shi Shanshan , Chen Wei , Sun Weining
期刊:Proteomics
日期:2011-11-23
DOI :10.1002/pmic.201100042
Many environmental stimuli, including light, biotic and abiotic stress factors, induce changes in cellular Ca(2+) concentrations in plants. Such Ca(2+) signatures are perceived by sensor molecules such as calcineurin B-like (CBL) proteins. AtCBL1, a member of the CBL family which is highly inducible by multiple stress signals, is known to function in the salt stress signal transduction pathway and to positively regulate the plant tolerance to salt. To shed light into the molecular mechanisms of the salt stress response mediated by AtCBL1, a two-dimensional DIGE proteomic approach was applied to identify the differentially expressed proteins in Arabidopsis wild-type and cbl1 null mutant plants in response to salt stress. Seventy-three spots were found altered in expression by least 1.2-fold and 50 proteins were identified by MALDI-TOF/TOF-MS, including some well-known and novel salt-responsive proteins. These proteins function in various processes, such as signal transduction, ROS scavenging, energy production, carbon fixation, metabolism, mRNA processing, protein processing and structural stability. Receptor for activated C kinase 1C (RACK1C, spot 715), a WD40 repeat protein, was up-regulated in the cbl1 null mutant, and two rack1c mutant lines showed decreased tolerance to salt stress, suggesting that RACK1C plays a role in salt stress resistance. In conclusion, our work demonstrated the advantages of the proteomic approach in studies of plant biology and identified candidate proteins in CBL1-mediated salt stress signaling network.
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4区Q1影响因子: 3.6
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英汉
4. miR393s regulate salt stress response pathway in Arabidopsis thaliana through scaffold protein RACK1A mediated ABA signaling pathways.
作者:Denver Jn Baptiste , Ullah Hemayet
期刊:Plant signaling & behavior
日期:2019-04-25
DOI :10.1080/15592324.2019.1600394
Scaffold protein Receptor for Activated C Kinase 1 (RACK1) is a negative regulator of plant stress hormone - abscisic acid (ABA) mediated pathways. RACK1 has been reported to regulate global miRNA biogenesis pathway in C. elegans, humans, and in Arabidopsis. RACK1 regulates different steps of miRNA biogenesis and stability in response to different stimuli in plants. miR393s is implicated in salt stress response pathway through an antagonistic response between the stress hormone ABA-mediated salt stress and growth hormone auxin. Specifically, the known auxin receptor clade transcripts TIR1/AFB2 are the target for the miR393s. By down-regulating the auxin signaling pathways, the miR393s inhibit the regulation of salt tolerance by auxin. Here we show that genetic loss of RACK1A- the predominant member of the three genes family of RACK1 in Arabidopsis, results in the inhibition of miR393 level causing the same salt sensitivities as the individual mir393a or mir393b or the double mutant mir393ab phenotypes. We propose that down-regulation of auxin signaling through RACK1A induced miR393 biogenesis potentially regulates the Arabidopsis acclimation to salinity. Our findings fill up a molecular gap in our understanding of the role of miR393 mediated ABA and auxin-regulated salt stress responses.
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2区Q1影响因子: 3.7
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5. Functional analysis of drought and salt tolerance mechanisms of mulberry RACK1 gene.
作者:Liu Changying , Zhu Panpan , Fan Wei , Feng Yang , Kou Min , Hu Jie , Zhao Aichun
期刊:Tree physiology
日期:2019-12-01
DOI :10.1093/treephys/tpz108
The receptor for activated C kinase 1 (RACK1) protein acts as a central hub for the integration of many physiological processes in eukaryotic organisms. Plant RACK1 is implicated in abiotic stress responses, but the underlying molecular mechanisms of stress adaptation remain largely unknown. Here, the overexpression of the mulberry (Morus alba L.) RACK1 gene in Arabidopsis decreased tolerance to drought and salt stresses and MaRACK1 overexpression changed expression levels of genes in response to stress and stimuli. We developed a simple and efficient transient transformation system in mulberry, and the mulberry seedlings transiently expressing MaRACK1 were hypersensitive to drought and salt stresses. The expression levels of guanine nucleotide-binding protein (G-protein) encoding genes in mulberry and Arabidopsis were not affected by MaRACK1 overexpression. The interactions between RACK1 and G-proteins were confirmed, and the RACK1 proteins from mulberry and Arabidopsis could not interact with their respective G-proteins, which indicated that RACK1 may regulate stress responses independently of G-proteins. Additionally, MaRACK1 may regulate drought and salt stress tolerances by interacting with a fructose 1, 6-bisphosphate aldolase. Our findings provide new insights into the mechanisms underlying RACK1 functions in abiotic stress responses and important information for their further characterization.