S-Nitrosoglutathione Reductase Contributes to Thermotolerance by Modulating High Temperature-Induced Apoplastic H(2)O(2) in Solanum lycopersicum.

S-Nitrosoglutathione Reductase Contributes to Thermotolerance by Modulating High Temperature-Induced Apoplastic H(2)O(2) in Solanum lycopersicum.
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S-亚硝基谷胱甘肽还原酶通过调节番茄中高温诱导的质外体 H2O2 来提高耐热性

DOI:
10.3389/fpls.2022.862649
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发表时间:
2022
影响因子:
5.6
通讯作者:
--
中科院分区:
生物学2区
文献类型:
--
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S-亚硝基谷胱甘肽还原酶(GSNOR)通过调节S-亚硝基硫醇(SNO)水平影响蛋白质S-亚硝基化,被认为是植物抗逆性的重要调节因子。然而,GSNOR介导的胁迫耐受机制仍不清楚。在这里,我们发现,GSNOR活性在番茄(Solanum lycopersicum)植物中被高温诱导,而SlGSNOR 1的mRNA水平表现出很小的响应。通过病毒诱导的基因沉默(VIGS)抑制SlGSNOR 1表达增加了高温下SNO和亚硝酸盐的积累,降低了耐热性。热耐受性降低与脱落酸(阿坝)和水杨酸(SA)积累减少、丝裂原活化蛋白激酶(MAPK)活化减弱和热休克蛋白表达减少有关。有趣的是,SlGSNOR 1沉默损害了响应于高温的植物爆裂氧化酶同源物1(SlRBOH 1)和质外体H2 O2积累的上调,而SlRBOH 1沉默废除了GSNOR的激活,并导致与SlGSNOR 1沉默植物中类似的耐热性下降。重要的是,H2 O2处理恢复了SlGSNOR 1沉默植物的耐热性和提高的抗氧化能力。我们的研究结果表明,GSNOR在调节SlRBOH 1依赖的质外体H2 O2的生产中起着重要作用,在响应高温,而SNO和H2 O2之间的平衡相互作用是维持细胞的氧化还原稳态和耐热性的关键。
S-nitrosoglutathione reductase (GSNOR) is considered as a critical regulator of plant stress tolerance for its impacts on protein S-nitrosylation through regulation of the S-nitrosothiol (SNO) level. However, the mechanism of GSNOR-mediated stress tolerance is still obscure. Here, we found that GSNOR activity was induced by high temperature in tomato (Solanum lycopersicum) plants, whereas mRNA level of SlGSNOR1 exhibited little response. Suppressing SlGSNOR1 expression by virus-induced gene silencing (VIGS) increased accumulation of SNO and nitrites under high temperature and reduced thermotolerance. The compromised thermotolerance was associated with less accumulation of abscisic acid (ABA) and salicylic acid (SA), attenuated activation of mitogen-activated protein kinase (MAPK) and reduced expression of heat shock protein. Intriguingly, SlGSNOR1 silencing impaired upregulation of RESPIRATORY BURST OXIDASE HOMOLOG1 (SlRBOH1) and apoplastic H2O2 accumulation in response to high temperature, whereas SlRBOH1 silencing abolished activation of GSNOR and led to a similar decline in thermotolerance as in SlGSNOR1-silenced plants. Importantly, H2O2 treatment recovered the thermotolerance and improved antioxidant capacity in SlGSNOR1-silenced plants. Our results suggest that GSNOR plays a role in regulating the SlRBOH1-dependent apoplastic H2O2 production in response to high temperature, while a balanced interaction between SNO and H2O2 is critical for maintaining the cellular redox homeostasis and thermotolerance.
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发表时间: 1998-08-06
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