S-Nitrosoglutathione Reductase Contributes to Thermotolerance by Modulating High Temperature-Induced Apoplastic HO in .

S-nitrosoglutathione reductase (GSNOR) is considered as a critical regulator of plant stress tolerance for its impacts on protein -nitrosylation through regulation of the -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 () plants, whereas mRNA level of exhibited little response. Suppressing 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, silencing impaired upregulation of () and apoplastic HO accumulation in response to high temperature, whereas silencing abolished activation of GSNOR and led to a similar decline in thermotolerance as in -silenced plants. Importantly, HO treatment recovered the thermotolerance and improved antioxidant capacity in -silenced plants. Our results suggest that GSNOR plays a role in regulating the -dependent apoplastic HO production in response to high temperature, while a balanced interaction between SNO and HO is critical for maintaining the cellular redox homeostasis and thermotolerance.