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This paper describes version 3 of the Simple Ocean Data Assimilation (SODA3) ocean reanalysis with enhancements to model resolution, observation, and forcing datasets, and the addition of active sea ice. SODA3 relies on the ocean component of the NOAA/Geophysical Fluid Dynamics Laboratory CM2.5 coupled model with nominal ¼° resolution. A scheme has also been implemented to reduce bias in the surface fluxes. A 37-yr-long ocean reanalysis, SODA3.4.2, created using this new SODA3 system is compared to the previous generation of SODA (SODA2.2.4) as well as to the Hadley Centre EN4.1.1 no-model statistical objective analysis. The comparison is carried out in the tropics, the midlatitudes, and the Arctic and includes examinations of the meridional overturning circulation in the Atlantic. The comparison shows that SODA3.4.2 has reduced systematic errors to a level comparable to those of the no-model statistical objective analysis in the upper ocean. The accuracy of variability has been improved particularly poleward of the tropics, with the greatest improvements seen in the Arctic, accompanying a substantial reduction in surface net heat and freshwater flux bias. These improvements justify increasing use of ocean reanalysis for climate studies including the higher latitudes.

Limited information is available regarding the exact function of specific WRKY transcription factors in plant responses to heat stress. We analyzed the roles of WRKY25, WRKY26, and WRKY33, three types of group I WRKY proteins, in the regulation of resistance to heat stress. Expression of WRKY25 and WRKY26 was induced upon treatment with high temperature, whereas WRKY33 expression was repressed. Heat-treated WRKY single mutants exhibited small responses, while wrky25wrky26 and wrky25wrky33 double mutants and the wrky25wrky26wrky33 triple mutants showed substantially increased susceptibility to heat stress, showing reduced germination, decreased survival, and elevated electrolyte leakage, compared with wild-type plants. In contrast, constitutive expression of WRKY25, WRKY26, or WRKY33 enhanced resistance to heat stress. Expression studies of selected heat-defense genes in single, double, and triple mutants, as well as in over-expressing lines, were correlated with their thermotolerance phenotypes and demonstrated that the three WRKY transcription factors modulate transcriptional changes of heat-inducible genes in response to heat treatment. In addition, our findings provided evidence that WRKY25, WRKY26, and WRKY33 were involved in regulation of the heat-induced ethylene-dependent response and demonstrated positive cross-regulation within these three genes. Together, these results indicate that WRKY25, WRKY26, and WRKY33 positively regulate the cooperation between the ethylene-activated and heat shock proteins-related signaling pathways that mediate responses to heat stress; and that these three proteins interact functionally and play overlapping and synergetic roles in plant thermotolerance.

SUMMARYThe WRKY transcription factors have been demonstrated to play crucial roles in regulating stress responses; however, the exact mechanisms underlying their involvement in stress responses are not fully understood. Arabidopsis WRKY8 was predominantly expressed in roots and was highly upregulated by salt treatment. Disruption of WRKY8 rendered plants hypersensitive to salt, showing delayed germination, inhibited postgermination development and accelerated chlorosis. Further investigation revealed that WRKY8 interacted with VQ9, and their interaction decreased the DNA-binding activity of WRKY8. The VQ9 protein was exclusively localized in the nucleus, and VQ9 expression was strongly responsive to NaCl treatment. Mutation of VQ9 enhanced tolerance to salt stress, indicating that VQ9 acts antagonistically with WRKY8 to mediate responses to salt stress. The antagonist functions of WRKY8 and VQ9 were consistent with an increased or reduced Na + /K + concentration ratio, as well as contrasting expression patterns of downstream stressresponsive genes in salt-stressed wrky8 and vq9 mutants. Moreover, chromatin immunoprecipitation (ChIP) assays showed that WRKY8 directly bound the promoter of RD29A under salt conditions. These results provided strong evidence that the VQ9 protein acts as a repressor of the WRKY8 factor to maintain an appropriate balance of WRKY8-mediated signaling pathways to establish salinity stress tolerance.

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