As salinity stratification is necessary to form the barrier layer （BL）, the quantification of its role in BL interannual variability is crucial. This study assessed salinity variability and its effect on the BL in t...As salinity stratification is necessary to form the barrier layer （BL）, the quantification of its role in BL interannual variability is crucial. This study assessed salinity variability and its effect on the BL in the equatorial Pacific using outputs from Beijing Normal University Earth System Model （BNU-ESM） simulations. A comparison between observations and the BNU-ESM simulations demonstrated that BNU-ESM has good capability in reproducing most of the interannual features observed in nature. Despite some discrepancies in both magnitude and location of the interannual variability centers, the displacements of sea surface salinity （SSS）, barrier layer thickness （BLT）, and SST simulated by BNU-ESM in the equatorial Pacific are realistic. During E1 Nifio, for example, the modeled interannual anomalies of BLT, mixed layer depth, and isothermal layer depth, exhibit good correspondence with observations, including the development and decay of E1 Nifio in the central Pacific, whereas the intensity of the interannual variabilities is weaker relative to observations. Due to the bias in salinity simulations, the SSS front extends farther west along the equator, whereas BLT variability is weaker in the central Pacific than in observations. Further, the BNU-ESM simulations were examined to assess the relative effects of salinity and temperature variability on BLT. Consistent with previous observation-based analyses, the interannual salinity variability can make a significant contribution to BLT relative to temperature in the western-central equatorial Pacific.展开更多
Plants usually keep resistance(R)proteins in a static state under normal conditions to avoid autoimmunity and save energy for growth,but R proteins can be rapidly activated upon perceiving pathogen invasion.Pib,the fi...Plants usually keep resistance(R)proteins in a static state under normal conditions to avoid autoimmunity and save energy for growth,but R proteins can be rapidly activated upon perceiving pathogen invasion.Pib,the first cloned blast disease R gene in rice,encoding a nucleotide-binding leucine-rich repeat(NLR)protein,mediates resistance to the blast fungal(Magnaporthe oryzae)isolates carrying the avirulence gene AvrPib.However,the molecular mechanisms about how Pib recognizes AvrPib and how it is inactivated and activated remain largely unclear.In this study,through map-based cloning and CRISPR-Cas9 gene editing,we proved that Pib contributes to the blast disease resistance of rice cultivar Yunyin(YY).Furthermore,an SH3 domain-containing protein,SH3P2,was found to associate with Pib mainly at clathrin-coated vesicles in rice cells,via direct binding with the coiled-coil(CC)domain of Pib.Interestingly,overexpression of SH3P2 in YY compromised Pib-mediated resistance to M.oryzae isolates carrying AvrPib and Pib-AvrPib recognition-induced cell death.SH3P2 competitively inhibits the self-association of the Pib CC domain in vitro,suggesting that binding of SH3P2 with Pib undermines its homodimerization.Moreover,SH3P2 can also interact with AvrPib and displays higher affinity to AvrPib than to Pib,which leads to dissociation of SH3P2 from Pib in the presence of AvrPib.Taken together,our results suggest that SH3P2 functions as a“protector”to keep Pib in a static state by direct interaction during normal growth but could be triggered off by the invasion of AvrPib-carrying M.oryzae isolates.Our study reveals a new mechanism about how an NLR protein is inactivated under normal conditions but is activated upon pathogen infection.展开更多
基金This study was supported by National Key Research and Development Program of China （2016YFA0601801）, the State Key Program of National Natural Science Foundation of China （41530424）, National Program on Global Change and Air-Sea Interactions, State Oceanic Administration （SOA） （GASI-IPOVAI-03）, and the National Natural Science Foundation of China （41305121）. We sincerely thank two anonymous reviewers whose comments improved the paper.
基金supported by the National Natural Science Foundation of China(Grant Nos.41376039,41376019 and 41421005)the NSFC-Shandong Joint Fund for Marine Science Research Centers(Grant No.U1406401)+1 种基金the IOCAS through the CAS Strategic Priority Project[the Western Pacific Ocean System(WPOS)]the WPOS in the "Strategic Priority Research Program" of the Chinese Academy of Sciences(Grant No.XDA11010304)
文摘As salinity stratification is necessary to form the barrier layer （BL）, the quantification of its role in BL interannual variability is crucial. This study assessed salinity variability and its effect on the BL in the equatorial Pacific using outputs from Beijing Normal University Earth System Model （BNU-ESM） simulations. A comparison between observations and the BNU-ESM simulations demonstrated that BNU-ESM has good capability in reproducing most of the interannual features observed in nature. Despite some discrepancies in both magnitude and location of the interannual variability centers, the displacements of sea surface salinity （SSS）, barrier layer thickness （BLT）, and SST simulated by BNU-ESM in the equatorial Pacific are realistic. During E1 Nifio, for example, the modeled interannual anomalies of BLT, mixed layer depth, and isothermal layer depth, exhibit good correspondence with observations, including the development and decay of E1 Nifio in the central Pacific, whereas the intensity of the interannual variabilities is weaker relative to observations. Due to the bias in salinity simulations, the SSS front extends farther west along the equator, whereas BLT variability is weaker in the central Pacific than in observations. Further, the BNU-ESM simulations were examined to assess the relative effects of salinity and temperature variability on BLT. Consistent with previous observation-based analyses, the interannual salinity variability can make a significant contribution to BLT relative to temperature in the western-central equatorial Pacific.
基金This work was supported by the National Key R&D Program Foundation of China(grant no.2016YFD0300508)the National Rice Industry Technology System of Modern Agriculture for China(grant no.CARS-01-20)+2 种基金the“5511”Collaborative Innovation Project for High-Quality Development and Surpasses of Agriculture between Government of Fujian and Chinese Academy of Agricultural Sciences(grant no.XTCXGC2021001)Key Program of Science and Technology in Fujian province,China(no.2020NZ08016)the Special Foundation of Non-Profit Research Institutes of Fujian Province(grant no.2018R1021-5).
文摘Plants usually keep resistance(R)proteins in a static state under normal conditions to avoid autoimmunity and save energy for growth,but R proteins can be rapidly activated upon perceiving pathogen invasion.Pib,the first cloned blast disease R gene in rice,encoding a nucleotide-binding leucine-rich repeat(NLR)protein,mediates resistance to the blast fungal(Magnaporthe oryzae)isolates carrying the avirulence gene AvrPib.However,the molecular mechanisms about how Pib recognizes AvrPib and how it is inactivated and activated remain largely unclear.In this study,through map-based cloning and CRISPR-Cas9 gene editing,we proved that Pib contributes to the blast disease resistance of rice cultivar Yunyin(YY).Furthermore,an SH3 domain-containing protein,SH3P2,was found to associate with Pib mainly at clathrin-coated vesicles in rice cells,via direct binding with the coiled-coil(CC)domain of Pib.Interestingly,overexpression of SH3P2 in YY compromised Pib-mediated resistance to M.oryzae isolates carrying AvrPib and Pib-AvrPib recognition-induced cell death.SH3P2 competitively inhibits the self-association of the Pib CC domain in vitro,suggesting that binding of SH3P2 with Pib undermines its homodimerization.Moreover,SH3P2 can also interact with AvrPib and displays higher affinity to AvrPib than to Pib,which leads to dissociation of SH3P2 from Pib in the presence of AvrPib.Taken together,our results suggest that SH3P2 functions as a“protector”to keep Pib in a static state by direct interaction during normal growth but could be triggered off by the invasion of AvrPib-carrying M.oryzae isolates.Our study reveals a new mechanism about how an NLR protein is inactivated under normal conditions but is activated upon pathogen infection.
