Salt stress is a major abiotic stress which severely hinders crop production.However,the regulatory network controlling tomato resistance to salt remains unclear.Here,we found that the tomato WRKY transcription factor...Salt stress is a major abiotic stress which severely hinders crop production.However,the regulatory network controlling tomato resistance to salt remains unclear.Here,we found that the tomato WRKY transcription factor WRKY57 acted as a negative regulator in salt stress response by directly attenuating the transcription of salt-responsive genes(Sl RD29B and Sl DREB2)and an ion homeostasis gene(Sl SOS1).We further identified two VQ-motif containing proteins Sl VQ16 and Sl VQ21as Sl WRKY57-interacting proteins.Sl VQ16 positively,while Sl VQ21 negatively modulated tomato resistance to salt stress.Sl VQ16 and Sl VQ21 competitively interacted with Sl WRKY57 and antagonistically regulated the transcriptional repression activity of Sl WRKY57.Additionally,the Sl WRKY57-Sl VQ21/Sl VQ16 module was involved in the pathway of phytohormone jasmonates(JAs)by interacting with JA repressors JA-ZIM domain(JAZ)proteins.These results provide new insights into how the Sl WRKY57-Sl VQ21/Sl VQ16 module finely tunes tomato salt tolerance.展开更多
TGF-β and Foxp3 expressions are crucial for the induction and functional activity of CD4＋Foxp3＋ regulatory T （iTreg） cells. Here, we demonstrate that although TGF-β-primed CD8＋ cells display much lower Foxp3 ex...TGF-β and Foxp3 expressions are crucial for the induction and functional activity of CD4＋Foxp3＋ regulatory T （iTreg） cells. Here, we demonstrate that although TGF-β-primed CD8＋ cells display much lower Foxp3 expression, their suppressive capacity is equivalent to that of CD4＋ iTreg cells, and both Foxp3- and Foxp3＋ CD8＋ subsets have suppressive activities in vitro and in vivo. CD8＋Foxp3- iTreg cells produce little IFN-γ but almost no IL-2, and display a typical anergic phenotype. Among phenotypic markers expressed in CD8＋Foxp3- cells, we identify CD103 expression particularly crucial for the generation and function of this subset. Moreover, IL-IO and TGF-β signals rather than cytotoxicity mediate the suppressive effect of this novel Treg population. Therefore, TGF-β can induce both CD8＋Foxp3- and CD8＋Foxp3＋ iTreg subsets, which may represent the unique immunoregulatory means to treat autoimmune and inflammatory diseases.展开更多
基金supported by the Project of Cultivation for young top-notch Talents of Beijing Municipal Institutions (Grant No.BPHR202203099)。
文摘Salt stress is a major abiotic stress which severely hinders crop production.However,the regulatory network controlling tomato resistance to salt remains unclear.Here,we found that the tomato WRKY transcription factor WRKY57 acted as a negative regulator in salt stress response by directly attenuating the transcription of salt-responsive genes(Sl RD29B and Sl DREB2)and an ion homeostasis gene(Sl SOS1).We further identified two VQ-motif containing proteins Sl VQ16 and Sl VQ21as Sl WRKY57-interacting proteins.Sl VQ16 positively,while Sl VQ21 negatively modulated tomato resistance to salt stress.Sl VQ16 and Sl VQ21 competitively interacted with Sl WRKY57 and antagonistically regulated the transcriptional repression activity of Sl WRKY57.Additionally,the Sl WRKY57-Sl VQ21/Sl VQ16 module was involved in the pathway of phytohormone jasmonates(JAs)by interacting with JA repressors JA-ZIM domain(JAZ)proteins.These results provide new insights into how the Sl WRKY57-Sl VQ21/Sl VQ16 module finely tunes tomato salt tolerance.
文摘TGF-β and Foxp3 expressions are crucial for the induction and functional activity of CD4＋Foxp3＋ regulatory T （iTreg） cells. Here, we demonstrate that although TGF-β-primed CD8＋ cells display much lower Foxp3 expression, their suppressive capacity is equivalent to that of CD4＋ iTreg cells, and both Foxp3- and Foxp3＋ CD8＋ subsets have suppressive activities in vitro and in vivo. CD8＋Foxp3- iTreg cells produce little IFN-γ but almost no IL-2, and display a typical anergic phenotype. Among phenotypic markers expressed in CD8＋Foxp3- cells, we identify CD103 expression particularly crucial for the generation and function of this subset. Moreover, IL-IO and TGF-β signals rather than cytotoxicity mediate the suppressive effect of this novel Treg population. Therefore, TGF-β can induce both CD8＋Foxp3- and CD8＋Foxp3＋ iTreg subsets, which may represent the unique immunoregulatory means to treat autoimmune and inflammatory diseases.
