The Salt-Overly-Sensitive(SOS)signaling module,comprising the sodium-transport protein SOS1 and the regulatory proteins SOS2 and SOS3,is well known as the central salt excretion system,which helps protect plants again...The Salt-Overly-Sensitive(SOS)signaling module,comprising the sodium-transport protein SOS1 and the regulatory proteins SOS2 and SOS3,is well known as the central salt excretion system,which helps protect plants against salt stress.Here we report that VPS23A,a component of the ESCRT(endosomal sorting complex required for transport),plays an essential role in the function of the SOS module in conferring plant salt tolerance.VPS23A enhances the interaction of SOS2 and SOS3.In the presence of salt stress,VPS23A positively regulates the redistribution of SOS2 to the plasma membrane,which then activates the antiporter activity of SOS1 to reduce Na+accumulation in plant cells.Genetic evidence demonstrated that plant salt tolerance achieved by the overexpression of SOS2 and SOS3 dependeds on VPS23A.Taken together,our results revealed that VPS23A is a crucial regulator of the SOS module and affects the localization of SOS2 to the cell membrane.Moreover,the strong salt tolerance of Arabidopsis seedlings conferred by the engineered membrane-bound SOS2 revealed the significance of SOS2 sorting to the cell membrane in achieving its function,providing a potential strategy for crop salt tolerance engineering.展开更多
A myriad of abiotic stress responses in plants are controlled by abscisic acid(ABA)signaling.ABA receptors can be degraded by both the 26S proteasome pathway and vacuolar degradation pathway after processing via the e...A myriad of abiotic stress responses in plants are controlled by abscisic acid(ABA)signaling.ABA receptors can be degraded by both the 26S proteasome pathway and vacuolar degradation pathway after processing via the endosomal sorting complex required for transport(ESCRT)proteins.Despite being essential for ABA signaling,the upstream regulators of ESCRTs remain unknown.Here,we report that the ESCRT-I component VPS23A is an unstable protein that is degraded via the ubiquitin-proteasome system(UPS).The UEV domain of VPS23A physically interacts with the two PSAP motifs of XBAT35,an E3 ubiquitin ligase,and this interaction results in the deposition of K48 polyubiquitin chains on VPS23A,marking it for degradation by 26S proteasomes.We showed that XBAT35 in plants is a positive regulator of ABA responses that acts via the VPS23A/PYL4 complex,specifically by accelerating VPS23A turnover and thereby increasing accumulation of the ABA receptor PYL4.This work deciphers how an ESCRT component is regulated in plants and deepens our understanding of plant stress responses by illustrating a mechanism whereby crosstalk between the UPS and endosome-vacuole-mediated degradation pathways controls ABA signaling.展开更多
Dendronized hyperbranched polymer(DHP) is a new kind of polymer, which combines the advantages of dendrimers and hyperbranched polymers. In this work, two dendronized hyperbranched polymers, DHPG0 and DHPG1, were succ...Dendronized hyperbranched polymer(DHP) is a new kind of polymer, which combines the advantages of dendrimers and hyperbranched polymers. In this work, two dendronized hyperbranched polymers, DHPG0 and DHPG1, were successfully prepared through the simple "A_3+B_2" type Sonogashira coupling reaction. The nonlinear optical(NLO) effects of DHPG0 and DHPG1, characterized by the d33 values, were 183 and 220 pm V^(–1) respectively, higher than those of their analogues of dendronized polymers and dendrimers, thanks to the special topological structure. Also, the obtained polymers displayed excellent solubility, good processability, and high thermal stability.展开更多
The aim of this study is to explore inhibitory activity of Bifidobacterium adolescent combined with cis-platin on the growth of melanoma(B16)in mice and the underlying mechanism.C57 mice were inoculated with B16 cance...The aim of this study is to explore inhibitory activity of Bifidobacterium adolescent combined with cis-platin on the growth of melanoma(B16)in mice and the underlying mechanism.C57 mice were inoculated with B16 cancer cells to construct mouse model of melanoma and treated with bifidobacterium adolescent combined with cisplatin.Ratios of inhibitory activity on the growth of melanoma(B16)were calculated.Pathology changes of the tumor were observed by HE staining.B16 cell cycles were examined on a flow cytometer.Lymphocyte prolif-eration was measured with MTT assay and the T-cell sub-set was measured by double marked fluorescence.When bifidobacterium of 1010 cfu/L was injected,the ratio of inhibitory activity on the growth of melanoma(B16)reached 54%,which was similar to that of cisplatin group.The ratio of inhibitory activity reached 74.45%when the mice were treated by bifidobacterium combined with cis-platin.HE staining shows that bifidobacterium inhibited B16 cell proliferation and enhanced the cisplatin`s killing activity on B16 cells.The results of flow cytometry demonstrated that B16 cell proliferation was arrested at G1 stage after treatment with bifidobacterium.The B16 cell proliferation was arrested at S stage after treatment with cisplatin.The CD4+percentage increased and the difference was significant compared with the normal group after treatment with bifidobacterium,indicating that T-cell immune activity was enhanced.Treatment with bifidobacterium combined with cisplatin can enhance the inhibitory activity on the growth of melanoma(B16)of cisplatin.The mechanism of the inhibitory activity on B16 cell proliferation is correlated with the enhanced immune activity in mice.展开更多
基金This project was financially supported by grants from the National Key R&D Program of China(2016YFA0500501)the National Natural Science Foundation of China(31800228 and 31571441)also partially supported by the Transgenic Research Projects(2016ZX08009-003).
文摘The Salt-Overly-Sensitive(SOS)signaling module,comprising the sodium-transport protein SOS1 and the regulatory proteins SOS2 and SOS3,is well known as the central salt excretion system,which helps protect plants against salt stress.Here we report that VPS23A,a component of the ESCRT(endosomal sorting complex required for transport),plays an essential role in the function of the SOS module in conferring plant salt tolerance.VPS23A enhances the interaction of SOS2 and SOS3.In the presence of salt stress,VPS23A positively regulates the redistribution of SOS2 to the plasma membrane,which then activates the antiporter activity of SOS1 to reduce Na+accumulation in plant cells.Genetic evidence demonstrated that plant salt tolerance achieved by the overexpression of SOS2 and SOS3 dependeds on VPS23A.Taken together,our results revealed that VPS23A is a crucial regulator of the SOS module and affects the localization of SOS2 to the cell membrane.Moreover,the strong salt tolerance of Arabidopsis seedlings conferred by the engineered membrane-bound SOS2 revealed the significance of SOS2 sorting to the cell membrane in achieving its function,providing a potential strategy for crop salt tolerance engineering.
基金grant 2016YFA0500500 from the National Key R&D Program of Chinagrant 31800228 from the National Natural Science Foundation of China.
文摘A myriad of abiotic stress responses in plants are controlled by abscisic acid(ABA)signaling.ABA receptors can be degraded by both the 26S proteasome pathway and vacuolar degradation pathway after processing via the endosomal sorting complex required for transport(ESCRT)proteins.Despite being essential for ABA signaling,the upstream regulators of ESCRTs remain unknown.Here,we report that the ESCRT-I component VPS23A is an unstable protein that is degraded via the ubiquitin-proteasome system(UPS).The UEV domain of VPS23A physically interacts with the two PSAP motifs of XBAT35,an E3 ubiquitin ligase,and this interaction results in the deposition of K48 polyubiquitin chains on VPS23A,marking it for degradation by 26S proteasomes.We showed that XBAT35 in plants is a positive regulator of ABA responses that acts via the VPS23A/PYL4 complex,specifically by accelerating VPS23A turnover and thereby increasing accumulation of the ABA receptor PYL4.This work deciphers how an ESCRT component is regulated in plants and deepens our understanding of plant stress responses by illustrating a mechanism whereby crosstalk between the UPS and endosome-vacuole-mediated degradation pathways controls ABA signaling.
基金supported by the National Natural Science Foundation of China(21325416)
文摘Dendronized hyperbranched polymer(DHP) is a new kind of polymer, which combines the advantages of dendrimers and hyperbranched polymers. In this work, two dendronized hyperbranched polymers, DHPG0 and DHPG1, were successfully prepared through the simple "A_3+B_2" type Sonogashira coupling reaction. The nonlinear optical(NLO) effects of DHPG0 and DHPG1, characterized by the d33 values, were 183 and 220 pm V^(–1) respectively, higher than those of their analogues of dendronized polymers and dendrimers, thanks to the special topological structure. Also, the obtained polymers displayed excellent solubility, good processability, and high thermal stability.
文摘The aim of this study is to explore inhibitory activity of Bifidobacterium adolescent combined with cis-platin on the growth of melanoma(B16)in mice and the underlying mechanism.C57 mice were inoculated with B16 cancer cells to construct mouse model of melanoma and treated with bifidobacterium adolescent combined with cisplatin.Ratios of inhibitory activity on the growth of melanoma(B16)were calculated.Pathology changes of the tumor were observed by HE staining.B16 cell cycles were examined on a flow cytometer.Lymphocyte prolif-eration was measured with MTT assay and the T-cell sub-set was measured by double marked fluorescence.When bifidobacterium of 1010 cfu/L was injected,the ratio of inhibitory activity on the growth of melanoma(B16)reached 54%,which was similar to that of cisplatin group.The ratio of inhibitory activity reached 74.45%when the mice were treated by bifidobacterium combined with cis-platin.HE staining shows that bifidobacterium inhibited B16 cell proliferation and enhanced the cisplatin`s killing activity on B16 cells.The results of flow cytometry demonstrated that B16 cell proliferation was arrested at G1 stage after treatment with bifidobacterium.The B16 cell proliferation was arrested at S stage after treatment with cisplatin.The CD4+percentage increased and the difference was significant compared with the normal group after treatment with bifidobacterium,indicating that T-cell immune activity was enhanced.Treatment with bifidobacterium combined with cisplatin can enhance the inhibitory activity on the growth of melanoma(B16)of cisplatin.The mechanism of the inhibitory activity on B16 cell proliferation is correlated with the enhanced immune activity in mice.