Plant growth and development are significantly hampered in saline environments,limiting agricultural productivity.Thus,it is crucial to unravel the mechanism underlying plant responses to salt stress.β-1,4-Galactan(g...Plant growth and development are significantly hampered in saline environments,limiting agricultural productivity.Thus,it is crucial to unravel the mechanism underlying plant responses to salt stress.β-1,4-Galactan(galactan),which forms the side chains of pectic rhamnogalacturonan I,enhances plant sensitivity to high-salt stress.Galactan is synthesized by GALACTAN SYNTHASE1(GALS1).We previously showed that Na Cl relieves the direct suppression of GALS1 transcription by the transcription factors BPC1 and BPC2 to induce the excess accumulation of galactan in Arabidopsis(Arabidopsis thaliana).However,how plants adapt to this unfavorable environment remains unclear.Here,we determined that the transcription factors CBF1,CBF2,and CBF3 directly interact with the GALS1 promoter and repress its expression,leading to reduced galactan accumulation and enhanced salt tolerance.Salt stress enhances the binding of CBF1/CBF2/CBF3 to the GALS1 promoter by inducing CBF1/CBF2/CBF3 transcription and accumulation.Genetic analysis suggested that CBF1/CBF2/CBF3 function upstream of GALS1 to modulate salt-induced galactan biosynthesis and the salt response.CBF1/CBF2/CBF3 and BPC1/BPC2 function in parallel to regulate GALS1 expression,thereby modulating the salt response.Our results reveal a mechanism in which salt-activated CBF1/CBF2/CBF3 inhibit BPC1/BPC2-regulated GALS1 expression to alleviate galactan-induced salt hypersensitivity,providing an activation/deactivation fine-tune mechanism for dynamic regulation of GALS1 expression under salt stress in Arabidopsis.展开更多
Salinity severely reduces plant growth and limits agricultural productivity.Dynamic changes and rearrangement of the plant cell wall is an important response to salt stress,but relatively little is known about the bio...Salinity severely reduces plant growth and limits agricultural productivity.Dynamic changes and rearrangement of the plant cell wall is an important response to salt stress,but relatively little is known about the biological importance of specific cell wall components in the response.Here,we demonstrate a specific function ofβ-1,4-galactan in salt hypersensitivity.We found that salt stress induces the accumulation ofβ-1,4-galactan in root cell walls by up regulating the expression of GALACTAN SYNTHASE 1(GALS1),which encodes aβ-1,4-galactan synthase.The accumulation ofβ-1,4-galactan negatively affects salt tolerance.Exogenous application of D-galactose(D-Gal)causes an increase inβ-1,4-galactan levels in the wild type and GALS1 mutants,especially in GALS1 overexpressors,which correlated with the aggravated salt hypersensitivity.Furthermore,we discovered that the BARLEY B RECOMBINANT/BASIC PENTACYSTEINE transcription factors BPC1/BPC2 positively regulate plant salt tolerance by repressing GALS1 expression andβ-1,4-galactan accumulation.Genetic analysis suggested that GALS1 is genetically epistatic to BPC1/BPC2 with respect to the control of salt sensitivity as well as accumulation ofβ-1,4-galactan.Taken together,our results reveal a new regulatory mechanism by whichβ-1,4-galactan regulated by the BPC1/BPC2-GALS1 module aggravates salt sensitivity in Arabidopsis thaliana.展开更多
Background:This study aimed to construct and characterize a humanized influenza mouse model expressing hST6GAL1.Methods:Humanized fragments,consisting of the endothelial cell-specific K18 promoter,human ST6GAL1-encodi...Background:This study aimed to construct and characterize a humanized influenza mouse model expressing hST6GAL1.Methods:Humanized fragments,consisting of the endothelial cell-specific K18 promoter,human ST6GAL1-encoding gene,and luciferase gene,were microinjected into the fertilized eggs of mice.The manipulated embryos were transferred into the oviducts of pseudopregnant female mice.The offspring were identified using PCR.Mice exhibiting elevated expression of the hST6GAL1 gene were selectively bred for propagation,and in vivo analysis was performed for screening.Expression of the humanized gene was tested by performing immunohistochemical(IHC)analysis.Hematologic and biochemical analyses using the whole blood and serum of humanized hST6GAL1 mice were performed.Results:Successful integration of the human ST6GAL1 gene into the mouse genome led to the overexpression of human SiaT ST6GAL1.Seven mice were identified as carrying copies of the humanized gene,and the in vivo analysis indicated that hST6GAL1gene expression in positive mice mirrored influenza virus infection characteristics.The IHC results revealed that hST6GAL1 was expressed in the lungs of humanized mice.Moreover,the hematologic and biochemical parameters of the positive mice were within the normal range.Conclusion:A humanized influenza mouse model expressing the hST6GAL1 gene was successfully established and characterized.展开更多
基金supported by grants from the National Natural Science Foundation of China(32001445)。
文摘Plant growth and development are significantly hampered in saline environments,limiting agricultural productivity.Thus,it is crucial to unravel the mechanism underlying plant responses to salt stress.β-1,4-Galactan(galactan),which forms the side chains of pectic rhamnogalacturonan I,enhances plant sensitivity to high-salt stress.Galactan is synthesized by GALACTAN SYNTHASE1(GALS1).We previously showed that Na Cl relieves the direct suppression of GALS1 transcription by the transcription factors BPC1 and BPC2 to induce the excess accumulation of galactan in Arabidopsis(Arabidopsis thaliana).However,how plants adapt to this unfavorable environment remains unclear.Here,we determined that the transcription factors CBF1,CBF2,and CBF3 directly interact with the GALS1 promoter and repress its expression,leading to reduced galactan accumulation and enhanced salt tolerance.Salt stress enhances the binding of CBF1/CBF2/CBF3 to the GALS1 promoter by inducing CBF1/CBF2/CBF3 transcription and accumulation.Genetic analysis suggested that CBF1/CBF2/CBF3 function upstream of GALS1 to modulate salt-induced galactan biosynthesis and the salt response.CBF1/CBF2/CBF3 and BPC1/BPC2 function in parallel to regulate GALS1 expression,thereby modulating the salt response.Our results reveal a mechanism in which salt-activated CBF1/CBF2/CBF3 inhibit BPC1/BPC2-regulated GALS1 expression to alleviate galactan-induced salt hypersensitivity,providing an activation/deactivation fine-tune mechanism for dynamic regulation of GALS1 expression under salt stress in Arabidopsis.
基金This study was supported by grants from the National Natural Science Foundation of China(31871534 and 32001445)the Natural Science Foundation of Jiangsu Province(BK20200557)+2 种基金the China Postdoctoral Science Foundation(2019M651846)the Six Talent Peaks Program of Jiangsu Province(2016-NY-079)and the Natural Science Foundation of Guangdong Province(2018A030313686).H.V.S.was supported through the Joint BioEnergy Institute(http://www.jbei.org)by the U.S.Department of Energy,Office of Science,Office of Biological and Environmental Research,through contract DE-AC02-05CH11231 between Lawrence Berkeley National Laboratory and the U.S.Department of Energy.
文摘Salinity severely reduces plant growth and limits agricultural productivity.Dynamic changes and rearrangement of the plant cell wall is an important response to salt stress,but relatively little is known about the biological importance of specific cell wall components in the response.Here,we demonstrate a specific function ofβ-1,4-galactan in salt hypersensitivity.We found that salt stress induces the accumulation ofβ-1,4-galactan in root cell walls by up regulating the expression of GALACTAN SYNTHASE 1(GALS1),which encodes aβ-1,4-galactan synthase.The accumulation ofβ-1,4-galactan negatively affects salt tolerance.Exogenous application of D-galactose(D-Gal)causes an increase inβ-1,4-galactan levels in the wild type and GALS1 mutants,especially in GALS1 overexpressors,which correlated with the aggravated salt hypersensitivity.Furthermore,we discovered that the BARLEY B RECOMBINANT/BASIC PENTACYSTEINE transcription factors BPC1/BPC2 positively regulate plant salt tolerance by repressing GALS1 expression andβ-1,4-galactan accumulation.Genetic analysis suggested that GALS1 is genetically epistatic to BPC1/BPC2 with respect to the control of salt sensitivity as well as accumulation ofβ-1,4-galactan.Taken together,our results reveal a new regulatory mechanism by whichβ-1,4-galactan regulated by the BPC1/BPC2-GALS1 module aggravates salt sensitivity in Arabidopsis thaliana.
基金National Key Research and Development Program of China,Grant/Award Number:2021YFC2301403 and 2022YFF0711000。
文摘Background:This study aimed to construct and characterize a humanized influenza mouse model expressing hST6GAL1.Methods:Humanized fragments,consisting of the endothelial cell-specific K18 promoter,human ST6GAL1-encoding gene,and luciferase gene,were microinjected into the fertilized eggs of mice.The manipulated embryos were transferred into the oviducts of pseudopregnant female mice.The offspring were identified using PCR.Mice exhibiting elevated expression of the hST6GAL1 gene were selectively bred for propagation,and in vivo analysis was performed for screening.Expression of the humanized gene was tested by performing immunohistochemical(IHC)analysis.Hematologic and biochemical analyses using the whole blood and serum of humanized hST6GAL1 mice were performed.Results:Successful integration of the human ST6GAL1 gene into the mouse genome led to the overexpression of human SiaT ST6GAL1.Seven mice were identified as carrying copies of the humanized gene,and the in vivo analysis indicated that hST6GAL1gene expression in positive mice mirrored influenza virus infection characteristics.The IHC results revealed that hST6GAL1 was expressed in the lungs of humanized mice.Moreover,the hematologic and biochemical parameters of the positive mice were within the normal range.Conclusion:A humanized influenza mouse model expressing the hST6GAL1 gene was successfully established and characterized.
