In response to competition for light from their neighbors,shade-intolerant plants flower precociously to ensure reproductive success and survival.However,the molecular mechanisms underlying this key developmental swit...In response to competition for light from their neighbors,shade-intolerant plants flower precociously to ensure reproductive success and survival.However,the molecular mechanisms underlying this key developmental switch are not well understood.Here,we show that a pair of Arabidopsis transcription factors essential for phytochrome A signaling,FAR-RED ELONGATED HYPOCOTYL3(FHY3)and FAR-RED IMPAIRED RESPONSE1(FAR1),regulate flowering time by integrating environmental light signals with the miR156-SPL module-mediated aging pathway.We found that FHY3 and FAR1 directly interact with three flowering-promoting SQUAMOSA-PROMOTER BINDING PROTEIN-LIKE(SPL)transcription factors,SPL3,SPL4,and SPL5,and inhibit their binding to the promoters of several key flowering regulatory genes,including FRUITFUL(FUL),LEAFY(LFY),APETALA1(AP1),and MIR172C,thus downregulating their transcript levels and delaying flowering.Under simulated shade conditions,levels of SPL3/4/5 proteins increase,whereas levels of FHY3 and FAR1 proteins decline,thus releasing SPL3/4/5 from FHY3/FAR1 inhibition to allow activation of FUL,LFY,AP1,and MIR172C and,consequently,early flowering.Taken together,these results unravel a novel mechanism whereby plants regulate flowering time by integrating environmental cues(such as light conditions)and an internal developmental program(the miR156-SPL module-mediated aging pathway).展开更多
myo-lnositol-l-phosphate synthase （MIPS） catalyzes the limiting step of inositol biosynthesis and has crucial roles in plant growth and development. In response to stress, the transcription of MIPS1 is induced and t...myo-lnositol-l-phosphate synthase （MIPS） catalyzes the limiting step of inositol biosynthesis and has crucial roles in plant growth and development. In response to stress, the transcription of MIPS1 is induced and the biosynthesis of inositol or inositol derivatives is promoted by unknown mechanisms. Here, we found that the light signaling protein FAR-RED ELONGATED HYPOCOTYL3 （FHY3） and its homolog FAR- RED IMPAIRED RESPONSE1 （FAR1） regulate light-induced inositol biosynthesis and oxidative stress re- sponses by activating the transcription of MIPS1. Disruption of FHY3 and FAR1 caused light-induced cell death after dark-light transition, precocious leaf senescence, and increased sensitivity to oxidative stress. Reduction of salicylic acid （SA） accumulation by overexpression of SALICYLIC ACID 3-HYDROXYLASE largely suppressed the cell death phenotype of fhy3 far1 mutant plants, suggesting that FHY3- and FARl-mediated cell death is dependent on SA. Furthermore, comparative analysis of chromatin immuno- precipitation sequencing and microarray results revealed that FHY3 and FAR1 directly target both MIPS1 and MIPS2. The fhy3 far1 mutant plants showed severely decreased MIPS1/2 transcript levels and reduced inositol levels. Conversely, constitutive expression of MIPSl partially rescued the inositol contents, caused reduced transcript levels of SA-biosynthesis genes, and prevented oxidative stress in fhy3 far1. Taken together, our results indicate that the light signaling proteins FHY3 and FAR1 directly bind the promoter of MIPS1 to activate its expression and thereby promote inositol biosynthesis to prevent light-induced oxidative stress and SA-dependent cell death.展开更多
Light and chloroplast function is known to affect the plant immune response; however, the underlying mechanism remains elusive. We previously demonstrated that two light signaling factors, FAR-RED ELONGATED HYPOCOTYL ...Light and chloroplast function is known to affect the plant immune response; however, the underlying mechanism remains elusive. We previously demonstrated that two light signaling factors, FAR-RED ELONGATED HYPOCOTYL 3（FHY3）and FAR-RED IMPAIRED RESPONSE 1（FAR1）, regulate chlorophyll biosynthesis and seedling growth via controlling HEMB1 expression in Arabidopsis thaliana. In this study, we reveal that FHY3 and FAR1 are involved in modulating plant immunity. We showed that the fhy3 far1 double null mutant displayed high levels of reactive oxygen species and salicylic acid（SA） and increased resistance to Pseudomonas syringae pathogen infection. Microarray analysis revealed that a large proportion of pathogen-related genes, particularly genes encoding nucleotide-binding and leucine-rich repeat domain resistant proteins, are highly induced in fhy3 far1. Genetic studies indicated that the defects of fhy3 far1 can be largely rescued by reducing SA signaling or blocking SA accumulation, and by overexpression of HEMB1, which encodes a 5-aminolevulinic acid dehydratase in the chlorophyll biosynthetic pathway.Furthermore, we found that transgenic plants with reduced expression of HEMB1 exhibit a phenotype similar to fhy3 far1.Taken together, this study demonstrates an important role of FHY3 and FAR1 in regulating plant immunity, through integrating chlorophyll biosynthesis and the SA signaling pathway.展开更多
基金supported by grants from National Natural Science Foundation of China(31770210 and 31570191)National Key Research and D evelopm ent Program of China(2016YFD0100303).
文摘In response to competition for light from their neighbors,shade-intolerant plants flower precociously to ensure reproductive success and survival.However,the molecular mechanisms underlying this key developmental switch are not well understood.Here,we show that a pair of Arabidopsis transcription factors essential for phytochrome A signaling,FAR-RED ELONGATED HYPOCOTYL3(FHY3)and FAR-RED IMPAIRED RESPONSE1(FAR1),regulate flowering time by integrating environmental light signals with the miR156-SPL module-mediated aging pathway.We found that FHY3 and FAR1 directly interact with three flowering-promoting SQUAMOSA-PROMOTER BINDING PROTEIN-LIKE(SPL)transcription factors,SPL3,SPL4,and SPL5,and inhibit their binding to the promoters of several key flowering regulatory genes,including FRUITFUL(FUL),LEAFY(LFY),APETALA1(AP1),and MIR172C,thus downregulating their transcript levels and delaying flowering.Under simulated shade conditions,levels of SPL3/4/5 proteins increase,whereas levels of FHY3 and FAR1 proteins decline,thus releasing SPL3/4/5 from FHY3/FAR1 inhibition to allow activation of FUL,LFY,AP1,and MIR172C and,consequently,early flowering.Taken together,these results unravel a novel mechanism whereby plants regulate flowering time by integrating environmental cues(such as light conditions)and an internal developmental program(the miR156-SPL module-mediated aging pathway).
文摘myo-lnositol-l-phosphate synthase （MIPS） catalyzes the limiting step of inositol biosynthesis and has crucial roles in plant growth and development. In response to stress, the transcription of MIPS1 is induced and the biosynthesis of inositol or inositol derivatives is promoted by unknown mechanisms. Here, we found that the light signaling protein FAR-RED ELONGATED HYPOCOTYL3 （FHY3） and its homolog FAR- RED IMPAIRED RESPONSE1 （FAR1） regulate light-induced inositol biosynthesis and oxidative stress re- sponses by activating the transcription of MIPS1. Disruption of FHY3 and FAR1 caused light-induced cell death after dark-light transition, precocious leaf senescence, and increased sensitivity to oxidative stress. Reduction of salicylic acid （SA） accumulation by overexpression of SALICYLIC ACID 3-HYDROXYLASE largely suppressed the cell death phenotype of fhy3 far1 mutant plants, suggesting that FHY3- and FARl-mediated cell death is dependent on SA. Furthermore, comparative analysis of chromatin immuno- precipitation sequencing and microarray results revealed that FHY3 and FAR1 directly target both MIPS1 and MIPS2. The fhy3 far1 mutant plants showed severely decreased MIPS1/2 transcript levels and reduced inositol levels. Conversely, constitutive expression of MIPSl partially rescued the inositol contents, caused reduced transcript levels of SA-biosynthesis genes, and prevented oxidative stress in fhy3 far1. Taken together, our results indicate that the light signaling proteins FHY3 and FAR1 directly bind the promoter of MIPS1 to activate its expression and thereby promote inositol biosynthesis to prevent light-induced oxidative stress and SA-dependent cell death.
基金supported by grants from the National Natural Science Foundation of China(31170221,31325002 and 31300206)the Ministry of Agriculture of China(2014ZX08009-003)
文摘Light and chloroplast function is known to affect the plant immune response; however, the underlying mechanism remains elusive. We previously demonstrated that two light signaling factors, FAR-RED ELONGATED HYPOCOTYL 3（FHY3）and FAR-RED IMPAIRED RESPONSE 1（FAR1）, regulate chlorophyll biosynthesis and seedling growth via controlling HEMB1 expression in Arabidopsis thaliana. In this study, we reveal that FHY3 and FAR1 are involved in modulating plant immunity. We showed that the fhy3 far1 double null mutant displayed high levels of reactive oxygen species and salicylic acid（SA） and increased resistance to Pseudomonas syringae pathogen infection. Microarray analysis revealed that a large proportion of pathogen-related genes, particularly genes encoding nucleotide-binding and leucine-rich repeat domain resistant proteins, are highly induced in fhy3 far1. Genetic studies indicated that the defects of fhy3 far1 can be largely rescued by reducing SA signaling or blocking SA accumulation, and by overexpression of HEMB1, which encodes a 5-aminolevulinic acid dehydratase in the chlorophyll biosynthetic pathway.Furthermore, we found that transgenic plants with reduced expression of HEMB1 exhibit a phenotype similar to fhy3 far1.Taken together, this study demonstrates an important role of FHY3 and FAR1 in regulating plant immunity, through integrating chlorophyll biosynthesis and the SA signaling pathway.
