After germination in the dark,plants produce a shoot apical hook and closed cotyledons to protect the quiescent shoot apical meristem(SAM),which is critical for seedling survival during skotomorphogenesis.The factors ...After germination in the dark,plants produce a shoot apical hook and closed cotyledons to protect the quiescent shoot apical meristem(SAM),which is critical for seedling survival during skotomorphogenesis.The factors that coordinate these processes,particularly SAM repression,remain enigmatic.Plant cuticles,multilayered structures of lipid components on the outermost surface of the aerial epidermis of all land plants,provide protection against desiccation and external environmental stresses.Whether and how cuticles regulate plant development are still unclear.Here,we demonstrate that mutants of BODYGUARD1(BDG1)and long-chain acyl-CoA synthetase2(LACS2),key genes involved in cutin biosynthesis,produce a short hypocotyl with an opened apical hook and cotyledons in which the SAM is activated during skotomorphogenesis.Light signaling represses expression of BDG1 and LACS2,as well as cutin biosynthesis.Transcriptome analysis revealed that cuticles are critical for skotomorphogenesis,particularly for the development and function of chloroplasts.Genetic and molecular analyses showed that decreased HOOKLESS1 expression results in apical hook opening in the mutants.When hypoxia-induced expression of LITTLE ZIPPER2 at the SAM promotes organ initiation in the mutants,the de-repressed expression of cell-cycle genes and the cytokinin response induce the growth of true leaves.Our results reveal previously unrecognized developmental functions of the plant cuticle during skotomorphogenesis and demonstrate a mechanism by which light initiates photomorphogenesis through dynamic regulation of cuticle synthesis to induce coordinated and systemic changes in organ development and growth during the skotomorphogenesis-to-photomorphogenesis transition.展开更多
基金supported by the National Natural Science Foundation of China(32270340 and 31970824 to X.L.and 32300304 to H.Z.)the project“Fulltime introduction of high-end talent research project”(2020HBQZYC004 and A202105008 to X.L.)from Hebei provincefunding from the Hebei Natural Science Foundation(C2021205013 to X.L.,C2021205043 to L.G.,and C2023205049 to Y.Sun).
文摘After germination in the dark,plants produce a shoot apical hook and closed cotyledons to protect the quiescent shoot apical meristem(SAM),which is critical for seedling survival during skotomorphogenesis.The factors that coordinate these processes,particularly SAM repression,remain enigmatic.Plant cuticles,multilayered structures of lipid components on the outermost surface of the aerial epidermis of all land plants,provide protection against desiccation and external environmental stresses.Whether and how cuticles regulate plant development are still unclear.Here,we demonstrate that mutants of BODYGUARD1(BDG1)and long-chain acyl-CoA synthetase2(LACS2),key genes involved in cutin biosynthesis,produce a short hypocotyl with an opened apical hook and cotyledons in which the SAM is activated during skotomorphogenesis.Light signaling represses expression of BDG1 and LACS2,as well as cutin biosynthesis.Transcriptome analysis revealed that cuticles are critical for skotomorphogenesis,particularly for the development and function of chloroplasts.Genetic and molecular analyses showed that decreased HOOKLESS1 expression results in apical hook opening in the mutants.When hypoxia-induced expression of LITTLE ZIPPER2 at the SAM promotes organ initiation in the mutants,the de-repressed expression of cell-cycle genes and the cytokinin response induce the growth of true leaves.Our results reveal previously unrecognized developmental functions of the plant cuticle during skotomorphogenesis and demonstrate a mechanism by which light initiates photomorphogenesis through dynamic regulation of cuticle synthesis to induce coordinated and systemic changes in organ development and growth during the skotomorphogenesis-to-photomorphogenesis transition.