title: Metabolic sugar signal promotes Arabidopsis meristematic proliferation via G2.
abstract: Most organs in higher plants are generated postembryonically from the meristems, which harbor continuously dividing stem cells throughout a plant's life cycle. In addition to developmental regulations, mitotic activities in the meristematic tissues are modulated by nutritional cues, including carbon source availability. Here we further analyze the relationship between the sugar signal and seedling meristem establishment, taking advantage of our previous observation that exogenously supplied metabolic sugars can rescue the meristem growth arrest phenotype of the Arabidopsis stip mutant seedlings. Our results show that metabolic sugars reactivate the stip meristems by activating the expression of key cell cycle regulators, and therefore, promoting G2 to M transition in Arabidopsis meristematic tissues. One of the early events in this process is the transcriptional repression of TSS, a genetic suppressor of the stip mutations, by sugar signals, suggesting that TSS may act as an integrator of developmental and nutritional signals in regulating meristematic proliferation. We also present evidence that metabolic sugar signals are required for the activation of mitotic entry during de novo meristem formation from G2 arrested cells. Our observations, together with the recent findings that nutrient deprivation leads to G2 arrest of animal germline stem cells, suggest that carbohydrate availability-regulated G2 to M transition may represent a common mechanism in stem cell division regulation in multicellular organisms.
authors.affiliation: Molecular and Computational Biology, University of Southern California, Los Angeles, CA 90089, USA.
authors.forename: Anna
authors.initials: A
authors.lastname: Skylar
authors.forename: Frances
authors.initials: F
authors.lastname: Sung
authors.forename: Fangxin
authors.initials: F
authors.lastname: Hong
authors.forename: Joanne
authors.initials: J
authors.lastname: Chory
authors.forename: Xuelin
authors.initials: X
authors.lastname: Wu
mesh_terms: D015084:2,4-Dichlorophenoxyacetic Acid / Q000494:pharmacology; D017360:Arabidopsis / Q000254:growth & development*; D029681:Arabidopsis Proteins / Q000502:physiology; D002241:Carbohydrates / Q000502:physiology*; D002244:Carbon / Q000378:metabolism; D002455:Cell Division; D049109:Cell Proliferation; D018844:Cyclin-Dependent Kinases / Q000502:physiology; D016195:G2 Phase; D018398:Homeodomain Proteins / Q000502:physiology; D007210:Indoleacetic Acids / Q000378:metabolism; D028861:Nuclear Pore Complex Proteins / Q000502:physiology
chemical_list: D029681:Arabidopsis Proteins; D002241:Carbohydrates; D018398:Homeodomain Proteins; D007210:Indoleacetic Acids; D028861:Nuclear Pore Complex Proteins; C500834:STIMPY protein, Arabidopsis; C524167:TPR protein, Arabidopsis; D015084:2,4-Dichlorophenoxyacetic Acid; D002244:Carbon; C434472:CDKA1 protein, Arabidopsis; D018844:Cyclin-Dependent Kinases