title: Effect of sugar-induced senescence on gene expression and implications for the regulation of senescence in Arabidopsis.
abstract: There has been some debate whether leaf senescence is induced by sugar starvation or by sugar accumulation. External supply of sugars has been shown to induce symptoms of senescence such as leaf yellowing. However, it was so far not clear if sugars have a signalling function during developmental senescence. Glucose and fructose accumulate strongly during senescence in Arabidopsis thaliana (L.) Heynh. leaves. Using Affymetrix GeneChip analysis we determined the effect of sugar-induced senescence on gene expression. Growth on glucose in combination with low nitrogen supply induced leaf yellowing and changes in gene expression that are characteristic of developmental senescence. Most importantly, the senescence-specific gene SAG12, which was previously thought to be sugar-repressible, was induced over 900-fold by glucose. Induction of SAG12, which is expressed during late senescence, demonstrates that processes characteristic for late stages are sugar-inducible. Two MYB transcription factor genes, PAP1 and PAP2, were identified as senescence-associated genes that are induced by glucose. Moreover, growth on glucose induced genes for nitrogen remobilisation that are typically enhanced during developmental senescence, including the glutamine synthetase gene GLN1;4 and the nitrate transporter gene AtNRT2.5. In contrast to wild-type plants, the hexokinase-1 mutant gin2-1 did not accumulate hexoses and senescence was delayed. Induction of senescence by externally supplied glucose was partially abolished in gin2-1, indicating that delayed senescence was a consequence of decreased sugar sensitivity. Taken together, our results show that Arabidopsis leaf senescence is induced rather than repressed by sugars.
authors.affiliation: Department of Biology, University College London, Gower Street, London WC1E 6BT, UK.
authors.forename: Nathalie
authors.initials: N
authors.lastname: Pourtau
authors.forename: Richard
authors.initials: R
authors.lastname: Jennings
authors.forename: Elise
authors.initials: E
authors.lastname: Pelzer
authors.forename: Jacqueline
authors.initials: J
authors.lastname: Pallas
authors.forename: Astrid
authors.initials: A
authors.lastname: Wingler
mesh_terms: D027321:Anion Transport Proteins / Q000235:genetics / Q000378:metabolism; D017360:Arabidopsis / Q000235:genetics / Q000254:growth & development* / Q000378:metabolism*; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism; D002244:Carbon / Q000378:metabolism; D016000:Cluster Analysis; D003546:Cysteine Endopeptidases / Q000235:genetics / Q000378:metabolism; D005632:Fructose / Q000378:metabolism* / Q000502:physiology; D020869:Gene Expression Profiling; D018506:Gene Expression Regulation, Plant; D005947:Glucose / Q000378:metabolism* / Q000502:physiology; D005974:Glutamate-Ammonia Ligase / Q000235:genetics / Q000378:metabolism; D006593:Hexokinase / Q000235:genetics / Q000378:metabolism; D009154:Mutation; D000091285:Nitrate Transporters; D009584:Nitrogen / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis; D000073718:Pancreatitis-Associated Proteins; D018515:Plant Leaves / Q000235:genetics / Q000254:growth & development / Q000378:metabolism; D015398:Signal Transduction; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism
chemical_list: D027321:Anion Transport Proteins; D029681:Arabidopsis Proteins; D002244:Carbon; D003546:Cysteine Endopeptidases; D005632:Fructose; D005947:Glucose; D005974:Glutamate-Ammonia Ligase; D006593:Hexokinase; D000091285:Nitrate Transporters; D009584:Nitrogen; D000073718:Pancreatitis-Associated Proteins; D014157:Transcription Factors; C502612:AT1G56650 protein, Arabidopsis; C514560:PAP2 protein, Arabidopsis; C000612141:REG3A protein, human; C402082:SAG12 protein, Arabidopsis