Blocking the Metabolism of Starch Breakdown Products in Arabidopsis Leaves Triggers Chloroplast Degradation
| Autor: | Simona Eicke, Tabea Mettler, Stefan Hörtensteiner, Michaela Stettler, Samuel C. Zeeman, Gaëlle Messerli |
|---|---|
| Přispěvatelé: | University of Zurich |
| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
autophagy
senescence Chloroplasts Starch Arabidopsis Plant Science Carbohydrate metabolism 580 Plants (Botany) Chloroplast membrane SX13 Plant Growth chemistry.chemical_compound 10126 Department of Plant and Microbial Biology SX00 SystemsX.ch 1110 Plant Science Maltotriose 1312 Molecular Biology Arabidopsis thaliana Molecular Biology Research Articles Chlorosis photosynthesis biology food and beverages Maltose biology.organism_classification Chloroplast Plant Leaves Phenotype Biochemistry chemistry chloroplast biology Mutation 570 Life sciences |
| Zdroj: | Molecular Plant |
| ISSN: | 1752-9867 1674-2052 |
| Popis: | In most plants, a large fraction of photo-assimilated carbon is stored in the chloroplasts during the day as starch and remobilized during the subsequent night to support metabolism. Mutations blocking either starch synthesis or starch breakdown in Arabidopsis thaliana reduce plant growth. Maltose is the major product of starch breakdown exported from the chloroplast at night. The maltose excess 1 mutant (mex1), which lacks the chloroplast envelope maltose transporter, accumulates high levels of maltose and starch in chloroplasts and develops a distinctive but previously unexplained chlorotic phenotype as leaves mature. The introduction of additional mutations that prevent starch synthesis, or that block maltose production from starch, also prevent chlorosis of mex1. In contrast, introduction of mutations in disproportionating enzyme (DPE1) results in the accumulation of maltotriose in addition to maltose, and greatly increases chlorosis. These data suggest a link between maltose accumulation and chloroplast homeostasis. Microscopic analyses show that the mesophyll cells in chlorotic mex1 leaves have fewer than half the number of chloroplasts than wild-type cells. Transmission electron microscopy reveals autophagy-like chloroplast degradation in both mex1 and the dpe1/mex1 double mutant. Microarray analyses reveal substantial reprogramming of metabolic and cellular processes, suggesting that organellar protein turnover is increased in mex1, though leaf senescence and senescence-related chlorophyll catabolism are not induced. We propose that the accumulation of maltose and malto-oligosaccharides causes chloroplast dysfunction, which may by signaled via a form of retrograde signaling and trigger chloroplast degradation. |
| Databáze: | OpenAIRE |
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