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Blocking the Metabolism of Starch Breakdown Products in Arabidopsis Leaves Triggers Chloroplast Degradation

Molecular Plant 2009年第6期2卷 1233-1246页

作者： Michaela Stettler Simona Eicke Tabea Mettler Gaelle Messerli stefan hortensteiner Samuel C. Zeeman Department of Biology ETH Zurich CH-8092 Zurich Switzerland Institute of Plant Biology University of Zurich CH-8008 Zurich Switzerland Present address: Max Planck Institute for Molecular Plant Physiology Potsdam-Golm 14476 Germany Present address: Johnson & Johnson Medical CH-8957 Spreitenbach Switzerland

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.

关键词： Carbohydrate metabolism photosynthesis senescence chloroplast biology Arabidopsis autophagy.

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Arabidopsis STAY-GREEN2 Is a Negative Regulator of Chlorophyll Degradation during Leaf Senescence

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Molecular Plant 2014年第8期7卷 1288-1302页

作者： Yasuhito Sakuraba So-Yon Park Ye-Sol Kim Seung-Hyun Wang Soo-Cheul Yoo stefan hortensteiner Nam-Chon Paek Department of Plant Science Plant Genomics and Breeding Institute Research Institute of Agriculture and Life Sciences Seoul NationalUniversity Seoul 151-921 Korea Present address: Department of Plant Pathology Physiology and Weed Science Virginia Tech Blacksburg VA 24061 USA Present address: Advanced Radiation Technology Institute Korea Atomic Energy Research Institute Jeongeup 580-185 Korea Department of Plant & Environmental Science Hankyong National University Ansung 456-749 Korea Institute of Plant Biology University of Zurich CH-8008 Zurich Switzerland

Chlorophyll （Chl） degradation causes leaf yellowing during senescence or under stress conditions. For Chl breakdown, STAY-GREEN1 （SGR1） interacts with Chl catabolic enzymes （CCEs） and light-harvesting complex II （LHCII） at the thylakoid membrane, possibly to allow metabolic channeling of potentially phototoxic Chl breakdown intermediates. Among these Chl catabolic components, SGR1 acts as a key regulator of leaf yellowing. In addition to SGR1 （At4g22920）, the Arabidopsis thaliana genome contains an additional homolog, SGR2 （At4g11910）, whose biological function remains elusive. Under senescence-inducing conditions, SGR2 expression is highly up-regulated, similarly to SGR1 expression. Here we show that SGR2 function counteracts SGR1 activity in leaf Chl degradation; SGR2-overexpressing plants stayed green and the sgr2-1 knockout mutant exhibited early leaf yellowing under age-, dark-, and stress-induced senescence conditions. Like SGR1, SGR2 interacted with LHCII but, in contrast to SGR1, SGR2 interactions with CCEs were very limited. Furthermore, SGR1 and SGR2 formed homo- or heterodimers, strongly suggesting a role for SGR2 in negatively regulat- ing Chl degradation by possibly interfering with the proposed CCE-recruiting function of SGR1. Our data indicate an antagonistic evolution of the functions of SGR1 and SGR2 in Arabidopsis to balance Chl catabolism in chloroplasts with the dismantling and remobilizing of other cellular components in senescing leaf cells.

关键词： Arabidopsis thaliana stay-green SGR1 SGR2 chlorophyll degradation leaf senescence abiotic stress.

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