Journal
SCIENCE
Volume 350, Issue 6259, Pages 450-454Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aac7444
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Funding
- Division of Chemical Sciences, Geosciences, and Biosciences, Office of Basic Energy Sciences of the U.S. Department of Energy [DE-FG02-04ER15540]
- Howard Hughes Medical Institute
- NIH [1F32GM096610]
- NCI P30 Cancer Center Support Grant [CA014195]
- NINDS P30 Neuroscience Center Core Grant [NS072031]
- W.M. Keck Foundation
- Gottfried Wilhelm Leibniz Award
- Max Planck Society
- Waitt Advanced Biophotonics Center
- U.S. Department of Energy (DOE) [DE-FG02-04ER15540] Funding Source: U.S. Department of Energy (DOE)
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Energy production by chloroplasts and mitochondria causes constant oxidative damage. A functioning photosynthetic cell requires quality-control mechanisms to turn over and degrade chloroplasts damaged by reactive oxygen species (ROS). Here, we generated a conditionally lethal Arabidopsis mutant that accumulated excess protoporphyrin IX in the chloroplast and produced singlet oxygen. Damaged chloroplasts were subsequently ubiquitinated and selectively degraded. A genetic screen identified the plant U-box 4 (PUB4) E3 ubiquitin ligase as being necessary for this process. pub4-6 mutants had defects in stress adaptation and longevity. Thus, we have identified a signal that leads to the targeted removal of ROS-overproducing chloroplasts.
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