Ubiquitin-dependent chloroplast-associated protein degradation in plants.

Autor: Ling Q; Department of Plant Sciences, University of Oxford, Oxford OX1 3RB, UK., Broad W; Department of Plant Sciences, University of Oxford, Oxford OX1 3RB, UK., Trösch R; Department of Biology, University of Leicester, Leicester LE1 7RH, UK., Töpel M; Department of Biology, University of Leicester, Leicester LE1 7RH, UK., Demiral Sert T; Department of Biology, University of Leicester, Leicester LE1 7RH, UK., Lymperopoulos P; Department of Biology, University of Leicester, Leicester LE1 7RH, UK., Baldwin A; Department of Biology, University of Leicester, Leicester LE1 7RH, UK., Jarvis RP; Department of Plant Sciences, University of Oxford, Oxford OX1 3RB, UK. paul.jarvis@plants.ox.ac.uk.; Department of Biology, University of Leicester, Leicester LE1 7RH, UK.
Jazyk: angličtina
Zdroj: Science (New York, N.Y.) [Science] 2019 Feb 22; Vol. 363 (6429).
DOI: 10.1126/science.aav4467
Abstrakt: Chloroplasts contain thousands of nucleus-encoded proteins that are imported from the cytosol by translocases in the chloroplast envelope membranes. Proteolytic regulation of the translocases is critically important, but little is known about the underlying mechanisms. We applied forward genetics and proteomics in Arabidopsis to identify factors required for chloroplast outer envelope membrane (OEM) protein degradation. We identified SP2, an Omp85-type β-barrel channel of the OEM, and CDC48, a cytosolic AAA+ (ATPase associated with diverse cellular activities) chaperone. Both proteins acted in the same pathway as the ubiquitin E3 ligase SP1, which regulates OEM translocase components. SP2 and CDC48 cooperated to bring about retrotranslocation of ubiquitinated substrates from the OEM (fulfilling conductance and motor functions, respectively), enabling degradation of the substrates by the 26S proteasome in the cytosol. Such chloroplast-associated protein degradation (CHLORAD) is vital for organellar functions and plant development.
(Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)
Databáze: MEDLINE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje