期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 116, 期 20, 页码 10162-10167出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1820426116
关键词
GUN1; retrograde signaling; RNA editing; MORF2/RIP2; PPR
资金
- NIH-National Cancer Institute [CCSG: P30 014195]
- Chapman Foundation
- Helmsley Charitable Trust
- Helmsley Center for Genomic Medicine
- US Department of Energy [DE-FG02-04ER15540]
- Howard Hughes Medical Institute
- U.S. Department of Energy (DOE) [DE-FG02-04ER15540] Funding Source: U.S. Department of Energy (DOE)
During development or under stress, chloroplasts generate signals that regulate the expression of a large number of nuclear genes, a process called retrograde signaling. GENOMES UNCOUPLED 1 (GUN1) is an important regulator of this pathway. In this study, we have discovered an unexpected role for GUN1 in plastid RNA editing, as gun1 mutations affect RNA-editing efficiency at multiple sites in plastids during retrograde signaling. GUN1 plays a direct role in RNA editing by physically interacting with MULTIPLE ORGANELLAR RNA EDITING FACTOR 2 (MORF2). MORF2 overexpression causes widespread RNA-editing changes and a strong genomes uncoupled (gun) molecular phenotype similar to gun1. MORF2 further interacts with RNA-editing site-specificity factors: ORGANELLE TRANSCRIPT PROCESSING 81 (OTP81), ORGANELLE TRANSCRIPT PROCESSING 84 (OTP84), and YELLOW SEEDLINGS 1 (YS1). We further show that otp81, otp84, and ys1 single mutants each exhibit a very weak gun phenotype, but combining the three mutations enhances the phenotype. Our study uncovers a role for GUN1 in the regulation of RNA-editing efficiency in damaged chloroplasts and suggests that MORF2 is involved in retrograde signaling.
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