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Extended leaf longevity in the ore4‐1 mutant of Arabidopsis with a reduced expression of a plastid ribosomal protein gene
Author(s) -
Woo Hye Ryun,
Goh ChangHyo,
Park JoonHyun,
de la Serve Bernard Teyssendier,
Kim JinHee,
Park YounIl,
Nam Hong Gil
Publication year - 2002
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.1365-313x.2002.01355.x
Subject(s) - mutant , biology , plastid , arabidopsis thaliana , arabidopsis , wild type , gene , mutation , ribosomal protein , genetics , longevity , abscisic acid , chloroplast , microbiology and biotechnology , ribosome , rna
Summary The longevity of plant leaf organs is genetically determined. However, the molecular mechanisms underlying the control of longevity are still largely unknown. Here, we describe a T‐DNA‐insertional mutation of Arabidopsis thaliana that confers extended leaf longevity. The mutation, termed ore4‐1 , delays a broad spectrum of age‐dependent leaf senescence, but has little effect on leaf senescence artificially induced by darkness, abscisic acid (ABA), methyl jasmonate (MeJA), or ethylene. The T‐DNA was inserted within the promoter region of the plastid ribosomal small subunit protein 17 ( PRPS17 ) gene, and this insertion dramatically reduced PRPS17 mRNA expression. In the ore4‐1 mutant, the leaf growth rate is decreased, while the maturation timing is similar to that of wild‐type. In addition, the activity of the photosystem I (PSI) is significantly reduced in the ore4‐1 mutant, as compared to wild‐type. Thus, the ore4‐1 mutation results in a deficiency in various chloroplast functions, including photosynthesis, which may decrease leaf growth. Our results suggest a possible link between reduced metabolism and extended longevity of the leaf organs in the ore4‐1 mutation.