Content area

Abstract

Plastid ribosomal proteins (PRPs) are essential for ribosome biogenesis, plastid protein biosynthesis, chloroplast differentiation, and early chloroplast development. This study identifies the first rice PRP mutant, asl1 (albino seedling lethality1), which exhibits an albino lethal phenotype at the seedling stage. This albino phenotype was associated with altered chlorophyll (Chl) content and chloroplast development. Map-based cloning revealed that ASL1 encodes PRP S20 (PRPS20), which localizes to the chloroplast. ASL1 showed tissue-specific expression, as it was highly expressed in plumule and young seedlings but expressed at much lower levels in other tissues. In addition, ASL1 expression was regulated by light. The transcript levels of nuclear genes for Chl biosynthesis and chloroplast development were strongly affected in asl1 mutants; transcripts of some plastid genes for photosynthesis were undetectable. Our findings indicate that nuclear-encoded PRPS20 plays an important role in chloroplast development in rice.

Details

Title
Disruption of the Rice Plastid Ribosomal Protein S20 Leads to Chloroplast Developmental Defects and Seedling Lethality
Author
Gong, Xiaodi 1 ; Jiang, Quan 1 ; Xu, Jianlong 2 ; Zhang, Jianhui 1 ; Teng, Sheng 3 ; Lin, Dongzhi 4 ; Dong, Yanjun 1 

 Development Center of Plant Germplasm Resources, College of Life and Environmental Sciences, Shanghai Normal University, Shanghai 200234 
 Institute of Crop Sciences, Chinese Academy of Agricultural Sciences, Beijing, 100081 
 Institute of Plant Physiology and Ecology, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences, Shanghai 200032, China 
 Development Center of Plant Germplasm Resources, College of Life and Environmental Sciences, Shanghai Normal University, Shanghai 200234; Development Center of Plant Germplasm Resources, College of Life and Environmental Sciences, Shanghai Normal University, Shanghai 200234 
Pages
1769-1777
Publication year
2013
Publication date
Oct 1, 2013
Publisher
Oxford University Press
e-ISSN
21601836
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
3169746544
Copyright
© 2013 Gong et al..