Premium
Single base substitution in OsCDC48 is responsible for premature senescence and death phenotype in rice
Author(s) -
Huang QiNa,
Shi YongFeng,
Zhang XiaoBo,
Song LiXin,
Feng BaoHua,
Wang HuiMei,
Xu Xia,
Li XiaoHong,
Guo Dan,
Wu JianLi
Publication year - 2016
Publication title -
journal of integrative plant biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.734
H-Index - 83
eISSN - 1744-7909
pISSN - 1672-9072
DOI - 10.1111/jipb.12372
Subject(s) - biology , senescence , mutant , phenotype , oryza sativa , complementation , gene , programmed cell death , genetics , wild type , microbiology and biotechnology , apoptosis
Abstract A premature senescence and death 128 ( psd128 ) mutant was isolated from an ethyl methane sulfonate‐induced rice IR64 mutant bank. The premature senescence phenotype appeared at the six‐leaf stage and the plant died at the early heading stage. psd128 exhibited impaired chloroplast development with significantly reduced photosynthetic ability, chlorophyll and carotenoid contents, root vigor, soluble protein content and increased malonaldehyde content. Furthermore, the expression of senescence‐related genes was significantly altered in psd128 . The mutant trait was controlled by a single recessive nuclear gene. Using map‐based strategy, the mutation Oryza sativa cell division cycle 48 ( OsCDC48 ) was isolated and predicted to encode a putative AAA‐type ATPase with 809 amino‐acid residuals. A single base substitution at position C2347T in psd128 resulted in a premature stop codon. Functional complementation could rescue the mutant phenotype. In addition, RNA interference resulted in the premature senescence and death phenotype. OsCDC48 was expressed constitutively in the root, stem, leaf and panicle. Subcellular analysis indicated that OsCDC48:YFP fusion proteins were located both in the cytoplasm and nucleus. OsCDC48 was highly conserved with more than 90% identity in the protein levels among plant species. Our results indicated that the impaired function of OsCDC48 was responsible for the premature senescence and death phenotype.