Down-Regulation of a Nicotinate Phosphoribosyltransferase Gene, OsNaPRT1, Leads to Withered Leaf Tips.
Li-Wen WuDeyong RenShikai HuGengmi LiGuojun DongLiang JiangXingming HuWeijun YeYongtao CuiLi ZhuJiang HuGuangheng ZhangZhenyu GaoDa-Li ZengQian QianLongbiao GuoPublished in: Plant physiology (2016)
Premature leaf senescence affects plant growth and yield in rice. NAD plays critical roles in cellular redox reactions and remains at a sufficient level in the cell to prevent cell death. Although numerous factors affecting leaf senescence have been identified, few involving NAD biosynthetic pathways have been described for plants. Here, we report the cloning and characterization of Leaf Tip Senescence 1 (LTS1) in rice (Oryza sativa), a recessive mutation in the gene encoding O. sativa nicotinate phosphoribosyltransferase (OsNaPRT1) in the NAD salvage pathway. A point mutation in OsNaPRT1 leads to dwarfism and the withered leaf tip phenotype, and the lts1 mutant displays early leaf senescence compared to the wild type. Leaf nicotinate and nicotinamide contents are elevated in lts1, while NAD levels are reduced. Leaf tissue of lts1 exhibited significant DNA fragmentation and H2O2 accumulation, along with up-regulation of genes associated with senescence. The lts1 mutant also showed reduced expression of SIR2-like genes (OsSRT1 and OsSRT2) and increased acetylation of histone H3K9. Down-regulation of OsSRTs induced histone H3K9 acetylation of senescence-related genes. These results suggest that deficiency in the NAD salvage pathway can trigger premature leaf senescence due to transcriptional activation of senescence-related genes.
Keyphrases
- dna damage
- endothelial cells
- stress induced
- cell death
- wild type
- genome wide
- high glucose
- gene expression
- poor prognosis
- signaling pathway
- copy number
- cell therapy
- bone marrow
- long non coding rna
- single molecule
- binding protein
- diabetic rats
- duchenne muscular dystrophy
- circulating tumor
- genome wide analysis
- nucleic acid
- replacement therapy
- heat shock protein