Character Identification, Physiological And Biochemical Characteristic And Gene Mapping Of A Rice Early Leaf Senescence Mutant (els-R7954)

A rice early leaf senescence mutant, temporarily named els-R7954, was obtained from rice mutation breeding. In this study, we performed a preliminary research and analysis on phenotype, physiological and biochemical characteristic, cytologic feature, genetic analysis as well as gene mapping of the els-R7954mutant. The main results are as follows:1. The premature senescence, development of dynamic, agronomic traits and rice quality traits of els-R7954mutant and the wild-type (WT) was investigated. The result indicated that:compared with WT, the mutant showed the weaker growth potential, growing period advanced, and obvious traits of premature senescence in the field. The leaves of mutant showed brown、dark red or yellow in the late of tillering stage. With the plant growth, the premature senescence phene(?)non is becoming more obvious, and leaves of the plant have all withered and died in filling stage. The agronomic traits of mutants showed scrubby plant, shorter leaves, smaller panicle, low seed setting rate, grain number per panicle^1000-grain weight and grain density reduced. At the same time, the rice quality of mutant showed a high degree of chalkiness and low degree of transparency. In conclusion, significant negative effect on the rice growth are suffered from els gene mutation.2. Analysis the physiological and biochemical indicators of the mutant and WT showed:the activity of SOD, content of GSH、VC、VE; both decreased with the growth period developed, and mutant kept a significantly lower from booting stage to mature stage. The content of MDA of mutant and WT both increased with the plant growth, and the mutant had a significantly higher content than WT from booting stage to mature stage. These indicated that mutant cannot protected the leaf cell from ROS and led the premature senescence. The content of chlorophyll(a、b、 a+b) of mutant and WT are both stable in the early of the growth period, and mutant had a significantly lower from WT. At the mature stage, the chlorophyll content of mutant is approaching zero.compared with mutant and WT, net photosynthetic rate and stomatal conductance of mutant and WT both declined with developing of growth period, and mutant showed a highly significantly lower from WT. This indicated photosynthetic performance of mutant was severely affected. The intercellular CO2concentration both rised from heading stage to mature stage, and mutant had a significantly higher. This also showed that the mutation adversely affected its ability of CO2assimilation. The photosynthesis, respiration, transpiration of mutant stay very low in the late of growth period, is consistent with the phenomenon that mutant withered and died early in the field.3. Using transmission electron microscope, we observed the cell structure of flag leaf and top second leaf of WT and mutant. The results showed that:compared with WT, the cytoplasm of mutant flag leaf shrank, grana thylakoid swollen and broke down, but membrane of grana lamellae and thylakoid was integral, and little osmiophilic particles can be found in chloroplast. The chloroplast of top second leaf shrank and swollen severely, a large number of them broke down. We can found lot of osmiophilic particles and accumulation of phenolics. This indicated that premature senescence caused a early broke down of mutant chloroplast, and also showed the reason how premature senescence led the color changing of leaf or decline of photosynthetic and respiration rate from a microscopic point of view.4. To investigate the inheritance pattern of the mutation, four crosses were made between the early leaf senescence mutant (male parent) and the wild-type Zhehui7954,9311, Minghui63, Shuhui527(female parents). Identifying the phenotype in the F2population, it suggested that F2plants segregated in a ratio of3normal:1els, indicating that the mutant phenotype is controlled by a single recessive gene. In this study, the mapping population were derived from a cross between els-R7954and9311, we attempted to map a els gene using SSR markers with this population. At last, the els locus was preliminarily mapped to chromosome2between SSR marker RM3774and RM530, with a distance of5.0cM from RM530. This result lays the foundation for fine mapping and cloning of premature senescence gene.