Phenotypic characterization and gene mapping of an <italic>early senescence leaf H5</italic>(<italic>esl-H5</italic>) mutant in rice (<italic>Oryza sativa</italic> L.)

Abstract

<p id="C3">A stable mutant <italic>esl-H5</italic> (<italic>early senescence leaf H5</italic>) was identified from the mutant library of<italic> japonica</italic> rice Huaidao 5 population induced by ethyl methane sulfonate (EMS) treatment. The mutant was normal at seedling stage. However, the lower leaves in <italic>esl-H5</italic> mutant displayed premature senescence at about 50 days after sowing. Compared with the wild type (WT), the heading date of the <italic>esl-H5</italic> mutant was delayed, while agronomical traits including plant height, panicle length, grain number per panicle, effective tiller numbers, and 1000-grain weight were significantly reduced. Moreover, chlorophyll content was also decreased in <italic>esl-H5</italic> mutant. Genetic analysis indicated that the early senescence trait in <italic>esl-H5 </italic>mutant was controlled by a single recessive gene. <italic>ESL-H5</italic> gene was localized on chromosome 1 using molecular marker. MutMap analysis further revealed that one nucleotide G to A replace occurred in the last exon of <italic>Os01g0533000</italic> gene which encodes callose synthase. The G to A replace in the <italic>ESL</italic>-<italic>H5</italic> introduced a premature stop codon. Phylogenetic analysis showed that ESL-H5 was homology with <italic>Arabidopsis </italic>AtGSL7 (Glucan Synthase-Like 7). At tillering stage, the contents of soluble sugar and starch were significantly increased in the leaves of the <italic>esl-H5 </italic>mutant compared with those of the WT. These results implied that the mutation of <italic>ESL-H5</italic> affected the transport of photosynthetic products, resulting in premature leaf senescence phenotypes. The qRT-PCR analysis revealed that the expression levels of disease resistance-related genes <italic>PR1a</italic>, <italic>PR1b</italic>, <italic>PR2</italic>, <italic>PR4</italic>, <italic>PR5</italic>, and <italic>PR10 </italic>in <italic>esl-H5</italic> mutant were higher than those in WT, which was consistent with the observation that <italic>esl-H5</italic> mutant improved bacterial blight resistance. The present results lay the foundation for studying the roles of sugar signal in regulating rice senescence and disease resistance.