Rice lesion mimic mutants play a crucial role in studying programmed cell death and broad-spectrum disease resistance in rice. In this study, we first report a novel panicle and leaf spot1 mutant (panicle and leaf spot 1, pls1), which develops reddish-brown spots on leaves starting from the three-leaf stage, expanding with plant growth and affecting other organs. Unlike previously reported rice lesion mimic mutants, pls1 exhibits reddish-brown lesions on the panicle branches and glumes after heading, and the panicles dry up at maturity, severely affecting yield. This represents a new type of rice lesion mimic. The combination of map-cloning and whole genome resequencing revealed that the pls1 mutant produced a large deletion of 173403 bp, resulting in 7 gene deletions and 1 gene promoter deletion. Gene function prediction and gene expression data in database confirm that PLS1 encodes tryptamine 5-hydroxylase (Os12g0268000).The pls1 mutant leads to excessive accumulation of reactive oxygen species (ROS), programmed cell death, and chloroplast degradation, reducing photosynthetic capacity. Melatonin plays an important role in plant salt tolerance. Further functional analysis showed that the loss of PLS1 significantly inhibits the expression of melatonin synthesis related enzyme genes OsTDC1, OsTDC3, OsSNAT1, OsASMT1, and OsCOMT in rice, resulting in decreased salt tolerance of the pls1 mutant. In summary, the panicle and leaf spot mutant pls1 is a new type of rice lesion mimic mutant, providing new germplasm for studying the mechanisms related to rice lesion mimics. The analysis of salt tolerance reveals a new function of tryptamine 5-hydroxylase, offering a new perspective for studying its mechanisms in programmed cell death and salt tolerance.