Plant architecture, one of the key factors that determine grain yield in rice, is mainly affected by components such as plant height, tiller number, and panicle morphology. For this paper, we obtained a multi-tillering and lazy mutant from a japonica rice cultivar, Wuyunjing 7 (WYJ7), via treatment with a heavy ion beam. Compared to WYJ7, the mutant showed a significant increase in tiller angle, tiller number, number of primary and secondary branches, and number of grains; however, the plant height and grain thickness of the mutant was significantly decreased. Phenotypic analysis of the F₁ hybrids revealed that the multi-tillering and lazy mutant phenotypes were regulated by a recessive gene. The segregation ratio of 1׃3 of the mutant phenotype and the wild-type plant in the F₂ population indicated that the former was controlled by a single gene named Multi-Tillering and Lazy 1 (MTL1). Bulked segregant analysis was performed using the individual plants with extremely typical tiller angles in the F₂ population. The MTL1 gene was initially mapped within a region of 5.58–17.64 Mb on chromosome 11. By using the F₂ segregated population for fine mapping, the MTL1 gene was ultimately fine mapped within the range of 66.67 kb on chromosome 11. The analysis of genes in this region revealed the presence of the previously identified LAZY1 (LA1) gene. Genomic PCR amplification and semi-quantitative RT-PCR assays showed that the LA1 gene could not be amplified and was not expressed, thus indicating that the MTL1 gene might be identical to the LA1 gene. This study suggests that the multi-tillering and lazy mutant phenotypes might be caused by the deletion of LA1 function. This finding can guide further investigations on the functional mechanisms of the LA1 gene, thus enriching the theoretical knowledge of plant architecture in relation to rice.

Panicle type is one of the important factors affecting rice (Oryza sativa L.) yield, and the identification of regulatory genes in panicle development can provide significant insights into the molecular network involved. This study identified a large and dense panicle 1 (ldp1) mutant produced from the Wuyunjing 7 (WYJ7) genotype, which displayed significant relative increases in panicle length, number of primary and secondary branches, number of grains per panicle, grain width, and grain yield per plant. Scanning electron microscopy results showed that the shoot apical meristem (SAM) of ldp1 was relatively larger at the bract stage (BM), with a significantly increased number of primary (PBM) and secondary branch (SBM) meristematic centers, indicating that the ldp1 mutation affects early stages in SAM development Comparative RNA-Seq analysis of meristem tissues from WYJ7 and ldp1 at the BM, PBM, and SBM developmental stages indicated that the number of differentially expressed genes (DEGs) were highest (1407) during the BM stage. Weighted gene coexpression network analysis (WGCNA) revealed that genes in one module (turquoise) are associated with the ldp1 phenotype and highly expressed during the BM stage, suggesting their roles in the identity transition and branch differentiation stages of rice inflorescences. Hub genes involved in auxin synthesis and transport pathways, such as OsAUX1, OsAUX4, and OsSAUR25, were identified. Moreover, GO and KEGG analysis of the DEGs in the turquoise module and the 1407 DEGs in the BM stage revealed that a majority of genes involved in tryptophan metabolism and auxin signaling pathway were differentially expressed between WYJ and ldp1. The genetic analysis indicated that the ldp1 phenotype is controlled by a recessive monogene (LDP1), which was mapped to a region between 16.9 and 18.1 Mb on chromosome seven. This study suggests that the ldp1 mutation may affect the expression of key genes in auxin synthesis and signal transduction, enhance the size of SAM, and thus affect panicle development. This study provides insights into the molecular regulatory network underlying rice panicle morphogenesis and lays an important foundation for further understanding the function and molecular mechanism of LDP1 during panicle development.