Plant height and tiller number are two major factors determining plant architecture and yield. However, in rice (Oryza sativa), the regulatory mechanism of plant architecture remains to be elucidated. Here, we reported a recessive rice mutant presenting dwarf and reduced tillering phenotypes (drt1). Map-based cloning revealed that the phenotypes are caused by a single point mutation in DRT1, which encodes the Class I formin protein O. sativa formin homolog 13 (OsFH13), binds with F-actin, and promotes actin polymerization for microfilament organization. DRT1 protein localized on the plasma membrane (PM) and chloroplast (CP) outer envelope. DRT1 interacted with rice phototropin 2 (OsPHOT2), and the interaction was interrupted in drt1. Upon blue light stimulus, PM localized DRT1 and OsPHOT2 were translocated onto the CP membrane. Moreover, deficiency of DRT1 reduced OsPHOT2 internalization and OsPHOT2-mediated CP relocation. Our study suggests that rice formin protein DRT1/OsFH13 is necessary for plant morphology and CP relocation by modulating the actin-associated cytoskeleton network.

Heat stress is one of the major factors affecting crop growth and yield. However, the molecular mechanisms underlying rice heat stress tolerance remain largely unclear. In this study, we identified and characterized the rice high temperature sensitive 2 (hts2) mutant, which is highly susceptible to heat stress. Map-based cloning revealed that the HTS2 encodes a cytochrome P450 protein (CYP71P1) involved in serotonin biosynthesis. HTS2 is ubiquitously expressed across plant tissues and shows strong upregulation in response to heat stress. The HTS2 mutation significantly impairs basal serotonin synthesis in rice, and the heat-sensitive phenotype of the hts2 mutant is completely rescued by exogenous serotonin supplementation. Compared to the wild type, the hts2 mutant exhibits reduced antioxidant capacity, leading to excessive reactive oxygen species (ROS) accumulation and severe oxidative damage, ultimately reducing heat stress tolerance. Furthermore, disruption of HTS2 significantly affects the rice heat shock response, with the heat-induced expression of HsfA2s and their downstream target genes, such as HSP18.0 (heat shock protein 18.0) and OsAPX2 (ascorbate peroxidase 2), markedly depressed in hts2 mutant. Our results suggest a pivotal role of HTS2 in modulating serotonin metabolism and maintaining ROS homeostasis during heat stress, offering new perspectives on the mechanisms underlying heat tolerance and potential strategies to enhance rice resilience to heat stress.

Leaf senescence is a crucial trait that significantly impacts crop quality and yield. However, whether plant leaf senescence genes are regulated by the same mechanisms in vitro and in vivo has not been determined. Here, we screened a rice (Oryza sativa) leaf senescence mutant exhibiting a delayed leaf senescence phenotype in vitro and an early leaf senescence phenotype in vivo. Map-based cloning revealed that these phenotypes were caused by OsELS6, which encodes ABERRANT LATERAL ROOT FORMATION4 (ALF4), a protein that inhibits SKP1-CUL1-F box protein (SCF) E3 ligase activity. In addition, OsELS6 interacted with the U-box E3 ligase OsHUB1, which may be involved in seed development, and with OsCDC48, which is involved in leaf senescence. Integrated transcriptomic, proteomic, and ubiquitomic analyses, as well as exogenous application of jasmonic acid (JA) , demonstrated that OsELS6 is related to OsCDC48 and plays opposite roles in rice leaf senescence in vitro and in vivo via the JA pathway. This study elucidated the regulatory mechanisms of OsELS6 in rice leaf senescence in vitro and in vivo, revealing that JA plays a key role in the regulation of leaf senescence by OsELS6 and OsCDC48.