Plant architecture is a key agronomic trait that is associated with plant growth, yield, and resistance to various stresses (Guo et al., 2020). One of the pivotal characteristics of plant architecture is leaf angle (also known as lamina inclination or lamina joint bending), which is the inclination between the leaf blade midrib and the vertical stem of a plant (Luo et al., 2016; Xu et al., 2021). Leaf angle has a direct relationship with light interception, photosynthetic efficiency, and plant density, which determines the yield of plants (Mantilla-Perez and Salas Fernandez, 2017). The degree of leaf angle is determined by the shape and structure of the lamina joint, which connects the leaf blade and the leaf sheath (Zhou et al., 2017; Huang et al., 2021). In the lamina joint, vascular bundles are located at both the abaxial and adaxial sides, sclerenchyma cells are situated at the fringe of the vascular bundles, aerenchyma tissues provide channels for water/nutrient transport and air circulation, and parenchyma cells fill the remaining space (Zhou et al., 2017). The division and expansion of sclerenchyma and parenchyma cells, the thickness of cell walls, and the occurrence of programmed cell death all affect the development of the lamina joint, which in turn determines the leaf angle phenotype (Xu et al., 2021).

Plant hormones play an important role in the regulation of rice leaf angle. Brassinosteroid (BR) promotes cell elongation at the adaxial side and inhibits cell division at the abaxial side to regulate leaf angle (Cao and Chen, 1995; Sun et al., 2015). Consistent with these findings, rice mutants impaired in BR biosynthesis and signal transduction, such as dwarf61 (d61), ebisu dwarf (d2), brassinosteroid-deficient dwarf2 (brd2), and dwarf11 (d11), exhibit erect leaf phenotypes (Yamamuro et al., 2000; Hong et al., 2003, 2005; Tanabe et al., 2005). The rice SPINDLY (OsSPY) gene, which encodes a negative regulator of gibberellin (GA) signaling, negatively regulates leaf angle by modulating the content of BR (Shimada et al., 2006). Subsequently, a study revealed that GA inhibits lamina inclination by regulating both BR biosynthesis and the BR response (Tong et al., 2014). Methyl jasmonate exerts a repressive effect on leaf angle in rice by inhibiting both BR biosynthesis and signaling pathways (Gan et al., 2015). The rice remorin gene, OsREM4.1, which is transcriptionally upregulated by abscisic acid (ABA), negatively regulates leaf angle by regulating BR signaling output (Gui et al., 2016). Later, ABA was reported to increase rice leaf angle at low concentrations, a process that depends on both BR biosynthesis and signaling pathways (Li et al., 2021). In addition, the loss-of-function mutants of Cytokinin OXIDASE/DEHYDROGENASE3 (OsCKX3) lead to increased levels of cytokinins in the lamina joint, resulting in an erect leaf angle phenotype (Huang et al., 2023).

Auxin biosynthesis and signal transduction pathways also contribute to the regulation of leaf angle. In maize (Zea mays L.), LIGULELESS1 (LG1), a SQUAMOSA BINDING PROTEIN (SBP) transcription factor, regulates leaf angle through directly activating three auxin transporter genes, ZmPIN1a, ZmPIN1b, and ZmPIN1c (Zhong et al., 2025). In rice, the knockdown mutants of the auxin receptors TRANSPORT INHIBITOR RESPONSE 1 (OsTIR1) or AUXIN SIGNALING F-BOX 2 (OsAFB2) result in enlarged leaf angles (Bian et al., 2012). LEAF INCLINATION1 (LC1) encodes an indole-3-acetic acid (IAA) amido synthetase (OsGH3-1), and the gain-of-function mutant lc1-D, with decreased free IAA content, displays enlarged leaf angles by stimulating cell elongation at the lamina joint (Zhao et al., 2013). The lack of LEAF INCLINATION3 (LC3) leads to enlarged leaf angles and increased expression levels of AUXIN/INDOLE-3-ACETIC ACID 12 (OsIAA12) and GRETCHEN HAGEN3-2 (OsGH3-2), and transgenic plants with overexpression of OsIAA12 or deficiency of AUXIN RESPONSE FACTOR17 (OsARF17) which interacts with OsIAA12 do display enlarged leaf angles (Chen et al., 2018). Later, a study revealed that OsARF17 cooperates with OsARF6 to negatively regulate leaf angles by modulating secondary cell wall biosynthesis in the lamina joint (Huang et al., 2021).

Gravitropism determines the upward growth of shoot and the downward growth of root (Chen et al., 1999). Research has demonstrated that the gravitropic response of shoots plays a pivotal role in determining rice leaf angle (Li et al., 2007; Wu et al., 2013). LAZY1 modulates shoot gravitropism by playing a negative role in polar auxin transport, thereby negatively regulating rice leaf angle (Li et al., 2007). Recently, a study revealed that the WRKY family transcription factor OsWRKY72 positively regulates leaf angle by modulating LAZY1-mediated shoot gravitropism (Liu et al., 2024). Loose Plant Architecture1 (LPA1), acting as a negative regulator of rice leaf angle, is also involved in the gravitropic response of shoots by modulating the sedimentation rate of amyloplasts (Wu et al., 2013). In addition, LPA1 affects the expression levels of three auxin efflux genes: OsPIN1a, OsPIN1c, and OsPIN3a, which implies that auxin flux might be involved in LPA1-mediated lamina inclination in rice (Liu et al., 2016). Subsequently, a study demonstrated that LPA1 activates the expression of OsPIN1a, thereby regulating rice leaf angle (Sun et al., 2019).

In this study, we found that OsARF12 was highly expressed in the leaf lamina joint and functioned as a transcriptional activator. Phenotypic analysis of OsARF12 transgenic plants revealed that OsARF12 was a negative regulator for rice leaf angle. Furthermore, we demonstrated that OsARF12 directly activated the expression of LPA1 and LAZY1 by binding to their promoters. Consistent with the phenotype of the lpa1 and lazy1 mutants, the osarf12 mutant exhibited impaired shoot gravitropism. Collectively, these findings reveal an auxin signaling pathway that regulates rice leaf angle through shoot gravitropism, highlighting its potential for application in crop architecture optimization.