Leaf angle is an important agronomic trait and influences crop architecture and yield. Studies have demonstrated the roles of phytohormones, particularly auxin and brassinosteroids, and various factors in controlling leaf inclination. However, the underlying mechanism especially the upstream regulatory networks still need being clarified. Here we report the functional characterization of rice leaf inclination3 (LC3), a SPOC domain-containing transcription suppressor, in regulating leaf inclination through interacting with LIP1 (LC3-interacting protein 1), a HIT zinc finger domain-containing protein. LC3 deficiency results in increased leaf inclination and enhanced expressions of OsIAA12 and OsGH3.2. Being consistent, transgenic plants with OsIAA12 overexpression or deficiency of OsARF17 which interacts with OsIAA12 do present enlarged leaf inclination. LIP1 directly binds to promoter regions of OsIAA12 and OsGH3.2, and interacts with LC3 to synergistically suppress auxin signaling. Our study demonstrate the distinct effects of IAA12-ARF17 interactions in leaf inclination regulation, and provide informative clues to elucidate the functional mechanism of SPOC domain-containing transcription suppressor and fine-controlled network of lamina joint development by LC3-regulated auxin homeostasis and auxin signaling through.