Updated project metadata. Starch accumulation is the key progress for the maturity of rice pollen grains. However, the regulatory mechanism underlying which remains less understood. Here, we isolated a rice male-sterile mutant ap1, which produces non-viable pollen grains with defective starch accumulation. Functional analysis revealed that AP1 encodes an active L-type lectin receptor-like kinase (L-LecRLK). AP1 is located on plasma membrane and its transcript is highly accumulated in pollen during the starch synthesis phase. RNA-seq analysis suggests that the mutation of AP1 significantly altered the expression of numerous genes involved in starch and sucrose metabolic pathway. Phosphoproteomic profiling revealed that the phosphorylation levels of several proteins within this pathway were significantly downregulated in the mutant. Among which, a rice UDP-glucose pyrophosphorylase (OsUGP2), which roles in pollen starch accumulation, was identified. Further protein–protein interaction assays suggest that OsUGP2 is a feasible target of AP1 to regulate pollen starch accumulation. Our findings thus revealed a novel role of L-LecRLK in controlling pollen maturity via modulating starch metabolism.