SummaryIn rice (Oryza sativa L.), floral organ development is an important trait. Although a role for PINOID in regulating floral organ development was reported recently, the underlying molecular mechanism remains unclear. Here, we isolated and characterized an abnormal floral organ mutant and mapped the causative gene through an improved MutMap method. Molecular study revealed that the observed phenotype is caused by a point mutation in OsPINOID (OsPID) gene; therefore, we named the mutation as ospid‐4. Our data demonstrate that OsPID interacts with OsPIN1a and OsPIN1b to regulate polar auxin transport as shown previously. Additionally, OsPID also interacts with OsMADS16 to regulate transcription during floral organ development in rice. Together, we propose a model that OsPID regulates floral organ development by modulating auxin polar transport and interaction with OsMADS16 and/or LAX1 in rice. These results provide a novel insight into the role of OsPID in regulating floral organ development of rice, especially in stigma development, which would be useful for genetic improvement of high‐yield breeding of rice.

During male gametogenesis in Arabidopsis, the haploid microspore undergoes an asymmetric division to produce a vegetative and a generative cell, the latter of which continues to divide symmetrically to form two sperms. This simple system couples cell cycle with cell fate specification.Here we addressed the role of DNA replication in male gametogenesis using a mutant bicellular pollen 1 (bice1), which produces bicellular, rather than tricellular, pollen grains as in the wild-type plant at anthesis.The mutation prolonged DNA synthesis of the generative cell, which resulted in c. 40% of pollen grains arrested at the two-nucleate stage. The extended S phase did not impact the cell fate of the generative cell as shown by cell-specific markers. BICE1 encodes a plant homolog of human D123 protein that is required for G1 progression, but the underlying mechanism is unknown.Here we showed that BICE1 interacts with MCM4 and MCM7 of the pre-replication complex. Consistently, double mutations in BICE1 and MCM4, or MCM7, also led to bicellular pollen and condensed chromosomes. These suggest that BICE1 plays a role in modulating DNA replication via interaction with MCM4 and MCM7.