Post-embryonic development depends on the activity of meristems in plants, and thus control of cell fate in the meristem is crucial to plant development and its architecture. In grasses such as rice and maize, the fate of reproductive meristems changes from indeterminate meristems, such as inflorescence and branch meristems, to determinate meristems, such as the spikelet meristem. Here we analyzed a recessive mutant of rice, aberrant spikelet and panicle1 (asp1), that showed pleiotropic phenotypes such as a disorganized branching pattern, aberrant spikelet morphology, and disarrangement of phyllotaxy. Close examination revealed that regulation of meristem fate was compromised in asp1: degeneration of the inflorescence meristem was delayed, transition from the branch meristem to the spikelet meristem was accelerated, and stem cell maintenance in both the branch meristem and the spikelet meristem was compromised. The genetic program was also disturbed in terms of spikelet development. Gene isolation revealed that ASP1 encodes a transcriptional co-repressor that is related to TOPLESS (TPL) in Arabidopsis and RAMOSA ENHANCER LOCUS2 (REL2) in maize. It is likely that the pleiotropic defects are associated with de-repression of multiple genes related to meristem function in the asp1 mutant. The asp1 mutant also showed de-repression of axillary bud growth and disturbed phyllotaxy in the vegetative phase, suggesting that the function of this gene is closely associated with auxin action. Consistent with these observations and the molecular function of Arabidopsis TPL, auxin signaling was also compromised in the rice asp1 mutant. Taken together, these results indicate that ASP1 regulates various aspects of developmental processes and physiological responses as a transcriptional co-repressor in rice.