Pedicel length and orientation (angle) contribute to the diversity of inflorescence architecture, and are important for optimal positioning of the flowers. However, relatively little is known about pedicel development. We previously described the ArabidopsisCORYMBOSA1(CRM1)/BIGgene, which affects inflorescence architecture by controlling pedicel elongation and orientation. Here, we performed a suppressor screen using the partial loss-of-function allelecrm1-13to identify genes and pathways that affect pedicel development. We identified a hypomorph allele of the meristem identity regulatorLEAFY(LFY) as the suppressor. Consistent with this,crm1pedicels had elevatedLFYlevels and conditional gain of LFY function produced downward-bending pedicels. Steroid activation of 35S:LFY-GR plants caused a reduction in the cortical cell length in the abaxial domain and additional defects associated with adaxialization. Further analyses of loss of LFY function revealed that LFY is required for reduced cortical cell elongation at the adaxial side of the pedicel base. Defects in conditionalLFYgain-of-function pedicels were correlated with decreasedBREVIPEDICELLUS(BP) expression, whileASYMMETRIC LEAVES2(AS2), a transcriptional repressor ofBP, andREVOLUTA, a promoter of adaxial cell fate, were highly and ectopically expressed inLFYgain-of-function pedicels. LFY bound tocis-regulatory regions upstream ofAS2, andas2mutations partially suppressed the pedicel length and orientation defects caused by increasedLFYactivity. These data suggest that LFY activity promotes adaxial cell fate and hence the proper orientation and length of the pedicel partly by directly activatingAS2expression, which suppressesBPexpression.