MiRNA172 represses the expression of APETALA2 (AP2) in Arabidopsis flower development through translational inhibition. This miRNA, which shows high sequence complementarity to AP2 mRNA, regulates AP2 expression primarily at the translational level. Elevated miRNA172 levels lead to floral organ identity defects similar to those in apetala2 mutants. Mutant AP2 RNA with disrupted miRNA172 base pairing results in increased AP2 protein and severe floral patterning defects, suggesting that miRNA172 acts as a translational repressor of AP2. MicroRNAs, including miRNA172, regulate protein-coding RNAs by guiding cleavage or inhibiting translation. In Arabidopsis, miRNA172 is processed by Dicer and requires HEN1 for accumulation. miRNA172 binds to AP2 mRNA, and its absence leads to floral homeotic transformations. AP2 is a class A gene that specifies perianth identity and acts antagonistically with AG, a class C gene. HEN1 is required for class C activity, and its loss leads to floral homeotic transformations. miRNA172 is highly complementary to AP2 mRNA and binds within the coding region but outside the conserved AP2 domain. Transgenic plants with elevated miRNA172 levels show floral homeotic phenotypes similar to ap2 loss-of-function mutants, indicating miRNA172's role in regulating AP2. RNA filter hybridization shows increased miRNA172 levels in transgenic lines, with higher levels in young seedlings than in inflorescences. AP2 RNA accumulation is similar in transgenic lines, but AP2 protein levels are significantly reduced in miRNA172-overexpressing plants, indicating translational regulation. Transgenic plants expressing wild-type AP2 or a mutant AP2 with mismatches to miRNA172 show different floral defects, with the mutant showing severe defects and elevated AP2 protein. This suggests that miRNA172 regulates AP2 at the translational level. The presence of miRNA172 in developing flowers indicates its role in regulating AP2 during floral patterning. miRNA172 is present in stage 1 floral primordia and persists in all four floral whorls, with later accumulation in the inner two whorls. This may cause AP2 protein to be concentrated in the outer two whorls, where it specifies perianth identities. In conclusion, miRNA172 represses AP2 expression during flower development, crucial for reproductive organ development and timely termination of floral stem cells. This regulation occurs at the translational level through direct sequence complementarity between AP2 mRNA and miRNA172. This study shows that plant miRNAs can regulate target mRNAs through translational inhibition or transcript cleavage.MiRNA172 represses the expression of APETALA2 (AP2) in Arabidopsis flower development through translational inhibition. This miRNA, which shows high sequence complementarity to AP2 mRNA, regulates AP2 expression primarily at the translational level. Elevated miRNA172 levels lead to floral organ identity defects similar to those in apetala2 mutants. Mutant AP2 RNA with disrupted miRNA172 base pairing results in increased AP2 protein and severe floral patterning defects, suggesting that miRNA172 acts as a translational repressor of AP2. MicroRNAs, including miRNA172, regulate protein-coding RNAs by guiding cleavage or inhibiting translation. In Arabidopsis, miRNA172 is processed by Dicer and requires HEN1 for accumulation. miRNA172 binds to AP2 mRNA, and its absence leads to floral homeotic transformations. AP2 is a class A gene that specifies perianth identity and acts antagonistically with AG, a class C gene. HEN1 is required for class C activity, and its loss leads to floral homeotic transformations. miRNA172 is highly complementary to AP2 mRNA and binds within the coding region but outside the conserved AP2 domain. Transgenic plants with elevated miRNA172 levels show floral homeotic phenotypes similar to ap2 loss-of-function mutants, indicating miRNA172's role in regulating AP2. RNA filter hybridization shows increased miRNA172 levels in transgenic lines, with higher levels in young seedlings than in inflorescences. AP2 RNA accumulation is similar in transgenic lines, but AP2 protein levels are significantly reduced in miRNA172-overexpressing plants, indicating translational regulation. Transgenic plants expressing wild-type AP2 or a mutant AP2 with mismatches to miRNA172 show different floral defects, with the mutant showing severe defects and elevated AP2 protein. This suggests that miRNA172 regulates AP2 at the translational level. The presence of miRNA172 in developing flowers indicates its role in regulating AP2 during floral patterning. miRNA172 is present in stage 1 floral primordia and persists in all four floral whorls, with later accumulation in the inner two whorls. This may cause AP2 protein to be concentrated in the outer two whorls, where it specifies perianth identities. In conclusion, miRNA172 represses AP2 expression during flower development, crucial for reproductive organ development and timely termination of floral stem cells. This regulation occurs at the translational level through direct sequence complementarity between AP2 mRNA and miRNA172. This study shows that plant miRNAs can regulate target mRNAs through translational inhibition or transcript cleavage.