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Hormone-activated proteolysis is a recurring theme of plant hormone signaling mechanisms.In strigolac-tone signaling,the enzyme receptor DWARF14(D14)and an F-box protein,MORE AXILLARY GROWTH2(MAX2),mark SUPPRESSOR OF MAX21-LIKE(SMXL)family proteins SMXL6,SMXL7,and SMXL8 for rapid degradation.Removal of these transcriptional corepressors initiates downstream growth responses.The homologous proteins SMXL3,SMXL4,and SMXL5,however,are resistant to MAX2-mediated degradation.We discovered that the smxl4 smxl5 mutant has enhanced responses to strigolactone.SMXL5 attenuates strigolactone signaling by interfering with AtD14-SMXL7 interactions.SMXL5 interacts with AtD14 and SMXL7,providing two possible ways to inhibit SMXL7 degradation.SMXL5 function is partially dependent on an ethylene-responsive-element binding-factor-associated amphiphilic repression(EAR)motif,which typically mediates interactions with the TOPLESS family of transcriptional corepressors.However,we found that loss of the EAR motif reduces SMXL5-SMXL7 interactions and the attenuation of strigolactone signaling by SMXL5.We hypothesize that integration of SMXL5 into heteromeric SMXL complexes reduces the susceptibility of SMXL6/7/8 proteins to strigolactone-activated degradation and that the EAR motif pro-motes the formation or stability of these complexes.This mechanism may provide a way to spatially or temporally fine-tune strigolactone signaling through the regulation of SMXL5 expression or translation.