The developmental plasticity of leaf size and shape is important for leaf function and plant survival.The CINCINNATA (CIN)-like TEOSINTE BRANCHED 1/CYCLOIDEA/PCF (TCP) transcription factors are key regulators of leaf development.However,the mechanisms by which plants form diverse leaves in response to environmental conditions are still largely unknown.We identified the TCP Interactor containing EAR motif protein 1 (TIE1),a novel transcriptional repressor,as a major modulator for TCP activity and leaf development.Overexpression of TIE1 leads to hyponastic and serrated leaves,whereas disruption of TIE1 causes epinastic leaves.TIE1 encodes a transcriptional repressor containing a C-terminal EAR motif,which mediates interactions with the TPL/TPR corepressors.In addition,TIE1 physically interacts with CIN-like TCPs,thus forming a bridge to link TPL/TPR corepressors to suppress the activity of TCP transcription factor.We further identified a RING-type E3 ligase TEAR1 (TIE1-associated RING-type E3 ligase 1),which regulated leaf development by promoting the degradation of TIE1.TEAR1 contains a typical C3H2C3-type RING domain and has E3 ligase activity.We find that TEAR1 interacts with TIE1,which is ubiquitinated in vivo and degraded by the 26S proteasome system.TEAR1 is developmentally regulated in leaves and TEAR1 is co-localized with TIE1 in nuclei,We demonstrate that TEAR1 negatively regulates TIE1 protein level.Overexpression of TEAR1 rescued leaf defects caused by TIE1 overexpression,whereas disruption of TEAR1 resulted in leaf phenotypes resembling those caused by TIE1 overexpression or TCP dysfunction.We propose that the TIE1-TEAR1 module provides fine and flexible regulation of CIN-like TCP activity and thus leaf size and shape in response to internal and external signals during leaf development.