The study identifies NINJA as a novel adaptor protein that links the co-repressor TOPLESS (TPL) to jasmonate (JA) signaling in plants. NINJA interacts with JAZ repressor proteins through a previously uncharacterized mechanism, recruiting TPL and TPL-related proteins (TPRs) to repress JA-responsive gene expression. This interaction is mediated by an EAR repression motif in NINJA, which is essential for its function as a negative regulator of JA signaling. NINJA functions in conjunction with TPL to modulate multiple signaling pathways, revealing a common molecular mechanism used by stress- and growth-related signaling cascades to regulate gene expression in plants. JA signaling is controlled by the SCF E3 ubiquitin ligase, with COI1 as the F-box subunit. Upon JA perception, JAZ proteins are degraded, releasing the transcriptional activator MYC2 to regulate early JA-responsive genes. Tandem affinity purification (TAP) was used to isolate the core JA signaling module and identify new JAZ interactors. NINJA was found to interact with JAZ proteins, particularly through the TIFY motif, and was shown to bind to JAZ1 fragments containing this motif. NINJA also interacts with other ZIM domain proteins, including PPD1, PPD2, and TIFY8. NINJA and TPL interact directly through the EAR motif of NINJA, confirming their role in transcriptional repression. NINJA functions as a transcriptional repressor of JA responses, as demonstrated by its ability to repress gene expression in tobacco protoplasts. NINJA overexpression reduces JA sensitivity, while its knock-down leads to derepressed JA responses, indicating its role as a negative regulator of JA signaling. The study highlights the parallelism between auxin and JA signaling pathways, where both hormones are perceived by F-box proteins that target repressor proteins for degradation, ultimately releasing transcription factors that activate downstream responses. NINJA, through its interaction with TPL, functions as a repressor in JA signaling, similar to the role of AUX/IAA proteins in auxin signaling. This suggests that TPL proteins act as general co-repressors in plants, recruited to different signaling pathways by specific adaptor proteins such as AUX/IAA, AFP, and the NINJA-JAZ complex. The findings reveal that NINJA is a key player in JA signaling, interacting with TPL and JAZ proteins to regulate gene expression. This interaction is essential for the repression of JA-responsive genes and the maintenance of proper signaling pathways. The study also highlights the importance of the TIFY motif in JAZ protein function and the role of NINJA in modulating this interaction. Overall, the research provides new insights into the molecular mechanisms underlying JA signaling and the role of NINJA in this process.The study identifies NINJA as a novel adaptor protein that links the co-repressor TOPLESS (TPL) to jasmonate (JA) signaling in plants. NINJA interacts with JAZ repressor proteins through a previously uncharacterized mechanism, recruiting TPL and TPL-related proteins (TPRs) to repress JA-responsive gene expression. This interaction is mediated by an EAR repression motif in NINJA, which is essential for its function as a negative regulator of JA signaling. NINJA functions in conjunction with TPL to modulate multiple signaling pathways, revealing a common molecular mechanism used by stress- and growth-related signaling cascades to regulate gene expression in plants. JA signaling is controlled by the SCF E3 ubiquitin ligase, with COI1 as the F-box subunit. Upon JA perception, JAZ proteins are degraded, releasing the transcriptional activator MYC2 to regulate early JA-responsive genes. Tandem affinity purification (TAP) was used to isolate the core JA signaling module and identify new JAZ interactors. NINJA was found to interact with JAZ proteins, particularly through the TIFY motif, and was shown to bind to JAZ1 fragments containing this motif. NINJA also interacts with other ZIM domain proteins, including PPD1, PPD2, and TIFY8. NINJA and TPL interact directly through the EAR motif of NINJA, confirming their role in transcriptional repression. NINJA functions as a transcriptional repressor of JA responses, as demonstrated by its ability to repress gene expression in tobacco protoplasts. NINJA overexpression reduces JA sensitivity, while its knock-down leads to derepressed JA responses, indicating its role as a negative regulator of JA signaling. The study highlights the parallelism between auxin and JA signaling pathways, where both hormones are perceived by F-box proteins that target repressor proteins for degradation, ultimately releasing transcription factors that activate downstream responses. NINJA, through its interaction with TPL, functions as a repressor in JA signaling, similar to the role of AUX/IAA proteins in auxin signaling. This suggests that TPL proteins act as general co-repressors in plants, recruited to different signaling pathways by specific adaptor proteins such as AUX/IAA, AFP, and the NINJA-JAZ complex. The findings reveal that NINJA is a key player in JA signaling, interacting with TPL and JAZ proteins to regulate gene expression. This interaction is essential for the repression of JA-responsive genes and the maintenance of proper signaling pathways. The study also highlights the importance of the TIFY motif in JAZ protein function and the role of NINJA in modulating this interaction. Overall, the research provides new insights into the molecular mechanisms underlying JA signaling and the role of NINJA in this process.