Abstract
COP9 signalosome (CSN) modulates signal transduction pathways involved in cell cycle, morphogenesis, and stress response, through its regulation on the ubiquitin-proteasome degradation pathway, in the animal and plant kingdoms. Null mutations for CSN results in lethal phenotypes, indicating its essential role in development.
Functional dissection of mammalian CSN revealed that the N-terminal portion of CSN1 (CSN1N) represses activated signals of the SAPK/JNK1 signaling pathway. CSN1N also reduces accumulation of JNK1, leading to suppression of c-Jun phosphorylation. To analyze this regulation, we have isolated proteins directly binding to CSN1N (NBPs). NBPs cover a novel spectrum of proteins, including SAP130, DDX15/hPrp43/mDEAH9, CFIm68, which are components of transcription/RNA processing complexes.
We are currently analyzing the Arabidopsis NBP orthologs and its knockout plants. Detailed biochemical analyses on CSN-NBP interactions together with in planta research should reveal this novel mechanism of CSN. Here we discuss the complex interaction between CSN, COP/DET/FUS, and their interacting partners.
