摘要：The COP9 signalosome (CSN) plays an important role in proteasome-mediated degradation by regulating CUL1 rubylation of the SCF ligase and is involved in many crucial biological processes. Here, we demonstrate a link between IDEF1 accumulation and the decline in COP9 derubylation activity in response to iron deficiency (-Fe) in rice (Oryza sativa). CSN6 expression is rapidly down-regulated during Fe depletion, contributing to reduced CSN activity, as judged by CSN5 and CUL1 expression, indicating CSN6 is involved in the early stage response of -Fe. In contrast to CSN6, the IDEF1 protein and expression of several iron uptake/utilisation-related genes are increased in response to -Fe. Thus, we constructed CSN6 transgenic sense and antisense lines and found that experimental depletion of CSN6 results in accumulation of the IDEF1 protein and up-regulation of several iron uptake/utilisation-related genes. Furthermore, IDEF1 can be decorated with K48-linked polyubiquitin and degraded via the 26S proteasome. Accumulated IDEF1 in antisense lines led to increased chlorophyll and Fe content in seedlings during -Fe. Collectively, the cellular CSN6 level is decreased during early stages of -Fe to ensure the rapid accumulation of IDEF1, which in turn up-regulates several iron uptake/utilisation-related genes to help overcome -Fe stress in rice.
