SCF^SNIPER4 controls the turnover of two redundant TRAF proteins in plant immunity.

In mammals, tumor necrosis factor receptor associated factors (TRAFs) are signaling adaptors that regulate diverse physiological processes, including immunity and stress responses. In Arabidopsis, MUSE13 and MUSE14 are redundant TRAF proteins serving as adaptors in the SCF^CRP1 complex to facilitate the turnover of nucleotide-binding domain and leucine-rich repeats (NLR) immune receptors. Degradation of MUSE13 is inhibited by proteasome inhibitor, suggesting that the MUSE13 stability is controlled by the 26S proteasome. However, the E3 ligase that regulates MUSE13 level is unknown. Here we report the identification of an F-box protein, SNIPER4 that regulates the turnover of MUSE13 and MUSE14. Protein levels of MUSE13 and MUSE14 are reduced by SNIPER4 overexpression, while higher accumulation of MUSE13 and MUSE14 is observed when dominant-negative SNIPER4 is expressed. Furthermore, SNIPER4 associates with MUSE13 or MUSE14. Taken together, the SCF^SNIPER4 complex controls the turnover of TRAF proteins for an optimum immune output.

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