The COP9 signalosome (CSN) is an evolutionarily conserved multiprotein complex 
that mediates the repression of photomorphogenesis in the dark in Arabidopsis 
through the degradation of transcription factors such as HY5 and HYH. 
CSN-mediated HY5 and HYH degradation also requires the activity of the putative 
E3 ubiquitin ligase (E3) component COP1 and the E2-conjugating enzyme variant 
COP10. Recently, it was shown that CSN also is required for auxin responses 
mediated by the SCF-type E3 SCF(TIR1). To determine whether Arabidopsis CSN is 
required for E3-mediated processes in a more general manner, we generated plants 
with reduced E3 function by suppressing AtRBX1, an essential core subunit of 
SCF-type E3s. We observed that AtRBX1 transgenic plants share multiple 
phenotypes with CSN reduced-function plants, such as morphological defects and 
reduced responses to auxin, jasmonic acid, and cold stress, suggesting that CSN 
is required for multiple AtRBX1-mediated processes. Furthermore, we observed 
that mutants with defects in AXR1, a protein that had been described only as a 
regulator of SCF(TIR1) function, also is required for other E3-mediated 
processes and for the COP1/COP10/CSN-mediated repression of photomorphogenesis 
in the dark. We conclude that CSN and AXR1 are of general importance for 
different pathways that are controlled by E3-mediated protein degradation.