Arabidopsis DDB1-CUL4 E3 ligase complexes in det1 salt/osmotic stress resistant germination.

A key regulatory mechanism in plant growth, development, and stress signaling utilizes E3 ubiquitin ligases, which target a variety of substrates for degradation. DE-ETIOLATED 1 (DET1) forms a complex with DDB1 (DAMAGED DNA BINDING protein 1) and CUL4 (CULLIN 4), and negatively regulates light signaling. Another DDB1-CUL4 complex containing DWA1 and DWA2 (DWD hypersensitive to ABA 1 and 2) has been shown to negatively regulate abscisic acid (ABA) signaling. Since distinct DDB1-CUL4 complexes have been shown to influence each other, we analyzed genetic interactions between DET1 and components of DDB1-CUL4 complexes during seed germination under salt and osmotic stress conditions. det1 germination was resistant to salt and osmotic stress and dwa1 and dwa2 enhanced this phenotype. In contrast, ddb1a partially suppressed the det1 germination phenotype on both salt and mannitol, while ddb1b had no effect. Mutations in DDB2, a DDB1-CUL4 complex component involved in DNA repair, also partially suppressed the det1 germination phenotype while mutants in COP1, another light signaling component, completely suppressed the det1 resistant germination phenotypes. Taken together these data suggest that components of E3 ubiquitin ligase complexes have variable but significant effects on det1 salt/osmotic stress responses.