Figure 3

Complementation of csn mutants. The indicated csn mutants in a pcu3-13myc background were transformed with pRep81 plasmids driving the expression of the respective 6 × histidine-Myc-tagged csn genes. Cells were maintained in the presence (promoter off) or absence of thiamin (promoter on) to regulate expression. Expression of endogenous Pcu3p-13Myc (a) and exogenous CSN subunits (b) was determined by immunoblotting with Myc antibodies. The weak complementing activity of some of the plasmids even in the repressed state may result from leakiness of the nmt1 promoter [34].