Targeted suppression of the ferroxidase and iron trafficking activities of the multicopper oxidase Fet3p from Saccharomyces cerevisiae

JBIC Journal of Biological Inorganic Chemistry - Tập 8 - Trang 611-620 - 2003
Tzu-Pin Wang1, Liliana Quintanar2, Scott Severance1, Edward I. Solomon2, Daniel J. Kosman1
1Department of Biochemistry, The University at Buffalo, Buffalo, USA
2Department of Chemistry Stanford University Stanford USA

Tóm tắt

The Fet3 protein in Saccharomyces cerevisiae is a multicopper oxidase tethered to the outer surface of the yeast plasma membrane. Fet3p catalyzes the oxidation of Fe2+ to Fe3+; this ferroxidation reaction is an obligatory first step in high-affinity iron uptake through the permease Ftr1p. Here, kinetic analyses of several Fet3p mutants identify residues that contribute to the specificity that Fet3p has for Fe2+, one of which is essential also to the coupling of the ferroxidase and uptake processes. The spectral and kinetic properties of the D278A, E185D and A, Y354F and A, and E185A/Y354A mutants of a soluble form of Fet3p showed that all of the mutants exhibited the normal absorbance at 330 nm and 608 nm due to the type 3 and type 1 copper sites in Fet3p, respectively. The EPR spectra of the mutants were also equivalent to wild-type, showing that the type 1 and type 2 Cu(II) sites in the proteins were not perturbed. The only marked kinetic defects measured in vitro were increases in K M for Fe2+ exhibited by the D278A, E185A, Y354A, and E185A/Y354A mutants. These results suggest that these three residues contribute to the ferroxidase specificity site in Fet3p. In vivo analysis of these mutant proteins in their membrane-bound form showed that only E185 mutants exhibited kinetic defects in 59Fe uptake. For the Fet3p(E185D) mutant, K M for iron was 300-fold greater than the wild-type K M, while Fet3p(E185A) was completely inactive in support of iron uptake. In situ fluorescence demonstrated that all of the mutant Fet3 proteins, in complex with an Ftr1p:YFP fusion protein, were trafficked normally to the plasma membrane. These results suggest that E185 contributes to Fe2+ binding to Fet3p and to the subsequent trafficking of the Fe3+ produced to Ftr1p.

Tài liệu tham khảo

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