Abstract

The mechanisms by which vanadate can affect important metabolic processes, such as cell growth and morphogenesis, are not fully understood. This is due to the variety of intracellular targets of the metal, and to the changes in chemical form and oxidation state that vanadium can undergo, both in the external environment and intracellularly. The yeast Hansenula polymorpha represents an interesting model for studies concerning vanadate tolerance. This yeast is able to grow on vanadate concentrations which are lethal to other organisms, showing at the same time ultrastructural and physiological modifications which suggest the existance of a vanadate-sensitive target in the invertase route to the plasma membrane, and the involvement of vacuoles in the activation of a detoxification mechanism for vanadate (Mannazzu et al 1997, 1998). In order to further understand the mechanisms responsible for this vanadate-tolerance in H. polymorpha, we isolated 61 vas (vanadate sensitive) mutants, characterized by altered sensitivity to vanadate. Fifty-four of these mutants, which show a recessive phenotype and are currently being subjected to complementation analysis, were tested for the expression of additional phenotypes related to defects in metal ion homeostasis and/or vacular functions. Interestingly, 24 of them are vas cos (copper sensitive) and 2 are vas cos vpa (vacuolar proteolitic activity defective), thus suggesting the existance of common determinants in the detoxification of vanadate and copper, and confirming the important role for vacuoles in the homeostatic control of metal ions. The isolation of the genes involved in vanadate tolerance is in progress.

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