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Pearce, D.A. et al.

Pearce, Carr, Das, Sherman,

Phenotypic reversal of the btn1 defects in yeast by chloroquine: a yeast model for Batten disease.

BTN1 of Saccharomyces cerevisiae encodes an ortholog of CLN3, the human Batten disease gene. We have reported previously that deletion of BTN1, btn1- Delta, resulted in a pH-dependent resistance to D-(-)-threo-2-amino-1-[p-nitrophenyl]-1,3-propanediol (ANP). This phenotype was caused by btn1- Delta strains having an elevated ability to acidify growth medium through an elevated activity of the plasma membrane H(+)-ATPase, resulting from a decreased vacuolar pH during early growth. We have determined that growing btn1- Delta strains in the presence of chloroquine reverses the resistance to ANP, decreases the rate of medium acidification, decreases the activity of plasma membrane H(+)-ATPase, and elevates vacuolar pH. However, an additional effect of this phenotypic reversal is that activity of plasma membrane H(+)-ATPase is decreased further and vacuolar pH is increased further as btn1- Delta strains continue to grow. This phenotypic reversal of btn1- Delta can be considered for developing a therapy for Batten disease.[1]

References

Phenotypic reversal of the btn1 defects in yeast by chloroquine: a yeast model for Batten disease. Pearce, D.A., Carr, C.J., Das, B., Sherman, F. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]

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