Byrne, L.J. and Cox, B.S. and Cole, D.J. and Ridout, M.S. and Morgan, B.J.T. and Tuite, M.F. (2007) Cell division is essential for elimination of the yeast [PSI+] prion by guanidine hydrochloride. Proceedings of the National Academy of Sciences of the United States of America, 104 (28). pp. 11688-11693. ISSN 0027-8424.
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Guanidine hydrochloride (Gdn center dot HCl) blocks the propagation of yeast prions by inhibiting Hsp104, a molecular chaperone that is absolutely required for yeast prion propagation. We had previously proposed that ongoing cell division is required for Gdn center dot HCl-induced loss of the [PSI+] prion. Subsequently, Wu et al. [Wu Y, Greene LE, Masison DC, Eisenberg E (2005) Proc Nat] Acad Sci USA 102:1278912794] claimed to show that Gdn center dot HCl can eliminate the [PSI+] prion from alpha-factor-arrested cells leading them to propose that in Gdn center dot HCl center dot treated cells the prion aggregates are degraded by an Hsp104-independent mechanism. Here we demonstrate that the results of Wu et al can be explained by an unusually high rate of alpha-factor-induced cell death in the [PSI+] strain (780-1D) used in their studies. What appeared to be no growth in their experiments was actually no increase in total cell number in a dividing culture through a counterbalancing level of cell death. Using media-exchange experiments, we provide further support for our original proposal that elimination of the [PSI+] prion by Gdn center dot HCl requires ongoing cell division and that prions are not destroyed during or after the evident curing phase.
|Uncontrolled keywords:||propagons; Hsp104; alpha-factor|
|Subjects:||Q Science > QA Mathematics (inc Computing science)
Q Science > QH Natural history > QH301 Biology
|Divisions:||Faculties > Science Technology and Medical Studies > School of Mathematics Statistics and Actuarial Science
Faculties > Science Technology and Medical Studies > School of Biosciences
|Depositing User:||Stephen Holland|
|Date Deposited:||19 Dec 2007 19:25|
|Last Modified:||14 Jan 2010 14:05|
|Resource URI:||http://kar.kent.ac.uk/id/eprint/2054 (The current URI for this page, for reference purposes)|
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