Curing of yeast [PSI+] prion by guanidine inactivation of Hsp104 does not require cell division.
Curing of yeast [PSI+] prion by guanidine inactivation of Hsp104 does not require cell division.
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通过 Hsp104 的胍灭活来治愈酵母 [PSI ] 朊病毒不需要细胞分裂。
DOI:
10.1073/pnas.0506384102
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发表时间:
2005
影响因子:
11.1
通讯作者:
Eisenberg,Evan
中科院分区:
文献类型:
--
作者:
Wu,Yue-Xuan;Greene,LoisE;Masison,DanielC;Eisenberg,Evan
Propagation of the yeast prion [PSI+], a self-replicating aggregated form of Sup35p, requires Hsp104. One model to explain this phenomenon proposes that, in the absence of Hsp104, Sup35p aggregates enlarge but fail to replicate thus becoming diluted out as the yeast divide. To test this model, we used live imaging of Sup35p-GFP to follow the changes that occur in [PSI+] cells after the addition of guanidine to inactivate Hsp104. After guanidine addition there was initially an increase in aggregation of Sup35p-GFP; but then, before the yeast divided, the aggregates began to dissolve, and after ≈6 h the Sup35-GFP looked identical to the Sup35-GFP in [psi+] cells. Although plating studies showed that the yeast were still [PSI+], this reduction in aggregation suggested that curing of [PSI+] by inactivation of Hsp104 might be independent of cell division. This was tested by measuring the rate of curing of [PSI+] cells in both dividing and nondividing cells. Cell division was inhibited by adding either alpha factor or farnesol. Remarkably, with both of these methods, we found that the rate of curing was not significantly affected by cell division. Thus, cell division is not a determining factor for curing [PSI+] by inactivating Hsp104 with guanidine. Rather, curing apparently occurs because Sup35-GFP polymers slowly depolymerize in the absence of Hsp104 activity. Hsp104 then counteracts this curing possibly by catalyzing formation of new polymers.
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影响因子:
5.3
作者:
Ness, F;Ferreira, P;Tuite, MF
通讯作者:
Tuite, MF
DOI:
--
发表时间:
2001
期刊:
Contributions to microbiology
影响因子:
--
作者:
K. Taylor;R. Wickner
通讯作者:
R. Wickner
影响因子:
13.8
作者:
E. C. Schirmer;J. Glover;M. Singer;S. Lindquist
通讯作者:
E. C. Schirmer;J. Glover;M. Singer;S. Lindquist
影响因子:
16
作者:
Sondheimer, N;Lindquist, S
通讯作者:
Lindquist, S
影响因子:
3.3
作者:
Derkatch,IL;Bradley,ME;Zhou,P;Chernoff,YO;Liebman,SW
通讯作者:
Liebman,SW