Nuclear factors and the control of suppressiveness in petite mutants of Saccharomyces cerevisiae

1974 ◽  
Vol 133 (1) ◽  
pp. 37-45 ◽  
Author(s):  
Michael F. Waxman ◽  
Norman R. Eaton
1969 ◽  
Vol 17 (3) ◽  
pp. 454-456 ◽  
Author(s):  
Vernon W. Mayer ◽  
Marvin S. Legator

1997 ◽  
Vol 34 (6) ◽  
pp. 382-384 ◽  
Author(s):  
Angelica Del Giudice ◽  
Domenica R. Massardo ◽  
Filomena Manna ◽  
Natalia Koltovaya ◽  
Hans Hartings ◽  
...  

1977 ◽  
Vol 26 (1) ◽  
pp. 373-385
Author(s):  
M.P. Rosin ◽  
A.M. Zimmerman

This study demonstrates that hydrostatic pressure is a potent inductive agent of the petite mutation in cultures of Saccharomyces cerevisiae. The inductive capacity of this mutagen is dependent on the magnitude and the duration of the pressure treatment. Furthermore, the extent of petite induction varies with the growth stage of the culture. Induction occurs in pressure-treated (1-4 X 1-(4) lbf in.-2 or 9–66 X 10(4) kN m-2 for 4 h) log growth cultures but not in stationary or lag phase cultures. Petite induction and cell survival are also dependent on the particular strain of yeast which is pressure-treated. Tetrad analysis and complementation assays demonstrate that pressure-induced petite cells are cytoplasmic in nature. Moreover, induced petite cells show a wide range of suppressivity (2–99%) with a large proportion of the petite cells being highly suppressive.


1999 ◽  
Vol 19 (8) ◽  
pp. 5474-5485 ◽  
Author(s):  
Martijn Rep ◽  
Vladimír Reiser ◽  
Ulrike Gartner ◽  
Johan M. Thevelein ◽  
Stefan Hohmann ◽  
...  

ABSTRACT After a sudden shift to high osmolarity, Saccharomyces cerevisiae cells respond by transiently inducing the expression of stress-protective genes. Msn2p and Msn4p have been described as two transcription factors that determine the extent of this response. Inmsn2 msn4 mutants, however, many promoters still show a distinct rise in transcriptional activity upon osmotic stress. Here we describe two structurally related nuclear factors, Msn1p and a newly identified protein, Hot1p (for high-osmolarity-induced transcription), which are also involved in osmotic stress-induced transcription.hot1 single mutants are specifically compromised in the transient induction of GPD1 and GPP2, which encode enzymes involved in glycerol biosynthesis, and exhibit delayed glycerol accumulation after stress exposure. Similar to agpd1 mutation, a hot1 defect can rescue cells from inappropriately high HOG pathway activity. In contrast, Hot1p has little influence on the osmotic stress induction of CTT1, where Msn1p appears to play a more prominent role. Cells lacking Msn1p, Msn2p, Msn4p, and Hot1p are almost devoid of the short-term transcriptional response of the genes GPD1,GPP2, CTT1, and HSP12 to osmotic stress. Such cells also show a distinct reduction in the nuclear residence of the mitogen-activated protein kinase Hog1p upon osmotic stress. Thus, Hot1p and Msn1p may define an additional tier of transcriptional regulators that control responses to high-osmolarity stress.


1971 ◽  
Vol 5 (5) ◽  
pp. 487-495 ◽  
Author(s):  
Georg Michaelis ◽  
Stephen Douglass ◽  
Ming-Jer Tsai ◽  
Richard S. Criddle

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