scholarly journals The Spemann organizer-expressed zinc finger gene Xegr-1 responds to the MAP kinase/Ets-SRF signal transduction pathway

1998 ◽  
Vol 17 (15) ◽  
pp. 4414-4425 ◽  
Author(s):  
F. Panitz
Genetics ◽  
1997 ◽  
Vol 147 (1) ◽  
pp. 19-32 ◽  
Author(s):  
Kathrin Schrick ◽  
Barbara Garvik ◽  
Leland H Hartwell

Abstract The mating process in yeast has two distinct aspects. One is the induction and activation of proteins required for cell fusion in response to a pheromone signal; the other is chemotropism, i.e., detection of a pheromone gradient and construction of a fusion site available to the signaling cell. To determine whether components of the signal transduction pathway necessary for transcriptional activation also play a role in chemotropism, we examined strains with null mutations in components of the signal transduction pathway for diploid formation, prezygote formation and the chemotropic process of mating partner discrimination when transcription was induced downstream of the mutation. Cells mutant for components of the mitogen-activated protein (MAP) kinase cascade (ste5, ste20, ste11, ste7 or fus3 kss1) formed diploids at a frequency 1% that of the wild-type control, but formed prezygotes as efficiently as the wild-type control and showed good mating partner discrimination, suggesting that the MAP kinase cascade is not essential for chemotropism. In contrast, cells mutant for the receptor (ste2) or the β or γ subunit (ste4 and stel8) of the G protein were extremely defective in both diploid and prezygote formation and discriminated poorly between signaling and nonsignaling mating partners, implying that these components are important for chemotropism.


2005 ◽  
Vol 48 (1) ◽  
pp. 60-68 ◽  
Author(s):  
Peter S. Solomon ◽  
Ormonde D. C. Waters ◽  
Joanne Simmonds ◽  
Richard M. Cooper ◽  
Richard P. Oliver

2004 ◽  
Vol 23 (24) ◽  
pp. 4780-4791 ◽  
Author(s):  
Ole-Morten Seternes ◽  
Theresa Mikalsen ◽  
Bjarne Johansen ◽  
Espen Michaelsen ◽  
Chris G Armstrong ◽  
...  

1994 ◽  
Vol 13 (7) ◽  
pp. 1628-1635 ◽  
Author(s):  
W.H. Biggs ◽  
K.H. Zavitz ◽  
B. Dickson ◽  
A. van der Straten ◽  
D. Brunner ◽  
...  

FEBS Letters ◽  
1995 ◽  
Vol 359 (2-3) ◽  
pp. 133-136 ◽  
Author(s):  
Markus Wartmann ◽  
Debra Campbell ◽  
Asha Subramanian ◽  
Sumner H. Burstein ◽  
Roger J. Davis

1994 ◽  
Vol 5 (3) ◽  
pp. 297-312 ◽  
Author(s):  
J A Brill ◽  
E A Elion ◽  
G R Fink

We have isolated dominant gain-of-function (gf) mutations in FUS3, a Saccharomyces cerevisiae mitogen-activated protein (MAP) kinase homolog, that constitutively activate the yeast mating signal transduction pathway and confer hypersensitivity to mating pheromone. Surprisingly, the phenotypes of dominant FUS3gf mutations require the two protein kinases, STE7 and STE11. FUS3gf kinases are hyperphosphorylated in yeast independently of STE7. Consistent with this, FUS3gf kinases expressed in Escherichia coli exhibit an increased ability to autophosphorylate on tyrosine in vivo. FUS3gf mutations suppress the signal transduction defect of a severely catalytically impaired allele of STE7. This finding suggests that the tyrosine-phosphorylated form of FUS3 is a better substrate for activation by STE7. Furthermore, these results imply that the degree of autophosphorylation of a MAP kinase determines its threshold of sensitivity to upstream signals.


Nature ◽  
1994 ◽  
Vol 370 (6488) ◽  
pp. 386-389 ◽  
Author(s):  
Damian Brunner ◽  
Klaus Dücker ◽  
Nadja Oellers ◽  
Ernst Hafen ◽  
Henrike Scholzi ◽  
...  

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