The UGA3 gene regulating the GABA catabolic pathway in Saccharomyces cerevisiae codes for a putative zinc-finger protein acting on RNA amount

1990 ◽  
Vol 220 (2) ◽  
pp. 269-276 ◽  
Author(s):  
Bruno André
1993 ◽  
Vol 13 (7) ◽  
pp. 3872-3881
Author(s):  
F Estruch ◽  
M Carlson

The MSN2 gene was selected as a multicopy suppressor in a temperature-sensitive SNF1 protein kinase mutant of Saccharomyces cerevisiae. MSN2 encodes a Cys2His2 zinc finger protein related to the yeast MIG1 repressor and to mammalian early growth response and Wilms' tumor zinc finger proteins. Deletion of MSN2 caused no phenotype. A second similar zinc finger gene, MSN4, was isolated, and deletion of both genes caused phenotypic defects related to carbon utilization. Overexpression of the zinc finger regions was deleterious to growth. LexA-MSN2 and LexA-MSN4 fusion proteins functioned as strong transcriptional activators when bound to DNA. Functional roles of this zinc finger protein family are discussed.


1993 ◽  
Vol 217 (3) ◽  
pp. 1049-1056 ◽  
Author(s):  
Ayako SAKAMOTO ◽  
Maki MINAMI ◽  
Gyung Hye HUH ◽  
Masaki IWABUCHI

1991 ◽  
Vol 55 (9) ◽  
pp. 2259-2264
Author(s):  
Yutaka Ogura ◽  
Tadashi Yoshida ◽  
Yasukazu Nakamura ◽  
Miho Takemura ◽  
Kenji Oda ◽  
...  

1994 ◽  
Vol 14 (5) ◽  
pp. 3150-3157 ◽  
Author(s):  
K Irie ◽  
K Yamaguchi ◽  
K Kawase ◽  
K Matsumoto

The STE4 gene encodes the beta subunit of a heterotrimeric G protein that is an essential component of the pheromone signal transduction pathway. To identify downstream component(s) of Ste4, we sought pseudo-revertants that restored mating competence to ste4 mutants. The suppressor mot2 was isolated as a recessive mutation that restored conjugational competence to a temperature-sensitive ste4 mutant and simultaneously conferred a temperature-sensitive growth phenotype. The MOT2 gene encodes a putative zinc finger protein, the deletion of which resulted in temperature-sensitive growth, increased expression of FUS1 in the absence of pheromones, and suppression of a deletion of the alpha-factor receptor. On the other hand, sterility resulting from deletion of STE4 was not suppressed by the mot2 deletion. These phenotypes are similar to those associated with temperature-sensitive mutations in CDC36 and CDC39, which are proposed to encode general negative regulators of transcription rather than factors involved in the pheromone response pathway. Deletion of MOT2 also caused increased transcription of unrelated genes such as GAL7 and PHO84. Overexpression of MOT2 suppresses the growth defect of temperature-sensitive mutations in CDC36 and CDC39. These observations suggest that Mot2 functions as a general negative regulator of transcription in the same processes as Cdc36 and Cdc39.


1995 ◽  
Vol 23 (23) ◽  
pp. 4907-4912 ◽  
Author(s):  
Malayannan Subramaniam ◽  
Steven A. Harris ◽  
Merry Jo Oursler ◽  
Kay Rasmussen ◽  
B. Lawrence Riggs ◽  
...  

DNA Sequence ◽  
2005 ◽  
Vol 16 (5) ◽  
pp. 391-396 ◽  
Author(s):  
Wenwen Tang ◽  
Jian Yuan ◽  
Xinya Chen ◽  
Yuxi Shan ◽  
Kuntian Luo ◽  
...  

1994 ◽  
Vol 14 (5) ◽  
pp. 3150-3157
Author(s):  
K Irie ◽  
K Yamaguchi ◽  
K Kawase ◽  
K Matsumoto

The STE4 gene encodes the beta subunit of a heterotrimeric G protein that is an essential component of the pheromone signal transduction pathway. To identify downstream component(s) of Ste4, we sought pseudo-revertants that restored mating competence to ste4 mutants. The suppressor mot2 was isolated as a recessive mutation that restored conjugational competence to a temperature-sensitive ste4 mutant and simultaneously conferred a temperature-sensitive growth phenotype. The MOT2 gene encodes a putative zinc finger protein, the deletion of which resulted in temperature-sensitive growth, increased expression of FUS1 in the absence of pheromones, and suppression of a deletion of the alpha-factor receptor. On the other hand, sterility resulting from deletion of STE4 was not suppressed by the mot2 deletion. These phenotypes are similar to those associated with temperature-sensitive mutations in CDC36 and CDC39, which are proposed to encode general negative regulators of transcription rather than factors involved in the pheromone response pathway. Deletion of MOT2 also caused increased transcription of unrelated genes such as GAL7 and PHO84. Overexpression of MOT2 suppresses the growth defect of temperature-sensitive mutations in CDC36 and CDC39. These observations suggest that Mot2 functions as a general negative regulator of transcription in the same processes as Cdc36 and Cdc39.


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