scholarly journals Simultaneous yet Independent Regulation of Actin Cytoskeletal Organization and Translation Initiation by Glucose inSaccharomyces cerevisiae

2004 ◽  
Vol 15 (4) ◽  
pp. 1544-1556 ◽  
Author(s):  
Yukifumi Uesono ◽  
Mark P. Ashe ◽  
Akio Toh-e
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Transcription Factors ◽  
Translation Initiation ◽  
Glucose Repression ◽  
Glucose Deprivation ◽  
Rapid Recovery ◽  
Cytoskeletal Organization ◽  
Translation Inhibition ◽  
Slow Adaptation ◽  
Glucose Recovery

Acute glucose deprivation rapidly but transiently depolarizes the actin cytoskeleton and inhibits translation initiation in Saccharomyces cerevisiae. Neither rapid actin depolarization nor translation inhibition upon glucose removal occurs in a reg1 disruptant, which is defective in glucose repression, or in the tpk1wmutant, which has weak cAPK activity. In the absence of additional glucose, recovery of either actin polarization or translation initiation relies upon respiration, the Snf1p protein kinase, and the transcription factors Msn2p and Msn4p. The readdition of glucose to glucose-starved cells causes a rapid recovery of actin polarization as well as translation initiation without respiration. These results indicate that the simultaneous regulation of actin polarization and translation initiation is divided into three reactions: 1) rapid shutdown depending on Reg1p and cAPK after glucose removal, 2) slow adaptation depending on Snf1p and Msn2p/4p in the absence of glucose, and 3) rapid recovery upon readdition of glucose. On glucose removal, translation initiation is rapidly inhibited in a rom2 disruptant, which is defective in rapid actin depolarization, whereas rapid actin depolarization occurs in a pop2/caf1 disruptant, which is defective in rapid inhibition of translation initiation. Thus, translation initiation and actin polarization seem to be simultaneously but independently regulated by glucose deprivation.

scholarly journals Molecular analysis of the SNF4 gene of Saccharomyces cerevisiae: evidence for physical association of the SNF4 protein with the SNF1 protein kinase.

1989 ◽  
Vol 9 (11) ◽  
pp. 5045-5054 ◽  
Author(s):  
J L Celenza ◽  
F J Eng ◽  
M Carlson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Protein Kinase ◽  
Glucose Repression ◽  
Gene Dosage ◽  
Essential Gene ◽  
Glucose Deprivation ◽  
Protein Kinase Activity ◽  
Lacz Gene ◽  
Physical Association

The SNF4 gene is required for expression of glucose-repressible genes in response to glucose deprivation in Saccharomyces cerevisiae. Previous evidence suggested that SNF4 is functionally related to SNF1, another essential gene in this global regulatory system that encodes a protein kinase. Increased SNF1 gene dosage partially compensates for a mutation in SNF4, and the SNF4 function is required for maximal SNF1 protein kinase activity in vitro. We have cloned SNF4 and identified its 1.2-kilobase RNA, which is not regulated by glucose repression. A 36-kilodalton SNF4 protein is predicted from the nucleotide sequence. Disruption of the chromosomal SNF4 locus revealed that the requirement for SNF4 function is less stringent at low temperature (23 degrees C). A bifunctional SNF4-lacZ gene fusion that includes almost the entire SNF4 coding sequence was constructed. The fusion protein was shown by immunofluorescence microscopy to be distributed throughout the cell, with partial localization to the nucleus. The SNF4-beta-galactosidase protein coimmunoprecipitated with the SNF1 protein kinase, thus providing evidence for the physical association of the two proteins.

Molecular analysis of SNF2 and SNF5, genes required for expression of glucose-repressible genes in Saccharomyces cerevisiae

1986 ◽  
Vol 6 (11) ◽  
pp. 3643-3651
Author(s):  
E Abrams ◽  
L Neigeborn ◽  
M Carlson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Acid Phosphatase ◽  
Molecular Analysis ◽  
Glucose Repression ◽  
Glucose Deprivation ◽  
Invertase Activity ◽  
Multiple Copy ◽  
High Level Expression ◽  
Chromosomal Locus ◽  
High Level

The SNF2 and SNF5 genes are required for derepression of SUC2 and other glucose-repressible genes of Saccharomyces cerevisiae in response to glucose deprivation. Previous genetic evidence suggested that SNF2 and SNF5 have functionally related roles. We cloned both genes by complementation and showed that the cloned DNA was tightly linked to the corresponding chromosomal locus. Both genes in multiple copy complemented only the cognate snf mutation. The SNF2 gene encodes a 5.7-kilobase RNA, and the SNF5 gene encodes a 3-kilobase RNA. Both RNAs contained poly(A) and were present in low abundance. Neither was regulated by glucose repression, and the level of SNF2 RNA was not dependent on SNF5 function or vice versa. Disruption of either gene at its chromosomal locus still allowed low-level derepression of secreted invertase activity, suggesting that these genes are required for high-level expression but are not directly involved in regulation. Further evidence was the finding that snf2 and snf5 mutants failed to derepress acid phosphatase, which is not regulated by glucose repression. The SNF2 and SNF5 functions were required for derepression of SUC2 mRNA.

Molecular analysis of the SNF4 gene of Saccharomyces cerevisiae: evidence for physical association of the SNF4 protein with the SNF1 protein kinase

1989 ◽  
Vol 9 (11) ◽  
pp. 5045-5054
Author(s):  
J L Celenza ◽  
F J Eng ◽  
M Carlson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Protein Kinase ◽  
Glucose Repression ◽  
Gene Dosage ◽  
Essential Gene ◽  
Glucose Deprivation ◽  
Protein Kinase Activity ◽  
Lacz Gene ◽  
Physical Association

The SNF4 gene is required for expression of glucose-repressible genes in response to glucose deprivation in Saccharomyces cerevisiae. Previous evidence suggested that SNF4 is functionally related to SNF1, another essential gene in this global regulatory system that encodes a protein kinase. Increased SNF1 gene dosage partially compensates for a mutation in SNF4, and the SNF4 function is required for maximal SNF1 protein kinase activity in vitro. We have cloned SNF4 and identified its 1.2-kilobase RNA, which is not regulated by glucose repression. A 36-kilodalton SNF4 protein is predicted from the nucleotide sequence. Disruption of the chromosomal SNF4 locus revealed that the requirement for SNF4 function is less stringent at low temperature (23 degrees C). A bifunctional SNF4-lacZ gene fusion that includes almost the entire SNF4 coding sequence was constructed. The fusion protein was shown by immunofluorescence microscopy to be distributed throughout the cell, with partial localization to the nucleus. The SNF4-beta-galactosidase protein coimmunoprecipitated with the SNF1 protein kinase, thus providing evidence for the physical association of the two proteins.

scholarly journals Molecular analysis of SNF2 and SNF5, genes required for expression of glucose-repressible genes in Saccharomyces cerevisiae.

1986 ◽  
Vol 6 (11) ◽  
pp. 3643-3651 ◽  
Author(s):  
E Abrams ◽  
L Neigeborn ◽  
M Carlson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Acid Phosphatase ◽  
Molecular Analysis ◽  
Glucose Repression ◽  
Glucose Deprivation ◽  
Invertase Activity ◽  
Multiple Copy ◽  
High Level Expression ◽  
Chromosomal Locus ◽  
High Level

The SNF2 and SNF5 genes are required for derepression of SUC2 and other glucose-repressible genes of Saccharomyces cerevisiae in response to glucose deprivation. Previous genetic evidence suggested that SNF2 and SNF5 have functionally related roles. We cloned both genes by complementation and showed that the cloned DNA was tightly linked to the corresponding chromosomal locus. Both genes in multiple copy complemented only the cognate snf mutation. The SNF2 gene encodes a 5.7-kilobase RNA, and the SNF5 gene encodes a 3-kilobase RNA. Both RNAs contained poly(A) and were present in low abundance. Neither was regulated by glucose repression, and the level of SNF2 RNA was not dependent on SNF5 function or vice versa. Disruption of either gene at its chromosomal locus still allowed low-level derepression of secreted invertase activity, suggesting that these genes are required for high-level expression but are not directly involved in regulation. Further evidence was the finding that snf2 and snf5 mutants failed to derepress acid phosphatase, which is not regulated by glucose repression. The SNF2 and SNF5 functions were required for derepression of SUC2 mRNA.

scholarly journals Improved Glucose Recovery from Sicyos angulatus by NaOH Pretreatment and Application to Bioethanol Production

Processes ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 245
Author(s):  
Hyung-Eun An ◽  
Kang Hyun Lee ◽  
Ye Won Jang ◽  
Chang-Bae Kim ◽  
Hah Young Yoo
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Alternative Energy ◽  
Invasive Plant ◽  
Food Resource ◽  
Raw Material ◽  
Control Group ◽  
Bioethanol Production ◽  
Naoh Pretreatment ◽  
Glucose Recovery ◽  
Harmful Species

As greenhouse gases and environmental pollution become serious, the demand for alternative energy such as bioethanol has rapidly increased, and a large supply of biomass is required for bioenergy production. Lignocellulosic biomass is the most abundant on the planet and a large part of it, the second-generation biomass, has the advantage of not being a food resource. In this study, Sicyos angulatus, known as an invasive plant (harmful) species, was used as a raw material for bioethanol production. In order to improve enzymatic hydrolysis, S. angulatus was pretreated with different NaOH concentration at 121 °C for 10 min. The optimal NaOH concentration for the pretreatment was determined to be 2% (w/w), and the glucan content (GC) and enzymatic digestibility (ED) were 46.7% and 55.3%, respectively. Through NaOH pretreatment, the GC and ED of S. angulatus were improved by 2.4-fold and 2.5-fold, respectively, compared to the control (untreated S. angulatus). The hydrolysates from S. angulatus were applied to a medium for bioethanol fermentation of Saccharomyces cerevisiae K35. Finally, the maximum ethanol production was found to be 41.3 g based on 1000 g S. angulatus, which was 2.4-fold improved than the control group.

scholarly journals Multicopy FZF1 (SUL1) Suppresses the Sulfite Sensitivity but Not the Glucose Derepression or Aberrant Cell Morphology of a grr1 Mutant of Saccharomyces cerevisiae

Genetics ◽  
1996 ◽  
Vol 144 (2) ◽  
pp. 511-521 ◽  
Author(s):  
Dorina Avram ◽  
Alan T Bakalinsky
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Transcription Factor ◽  
Glucose Metabolism ◽  
Cell Morphology ◽  
Glucose Repression ◽  
Carbon Sources ◽  
Single Copy ◽  
Aberrant Cell ◽  
Growth Defects ◽  
Putative Transcription Factor

Abstract An ssu2 mutation in Sacccharomyces cermisiae, previously shown to cause sulfite sensitivity, was found to be allelic to GRR1, a gene previously implicated in glucose repression. The suppressor rgt1, which suppresses the growth defects of grr1 strains on glucose, did not fully suppress the sensitivity on glucose or nonglucose carbon sources, indicating that it is not strictly linked to a defect in glucose metabolism. Because the Cln1 protein was previously shown to be elevated in grr1 mutants, the effect of CLN1 overexpression on sulfite sensitivity was investigated. Overexpression in GRR1 cells resulted in sulfite sensitivity, suggesting a connection between CLN1 and sulfite metabolism. Multicopy FZF1, a putative transcription factor, was found to suppress the sulfite sensitive phenotype of grr1 strains, but not the glucose derepression or aberrant cell morphology. Multicopy FZF1 was also found to suppress the sensitivity of a number of other unrelated sulfite-sensitive mutants, but not that of ssu1 or met20, implying that FZF1 may act through Ssulp and Met20p. Disruption of FZF1 resulted in sulfite sensitivity when the construct was introduced in single copy at the FZF1 locus in a GRR1 strain, providing evidence that FZF1 is involved in sulfite metabolism.

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