Induction and repression of the urea amidolyase gene in Saccharomyces cerevisiae

1986 ◽  
Vol 6 (11) ◽  
pp. 3954-3964
Author(s):  
F S Genbauffe ◽  
T G Cooper
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Steady State ◽  
Normal Control ◽  
Catabolite Repression ◽  
Gene Products ◽  
Nitrogen Catabolite Repression ◽  
Wild Type ◽  
Recombinant Plasmids ◽  
Control Pattern ◽  
Steady State Levels

The DUR1,2 gene from Saccharomyces cerevisiae has been isolated on recombinant plasmids along with all DNA between the DUR1,2 and MET8 loci. DUR1,2 was found to encode a 5.7-kilobase transcript, which is consistent with our earlier suggestion that the DUR1 and DUR2 loci are two domains of a single multifunctional gene. Steady-state levels of the DUR1,2 transcript responded to induction and nitrogen catabolite repression in the same way as urea amidolyase activity. dal81 mutants (grown with inducer) contained barely detectable amounts of DUR1,2 RNA, whereas dal80 mutants (grown without inducer) contained the same amount as a wild-type induced culture. These observations support our earlier hypothesis that DUR1,2 is transcriptionally regulated, with control being mediated by the DAL80 and DAL81 gene products. We cloned the DUR1,2-Oh mutation and found it to be a Ty insertion near sequences required for complementation of dur1,2 mutations. The ROAM phenotype of the DUR1,2-Oh mutation is sharply different from that of cis-dominant, DUR80 mutations, which enhance DUR1,2 expression but do not affect the normal control pattern of the gene. There is evidence that DUR80 mutations may also be Ty insertions, which generate phenotypes that are different from those in DUR1,2-Oh mutations.

scholarly journals Induction and repression of the urea amidolyase gene in Saccharomyces cerevisiae.

1986 ◽  
Vol 6 (11) ◽  
pp. 3954-3964 ◽  
Author(s):  
F S Genbauffe ◽  
T G Cooper
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Steady State ◽  
Normal Control ◽  
Catabolite Repression ◽  
Gene Products ◽  
Nitrogen Catabolite Repression ◽  
Wild Type ◽  
Recombinant Plasmids ◽  
Control Pattern ◽  
Steady State Levels

The DUR1,2 gene from Saccharomyces cerevisiae has been isolated on recombinant plasmids along with all DNA between the DUR1,2 and MET8 loci. DUR1,2 was found to encode a 5.7-kilobase transcript, which is consistent with our earlier suggestion that the DUR1 and DUR2 loci are two domains of a single multifunctional gene. Steady-state levels of the DUR1,2 transcript responded to induction and nitrogen catabolite repression in the same way as urea amidolyase activity. dal81 mutants (grown with inducer) contained barely detectable amounts of DUR1,2 RNA, whereas dal80 mutants (grown without inducer) contained the same amount as a wild-type induced culture. These observations support our earlier hypothesis that DUR1,2 is transcriptionally regulated, with control being mediated by the DAL80 and DAL81 gene products. We cloned the DUR1,2-Oh mutation and found it to be a Ty insertion near sequences required for complementation of dur1,2 mutations. The ROAM phenotype of the DUR1,2-Oh mutation is sharply different from that of cis-dominant, DUR80 mutations, which enhance DUR1,2 expression but do not affect the normal control pattern of the gene. There is evidence that DUR80 mutations may also be Ty insertions, which generate phenotypes that are different from those in DUR1,2-Oh mutations.

scholarly journals cis-Dominant mutations which dramatically enhance DUR1,2 gene expression without affecting its normal regulation.

1984 ◽  
Vol 4 (5) ◽  
pp. 947-955 ◽  
Author(s):  
G Chisholm ◽  
T Cooper
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Control System ◽  
Normal Control ◽  
Chromatin Structure ◽  
Catabolite Repression ◽  
Mutant Phenotype ◽  
Nitrogen Catabolite Repression ◽  
Upstream Control ◽  
Affect Gene Expression

We have isolated three cis-dominant mutations which dramatically enhance DUR1 ,2 gene expression in Saccharomyces cerevisiae. The mutant phenotype, which is expressed both in haploid and MATa/MAT alpha diploid strains, does not appear to be an alteration of the normal control system for this gene because its expression remained fully inducible and sensitive to nitrogen catabolite repression. Instead, we found much higher levels of DUR1 ,2-specific RNA under both uninduced and induced conditions, i.e., the overproduction trait was superimposed on normal regulation of the gene. The mutations seemed to affect gene expression in a unidirectional manner or to be specific for DUR1 ,2 gene expression, because other genes in proximity to the mutations were not affected. We feel that these mutations may alter the chromatin structure in the vicinity of the DUR1 ,2 upstream control sequences or, alternatively, may be Ty insertions which no longer possess the ROAM characteristics reported by others and ourselves.

cis-Dominant mutations which dramatically enhance DUR1,2 gene expression without affecting its normal regulation

1984 ◽  
Vol 4 (5) ◽  
pp. 947-955
Author(s):  
G Chisholm ◽  
T Cooper
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Control System ◽  
Normal Control ◽  
Chromatin Structure ◽  
Catabolite Repression ◽  
Mutant Phenotype ◽  
Nitrogen Catabolite Repression ◽  
Upstream Control ◽  
Affect Gene Expression

We have isolated three cis-dominant mutations which dramatically enhance DUR1 ,2 gene expression in Saccharomyces cerevisiae. The mutant phenotype, which is expressed both in haploid and MATa/MAT alpha diploid strains, does not appear to be an alteration of the normal control system for this gene because its expression remained fully inducible and sensitive to nitrogen catabolite repression. Instead, we found much higher levels of DUR1 ,2-specific RNA under both uninduced and induced conditions, i.e., the overproduction trait was superimposed on normal regulation of the gene. The mutations seemed to affect gene expression in a unidirectional manner or to be specific for DUR1 ,2 gene expression, because other genes in proximity to the mutations were not affected. We feel that these mutations may alter the chromatin structure in the vicinity of the DUR1 ,2 upstream control sequences or, alternatively, may be Ty insertions which no longer possess the ROAM characteristics reported by others and ourselves.

scholarly journals The critical role of T cells in glucocorticoid-induced osteoporosis

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Lin Song ◽  
Lijuan Cao ◽  
Rui Liu ◽  
Hui Ma ◽  
Yanan Li ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Steady State ◽  
Side Effects ◽  
Critical Role ◽  
Wild Type ◽  
Receptor Activator ◽  
Steady State Levels ◽  
Induced Apoptosis

AbstractGlucocorticoids (GC) are widely used clinically, despite the presence of significant side effects, including glucocorticoid-induced osteoporosis (GIOP). While GC are believed to act directly on osteoblasts and osteoclasts to promote osteoporosis, the detailed underlying molecular mechanism of GC-induced osteoporosis is still not fully elucidated. Here, we show that lymphocytes play a pivotal role in regulating GC-induced osteoporosis. We show that GIOP could not be induced in SCID mice that lack T cells, but it could be re-established by adoptive transfer of splenic T cells from wild-type mice. As expected, T cells in the periphery are greatly reduced by GC; instead, they accumulate in the bone marrow where they are protected from GC-induced apoptosis. These bone marrow T cells in GC-treated mice express high steady-state levels of NF-κB receptor activator ligand (RANKL), which promotes the formation and maturation of osteoclasts and induces osteoporosis. Taken together, these findings reveal a critical role for T cells in GIOP.

A gene product needed for induction of allantoin system genes in Saccharomyces cerevisiae but not for their transcriptional activation

1989 ◽  
Vol 9 (9) ◽  
pp. 3869-3877
Author(s):  
P A Bricmont ◽  
T G Cooper
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Gene Product ◽  
Transcriptional Activation ◽  
Nitrogen Catabolite Repression ◽  
Wild Type ◽  
Product Analysis ◽  
Cis Acting ◽  
Induction Sequence ◽  
Basal Level Expression ◽  
Activation Sequence

The allantoin-degradative pathway of Saccharomyces cerevisiae consists of several genes whose expression is highly induced by the presence of allophanic acid. Induced expression requires a functional DAL81 gene product. Analysis of these genes has demonstrated the presence of three cis-acting elements in the upstream regions: (i) an upstream activation sequence (UAS) required for transcriptional activation in an inducer-independent fashion, (ii) an upstream repression sequence (URS) that mediates inhibition of this transcriptional activation, and (iii) an upstream induction sequence (UIS) needed for a response to inducer. The UIS element mediates inhibition of URS-mediated function when inducer is present. We cloned and characterized the DAL81 gene and identified the element with which it was associated. The gene was found to encode a rare 3.2-kilobase-pair mRNA. The amount of DAL81-specific RNA responded neither to induction nor to nitrogen catabolite repression. Deletion of the DAL81 gene resulted in loss of induction but did not significantly affect basal level expression of the DAL7 and DUR1,2 genes or the UAS and URS functions present in plasmid constructions. These data suggest that (i) transcriptional activation of the DAL genes and their responses to inducer are mediated by different factors and cis-acting sequences and (ii) the UIS functions only when a wild-type DAL81 gene product is available.

scholarly journals Rrp6p/Rrp47p constitutes an independent nuclear turnover system of mature small non-coding RNAs in Saccharomyces cerevisiae

2020 ◽  
Author(s):  
Anusha Chaudhuri ◽  
Subhadeep Das ◽  
Mayukh Banerjea ◽  
Biswadip Das
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Steady State ◽  
Decay Rate ◽  
Nuclear Decay ◽  
Steady State Levels ◽  
Nuclear Exosome ◽  
Non Coding Rnas ◽  
Selective Enhancement

In Saccharomyces cerevisiae, the nuclear exosome/Rrp6p/TRAMP participates in the 3'-end processing of several precursor non-coding RNAs. Here we demonstrate that the depletion of nucleus-specific 3'to 5' exoribonuclease Rrp6p and its co-factor Rrp47p led to the specific and selective enhancement of steady-state levels of mature small non-coding RNAs (sncRNAs) that include 5S and 5.8S rRNAs, snRNAs and snoRNAs, but not 18S and 25S rRNAs. Most importantly, their steady-state enhancement does not require the exosome, TRAMP, CTEXT or Rrp6p-associated Mpp6p. Rrp6p/47p-dependent enhancement of the steady-state levels of sncRNAs is associated with the diminution of their nuclear decay-rate and requires their polyadenylation before targeting by Rrp6p, which is catalyzed by both the canonical and non-canonical poly(A) polymerases, Pap1p and Trf4p. Consistent with this finding, the Rrp6p and Rrp47p were demonstrated to exist as an exosome-independent complex. Thus, Rrp6p-Rrp47p defines a core nuclear exosome-independent novel turnover system that targets the small non-coding RNAs.

Multiple GCD genes required for repression of GCN4, a transcriptional activator of amino acid biosynthetic genes in Saccharomyces cerevisiae

1986 ◽  
Vol 6 (11) ◽  
pp. 3990-3998
Author(s):  
S Harashima ◽  
A G Hinnebusch
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Amino Acid ◽  
Lacz Gene ◽  
Gene Products ◽  
Wild Type ◽  
Double Mutation ◽  
Double Stranded Rna ◽  
Amino Acid Availability ◽  
Genes Encoding ◽  
New Alleles

GCN4 encodes a positive regulator of multiple unlinked genes encoding amino acid biosynthetic enzymes in Saccharomyces cerevisiae. Expression of GCN4 is coupled to amino acid availability by a control mechanism involving GCD1 as a negative effector and GCN1, GCN2, and GCN3 as positive effectors of GCN4 expression. We used reversion of a gcn2 gcn3 double mutation to isolate new alleles of GCD1 and mutations in four additional GCD genes which we designate GCD10, GCD11, GCD12, and GCD13. All of the mutations lead to constitutive derepression of HIS4 transcription in the absence of the GCN2+ and GCN3+ alleles. By contrast, the gcd mutations require the wild-type GCN4 allele for their derepressing effect, suggesting that each acts by influencing the level of GCN4 activity in the cell. Consistent with this interpretation, mutations in each GCD gene lead to constitutive derepression of a GCN4::lacZ gene fusion. Thus, at least five gene products are required to maintain the normal repressed level of GCN4 expression in nonstarvation conditions. Interestingly, the gcd mutations are pleiotropic and also affect growth rate in nonstarvation conditions. In addition, certain alleles lead to a loss of M double-stranded RNA required for the killer phenotype. This pleiotropy suggests that the GCD gene products contribute to an essential cellular function, in addition to, or in conjunction with, their role in GCN4 regulation.

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