Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.20 (alpha-glucosidase)
4,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Each of at least five unlinked MAL loci (MAL1 through MAL4 and MAL6) on the yeast genome controls the ability to synthesize an inducible alpha-D-glucosidase (maltase). A subcloned fragment of the coding sequence of the MAL6 maltase structural gene was used as a hybridization probe to investigate the physical structure of the family of MAL structural genes in the genomes of different Saccharomyces strains. MAL+ strains, each carrying a genetically defined MAL locus, were crossed with a MAL- strain and the segregation behavior of the functional locus and of sequences complementary to the maltase structural gene at that locus analyzed. The maltase structural gene sequences of each MaL locus were detected by Southern blot hybridization using BamH1 digests of genomic DNA of the meiotic products. This restriction enzyme was previously shown to cleave outside the confines of the MAL 6 locus. The results of such experiments indicate that each MAL locus encompasses at least one maltase structural gene sequence homologous to that of MAL6, that yeast strains that lack functional MAL loci may or may not contain the corresponding maltase structural gene sequence, that the MAL1 maltase structural gene sequence or one of its alleles can be detected in all laboratory yeast strains examined and that each MAL locus can be identified as a characteristic BamH1 fragment of genomic DNA which includes a maltase structural gene. Yeast strains vary in the number of maltase structural gene sequences that they carry. By using the approach described in this report, the ones corresponding to the different functional MAL loci and residing within a BamH1 generated restriction fragment can be identified.
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PMID:Identification and physical characterization of yeast maltase structural genes. 635 59

Fermentation of maltose by Saccharomyces strains depends on the presence of any one of five unlinked MAL loci (MAL1, MAL2, MAL3, MAL4 or MAL6). Earlier mutational analyses of MAL2 and MAL6 containing strains have identified a single complementation group at each of these two loci. However complementation analysis between naturally occurring Mal- Saccharomyces strains isolated from the wild demonstrated the presence of two complementation groups (designated MALp and MALg) at the MAL1, MAL3 and MAL6 loci. The available evidence suggests that the MALp gene is functionally equivalent to the complementation group identified by mutational analysis at the MAL6 locus and that this gene encodes a protein involved in the regulation of the coordinate induction of both maltase and maltose permease synthesis. In this paper we report the isolation, in a well characterized MAL1 strain, of 47 mutants unable to ferment maltose. All the mutants, with one exception, map at the MAL1 locus. These mal1 mutants, except for one, are recessive to MAL1 and fall into two major complementation groups. Evidence is presented that these two classes of mutants identify both a gene involved in the regulation of maltose identify both a gene involved in the regulation of maltose fermentation (MAL1R) and a gene involved in maltose transport (MAL1T). We also report here the isolation of a temperature sensitive maltose nonfermenting mutant mapping at the MAL1 locus identifying a third gene (MAL1S) at this locus. The maltase synthesized by this mutant, when assayed in cell-free extracts, is significantly more thermolabile than the wild type enzyme.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mutational analysis of the MAL1 locus of Saccharomyces: identification and functional characterization of three genes. 638 96

Yeast DNA pools were prepared by ligating partial Sau3A genomic digests from strains carrying various MAL genes into the BamHI site of the yeast-Escherichia coli shuttle vector YRp7. They were used to transform recipient yeast strains that could not utilize maltose since they lacked a classical MAL gene. Transformants were obtained that could use maltose and also formed normal levels of maltase. They were unstable. They would lose the selective marker TRP1 of YRp7 alone, together with the ability to utilize maltose or only the ability to utilize maltose. The insertion of one of the plasmids was used as a hybridization probe for the others and found to share homologous sequences with all. They were then shown to contain the replication origin of the yeast 2 micron circle plasmid and additional sequences. These additional sequences were used to probe genomic digests of total yeast DNA. They hybridized at various degrees of efficiency with several bands, indicating that they were part of a family of repeated sequences. Apparently, it was the combination of the replication origin of the 2 micron circles with the additional sequences that promoted maltose utilization.
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PMID:A hybrid DNA sequence containing the replication origin of the multicopy yeast plasmid 2 micron circle and an additional repeated sequence can convert maltose-negative into maltose-positive strains. 639 95

alpha-Glucosidases or maltases (EC 3.2.1.20) were purified to electrophoretic homogeneity from a respective strain of Saccharomyces cerevisiae which carries a single MAL gene, either MAL alpha, MAL beta, or MAL gamma, using gluconate-Sepharose affinity chromatography and isoelectrofocusing. Of these maltases, two types of maltase were obtained from the MAL gamma strain, the pI values of which were 5.6 and 5.9. From the MAL alpha and MAL beta strain was obtained only one type of maltase with the pI at 5.6 which was identical to one of the maltases from the MAL gamma strain. These four maltases possessed the same properties, except for pI. They were monomers with molecular weights of between 66 000 and 67 000. With regard to the substrate specificity, they hydrolyzed maltose and sucrose exclusively but not alpha-methylglucoside nor maltooligosaccharide. They did not differ in immunological properties.
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PMID:Purification and characterization of alpha-glucosidases produced by Saccharomyces in response to three distinct maltose genes. 642 30

We have studied the dependence on mitochondrial ATP of expression of MAL genes specifying maltose utilization in yeast. It was found that bongkrekic acid does not prevent the maltose induced synthesis of alpha-glucosidase in derepressed cells of the wild-type and corresponding respiratory-deficient mutant of Saacharomyces cerevisiae. The results suggest that expression of nuclear genes specifying alpha-glucosidase and maltose catabolism in yeast is apparently not dependent on the proper function of mitochondrial adenine nucleotide translocase and does not even require the presence of normal levels of ATP in mitochondria.
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PMID:Alpha-glucosidase synthesis in yeast cells depleted of intramitochondrial ATP. 700 49

Inbred haploid strains of Saccharomyces cerevisiae carrying MAL1, MAL2 or MAL6 in a common background have been crossed to each other and to strains carrying no active MAL loci. The kinetics of maltase induction and the induced maltase levels have been examined in the inbred strains and in haploid segregants of the crosses. Differences have been found in the kinetics of induction and induced maltase levels that segregate with the different MAL loci. In the strains tested, the relative rates of maltase induction were MAL2 greater than MAL6 much greater than MAL1; the relative induced maltase levels were MAL2 greater than MAL6 similar to MAL1. These results indicate that MAL1, MAL2 and MAL6 are (or include) regulatory genes that control the accumulation of the enzymes of maltose fermentation.
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PMID:The effects of three different mal loci on the regulation of maltase synthesis in yeast. 703 38

We report the DNA sequence of a segment located on the right arm of chromosome II from Saccharomyces cerevisiae S288C near the subtelomeric sequences. The sequence was determined using a random cloning strategy followed by an oligonucleotide-directed sequencing. The segment contains four non-overlapping open reading frames (ORFs) YBR297w, YBR298c, YBR299w and YBR301c, and two overlapping ones (YBR300c and YBR300w). Three of them--YBR297w, YBR298c and YBR299w--are the MAL3R (transcriptional regulatory protein), MAL3T (maltose permease) and MAL3S (maltase) genes of the MAL3 locus previously localized. The three other ORFs are unidentified. Another MAL locus (MALl) has been localized on chromosome VII. The Mal- phenotype of strain S288c cannot be explained by telomeric silencing.
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PMID:Sequence of a 9.8 kb segment of yeast chromosome II including the three genes of the MAL3 locus and three unidentified open reading frames. 748 39

In Saccharomyces cerevisiae, the gene functions required to ferment the disaccharide maltose are encoded by the MAL loci. Any one of five highly sequence homologous MAL loci identified in various S. cerevisiae strains (called MAL1, 2, 3, 4 and 6) is sufficient to ferment maltose. Each is a complex of three genes encoding maltose permease, maltase and a transcription activator. This family of loci maps to telomere-linked positions on different chromosomes and most natural strains contain more than one MAL locus. A number of naturally occurring, mutant alleles of MAL1 and MAL3 have been characterized which lack one or more of the gene functions encoded by the fully functional MAL loci. Loss of these gene functions appears to have resulted from mutation and/or rearrangement within the locus. Studies to date concentrated on the standard maltose fermenting strains of S. cerevisiae available from the Berkeley Yeast Stock Center collection. In this report we extend our genetic analysis of the MAL loci to a number of maltose fermenting and nonfermenting natural strains of S. cerevisiae and Saccharomyces paradoxus. No new MAL loci were discovered but several new mutant alleles of MAL1 were identified. The evolution of this gene family is discussed.
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PMID:Genetic variation of the repeated MAL loci in natural populations of Saccharomyces cerevisiae and Saccharomyces paradoxus. 800 35

Maltose utilization in yeast requires the presence of any one of the five unlinked, homologous MAL loci. Transcription of the two structural genes MALT (permease) and MALS (maltase) is induced by maltose and catabolite-repressed by glucose. MAL6T and MAL6S share a common 5' intergenic sequence; deletion studies within this sequence revealed a bi-directionally functioning upstream activation sequence (UASM) consisting of four 11 bp homologous sites. Activation of these sites by the MALR protein results in the coordinate expression of MAL6T and MAL6S. The basal promoter activates MALS expression to a greater extent than MALT and is located in a region that overlaps UASM. Deletion of several subsites within the UASM has an asymmetric effect on MAL gene expression, having a greater affect on MALT than on MALS. Catabolite repression of MAL6T and MAL6S by glucose is controlled at several levels. Using disruption mutants, the positively acting MAL1R protein was also found to play a role in catabolite repression of MAL6T and MAL6S.
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PMID:Shared control of maltose induction and catabolite repression of the MAL structural genes in Saccharomyces. 802 78

Maltose fermenting strains of Saccharomyces cerevisiae have one or more complex loci called MAL. Each locus comprises at least three genes: MALx1 encodes maltose permease, MALx2 encodes maltase, and MALx3 encodes an activator of MALx1 and MALx2 (x denotes one of five MAL loci, with x = 1, 2, 3, 4, or 6). The MAL43c allele is constitutive and relatively insensitive to glucose repression. To understand better this unique phenotype of MAL43c, we have isolated several MAL63c constitutive mutants from a MAL6 strain. All constitutive mutants remain glucose repressible, and all have multiple amino acid substitutions in the C-terminal region, now making this region of Mal63cp similar to that of Mal43cp. These changes have been generated by gene conversion, which transfers DNA from the telomeres of chromosome II and chromosome III or XVI to chromosome VIII (MAL6). The removal of a Mig1p binding site from the MAL63c promoter leads to a loss of glucose repression, imitating the phenotype of MAL43c. Conversely, addition of a Mig1p binding site to the promoter of MAL43c converts it to glucose sensitivity. Mig1p modulation of Mal63p and Mal43p expression therefore plays a substantial role in glucose repression of the MAL genes.
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PMID:Removal of Mig1p binding site converts a MAL63 constitutive mutant derived by interchromosomal gene conversion to glucose insensitivity. 877 May 84


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