A mutant of Aspergillus nidulans lacking NADP-linked glutamate dehydrogenase

Arst, Herbert N.; MacDonald, D

doi:10.1007/bf00278601

Cited by 70 publications

(47 citation statements)

References 23 publications

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“…3C). The gdhB gene encodes NAD-dependent glutamate dehydrogenase, which acts to convert glutamate to 2-oxoglutarate and ammonia and consequently is required for both proline and glutamate utilization (6). The gdhB101 mutation resulted in a loss of induction by both proline and glutamate but not acetate (Fig.…”

Section: Resultsmentioning

confidence: 99%

Regulation of theacuFGene, Encoding Phosphoenolpyruvate Carboxykinase in the Filamentous FungusAspergillus nidulans

2002

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Phosphoenolpyruvate carboxykinase (PEPCK) is a key enzyme required for gluconeogenesis when microorganisms grow on carbon sources metabolized via the tricarboxylic acid (TCA) cycle. Aspergillus nidulans acuF mutants isolated by their inability to use acetate as a carbon source specifically lack PEPCK. The acuF gene has been cloned and shown to encode a protein with high similarity to PEPCK from bacteria, plants, and fungi. The regulation of acuF expression has been studied by Northern blotting and by the construction of lacZ fusion reporters. Induction by acetate is abolished in mutants unable to metabolize acetate via the TCA cycle, and induction by amino acids metabolized via 2-oxoglutarate is lost in mutants unable to form 2-oxoglutarate. Induction by acetate and proline is not additive, consistent with a single mechanism of induction. Malate and succinate result in induction, and it is proposed that PEPCK is controlled by a novel mechanism of induction by a TCA cycle intermediate or derivative, thereby allowing gluconeogenesis to occur during growth on any carbon source metabolized via the TCA cycle. It has been shown that the facB gene, which mediates acetate induction of enzymes specifically required for acetate utilization, is not directly involved in PEPCK induction. This is in contrast to Saccharomyces cerevisiae, where Cat8p and Sip4p, homologs of FacB, regulate PEPCK as well as the expression of other genes necessary for growth on nonfermentable carbon sources in response to the carbon source present. This difference in the control of gluconeogenesis reflects the ability of A. nidulans and other filamentous fungi to use a wide variety of carbon sources in comparison with S. cerevisiae. The acuF gene was also found to be subject to activation by the CCAAT binding protein AnCF, a protein homologous to the S. cerevisiae Hap complex and the mammalian NFY complex.

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Section: Resultsmentioning

confidence: 99%

Regulation of theacuFGene, Encoding Phosphoenolpyruvate Carboxykinase in the Filamentous FungusAspergillus nidulans

2002

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“…These include not only sources of acetylCoA (ethanol, acetate, fatty acids) but also sources of 2-oxoglutarate (amino acids) and sources of both succinate and acetyl-CoA (aromatic acids and fatty acids containing odd numbers of carbon), which are not dependent on the glyoxalate cycle (Arst et al 1975;Kinghorn and Pateman 1976;Kuswandi and Roberts 1992;Brock et al 2000;Brock 2005).…”

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confidence: 99%

Transcriptional Control of Gluconeogenesis in Aspergillus nidulans

et al. 2007

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Aspergillus nidulans can utilize carbon sources that result in the production of TCA cycle intermediates, thereby requiring gluconeogenesis. We have cloned the acuG gene encoding fructose-1,6 bisphosphatase and found that expression of this gene is regulated by carbon catabolite repression as well as by induction by a TCA cycle intermediate similar to the induction of the previously studied acuF gene encoding phosphoenolpyruvate carboxykinase. The acuN356 mutation results in loss of growth on gluconeogenic carbon sources. Cloning of acuN has shown that it encodes enolase, an enzyme involved in both glycolysis and gluconeogenesis. The acuN356 mutation is a translocation with a breakpoint in the 59 untranslated region resulting in loss of expression in response to gluconeogenic but not glycolytic carbon sources. Mutations in the acuK and acuM genes affect growth on carbon sources requiring gluconeogenesis and result in loss of induction of the acuF, acuN, and acuG genes by sources of TCA cycle intermediates. Isolation and sequencing of these genes has shown that they encode proteins with similar but distinct Zn(2) Cys(6) DNA-binding domains, suggesting a direct role in transcriptional control of gluconeogenic genes. These genes are conserved in other filamentous ascomycetes, indicating their significance for the regulation of carbon source utilization.

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“…In addition to ten gdhA mutants already known (Kinghorn & Pateman, 1973a;Arst & MacDonald, 1973) a further 31 mutants, gdhAII to A 4 4 were isolated on the basis of sensitivity to high concentrations of ammonium (-N medium+ 200 mwammonium) at 25 "C. They were found to have decreased NADP-GDH activities, from zero to 20 % of wild type. These mutants were crossed to gdhAr and all but three gave no wild-type recombinants in 5000 progeny.…”

Section: Isolation and Genetics Of Mutants Lacking Nadp-gdhmentioning

confidence: 99%

“…Since it was not practical to construct diploids between all combinations of g d h h to gdhA41, complementation was tested in heterokaryons. These tests were carried out on media on which gdhA mutants grow poorly compared with the wild type: -N mediumf200 mMammonium at 25 "C (Kinghorn & Pateman, 1973a), and -CN medium+ I yo acetate+ 10 mM-ammonium at 37 "C (Arst & MacDonald, 1973). No increased growth was observed in heterokaryons between all combinations of gdhAI to gdhAqr on either medium.…”

Section: Complementation Testsmentioning

confidence: 99%

The Structural Gene for NADP L-Glutamate Dehydrogenase in Aspergillus Nidulans

Kinghorn

Pateman

1975

Journal of General Microbiology

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A total of 41 mutants lacking NADP L-glutamate dehydrogenase (NADP-GDH) activity have been studied. All the mutations were located at the gdhA locus within 0-1 % recombination of gdhAI. Two mutants, gdhAI and gdhA2, out of five examined, produced cross-reacting material which neutralized NADP-GDH antiserum. The mutant gdhA9 has altered K, values for all five substrates : ammonium, a-ketoglutarate, L-glutamate, NADPH and NADP. The mutant gdhA2o had temperaturesensitive growth, abnormal ammonium-regulation characteristics and thermolabile NADP-GDH activity. These results show that gdhA is the structural gene for NADP-CDH.

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A mutant of Aspergillus nidulans lacking NADP-linked glutamate dehydrogenase

Cited by 70 publications

References 23 publications

Regulation of theacuFGene, Encoding Phosphoenolpyruvate Carboxykinase in the Filamentous FungusAspergillus nidulans

Regulation of theacuFGene, Encoding Phosphoenolpyruvate Carboxykinase in the Filamentous FungusAspergillus nidulans

Transcriptional Control of Gluconeogenesis in Aspergillus nidulans

The Structural Gene for NADP L-Glutamate Dehydrogenase in Aspergillus Nidulans

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