Genetic analysis of the role of peroxisomes in the utilization of acetate and fatty acids in Aspergillus nidulans

Peroxisomes are organelles containing a diverse array of enzymes. In fungi they are important for carbon source utilization, pathogenesis, development, and secondary metabolism. We have studied Aspergillus nidulans peroxin (pex) mutants isolated by virtue of their inability to grow on butyrate or by...

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Veröffentlicht in:Genetics (Austin) 2008-03, Vol.178 (3), p.1355-1369
Hauptverfasser: Hynes, M.J, Murray, S.L, Khew, G.S, Davis, M.A
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Murray, S.L
Khew, G.S
Davis, M.A
description Peroxisomes are organelles containing a diverse array of enzymes. In fungi they are important for carbon source utilization, pathogenesis, development, and secondary metabolism. We have studied Aspergillus nidulans peroxin (pex) mutants isolated by virtue of their inability to grow on butyrate or by the inactivation of specific pex genes. While all pex mutants are able to form colonies, those unable to import PTS1 proteins are partially defective in asexual and sexual development. The pex mutants are able to grow on acetate but are affected in growth on fatty acids, indicating a requirement for the peroxisomal localization of beta-oxidation enzymes. However, mislocalization of malate synthase does not prevent growth on either fatty acids or acetate, showing that the glyoxylate cycle does not require peroxisomal localization. Proliferation of peroxisomes is dependent on fatty acids, but not on acetate, and on PexK (Pex11), expression of which is activated by the FarA transcription factor. Proliferation was greatly reduced in a farADelta strain. A mutation affecting a mitochodrial ketoacyl-CoA thiolase and disruption of a mitochondrial hydroxy-acyl-CoA dehydrogenase gene prevented growth on short-chain but not long-chain fatty acids. Together with previous results, this is consistent with growth on even-numbered short-chain fatty acids requiring a mitochondrial as well as a peroxisomal beta-oxidation pathway. The mitochondrial pathway is not required for growth on valerate or for long-chain fatty acid utilization.
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A mutation affecting a mitochodrial ketoacyl-CoA thiolase and disruption of a mitochondrial hydroxy-acyl-CoA dehydrogenase gene prevented growth on short-chain but not long-chain fatty acids. Together with previous results, this is consistent with growth on even-numbered short-chain fatty acids requiring a mitochondrial as well as a peroxisomal beta-oxidation pathway. 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subjects Acetates - metabolism
acetic acid
Aspergillus nidulans - cytology
Aspergillus nidulans - genetics
Aspergillus nidulans - growth & development
Aspergillus nidulans - metabolism
Aspergillus nidulellus
Carbon - pharmacology
Ethanol
Fatty acids
Fatty Acids - metabolism
fungal proteins
Fungal Proteins - isolation & purification
Fungal Proteins - metabolism
gene expression
hydroxy-acyl-CoA dehydrogenase
Investigations
ketoacyl-CoA thiolase
lipid metabolism
metabolism
Mitochondria - drug effects
Mitochondria - metabolism
Mutant Proteins - isolation & purification
Mutant Proteins - metabolism
Mutation - genetics
peroxin
peroxisomes
Peroxisomes - drug effects
Peroxisomes - genetics
Peroxisomes - metabolism
Phenotype
Protein Transport - drug effects
Proteins
PTS1 protein
Spores, Fungal - drug effects
transcription factors
title Genetic analysis of the role of peroxisomes in the utilization of acetate and fatty acids in Aspergillus nidulans
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