Aspergillus nidulans mutants unable to localise glyoxylate cycle enzymes to the peroxisomes are able to utilise acetate.

Gillian S. Khew, Sandra L. Murray, Meryl A. Davis and Michael J. Hynes.

Author address: 

Department of Genetics, University of Melbourne, Victoria 3010, Australia.

Abstract: 

Growth on acetate and fatty acids results in the production of acetyl-CoA which is channeled into the TCA and glyoxylate cycles. The TCA cycle occurs in the mitochondria and the glyoxylate cycle in the peroxisomes. Peroxisomal proteins are directed to the peroxisomes via one of two classes of peroxisomal targeting signals PTS1 and PTS2. PTS1 targeting occurs via the Pex5 receptor and PTS2 via the Pex7 receptor. These receptors are recycled to the cytosol by Pex6, an ATPase. The A. nidulans genes, acuD (isocitrate lyase) and acuE (malate synthase), encode enzymes specific to the glyoxylate cycle. AcuE possesses a peroxisomal targeting signal 1 (PTS1) whereas AcuD lacks any identifiable PTS1 or PTS2. We are interested in the effects of peroxisomal protein localisation on fatty acid utilisation in A. nidulans. A knockout mutant of the A. nidulans PEX5 orthologue (pexE) mislocalises AcuE to the cytoplasm but is able to target AcuD to the peroxisomes. A mutant in the PEX7 orthologue (pexG), however, mislocalises AcuD but is unaffected in peroxisomal targeting of AcuE. A mutant defective in the PEX6 orthologue (pexF) mislocalises both AcuD and AcuE to the cytoplasm but is nonetheless able to utilise acetate. Most of the peroxisomal mutants studied in our laboratory are sensitive to the presence of fatty acids. The growth of the pexE mutant is particularly inhibited by the presence of all fatty acids tested, including acetate. A pexE/pexG double mutant shows relief of acetate inhibition and is able to grow on acetate.
2005

abstract No: 

535

Full conference title: 

23rd Fungal Genetics Conference
    • Fungal Genetics Conference 23rd (2002)