Evidence map›Paper›PMID 17041184›Full record

ArticleEukaryotic cell2007

Peroxisome function regulates growth on glucose in the basidiomycete fungus Cryptococcus neoformans.

Alexander Idnurm, Steven S Giles, John R Perfect, Joseph Heitman

Open access · diamondAbstract read
In one paragraph

Article in Eukaryotic cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Microbiology spectrum · 2022
    Article
  5. Review
  6. Article
  7. Influence of Pathogen Carbon Metabolism on Interactions With Host Immunity.Frontiers in cellular and infection microbiology · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. International journal of molecular sciences · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Roles of Peroxisomes in the Rice Blast Fungus.BioMed research international · 2016
    Review
  20. Metabolism in fungal pathogenesis.Cold Spring Harbor perspectives in medicine · 2014
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Alexander IdnurmRoom 322 CARL Building, Box 3546, Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710, USA.
Steven S Giles
John R Perfect
Joseph Heitman
Duke Medical Center · US

Funding

Genetic analysis of Cryptococcus neoformans virulenceR01AI063443 · NIAID · DUKE UNIVERSITY · PI HEITMAN, JOSEPH · 2005 to 2009
$2.0M
GENTIC &MOLECULAR BIOLOGY OF VIRULENCE IN C. NEOFORMANSR01AI028388 · NIAID · DUKE UNIVERSITY · PI PERFECT, JOHN R. · 1991 to 2004
$1.9M
Genetic molecular biology of virulence in C. neoformansR56AI028388 · NIAID · DUKE UNIVERSITY · PI PERFECT, JOHN R. · 2006 to 2006
$389k
NIAID NIH HHS AI028388NIAID NIH HHS AI063443NIAID NIH HHS R01 AI028388NIAID NIH HHS R01 AI063443NIAID NIH HHS R56 AI028388
6 · The paper itself

Abstract

The function of the peroxisomes was examined in the pathogenic basidiomycete Cryptococcus neoformans. Recent studies reveal the glyoxylate pathway is required for virulence of diverse microbial pathogens of plants and animals. One exception is C. neoformans, in which isocitrate lyase (encoded by ICL1) was previously shown not to be required for virulence, and here this was extended to exclude also a role for malate synthase (encoded by MLS1). The role of peroxisomes, in which the glyoxylate pathway enzymes are localized in many organisms, was examined by mutation of two genes (PEX1 and PEX6) encoding AAA (ATPases associated with various cellular activities)-type proteins required for peroxisome formation. The pex1 and pex6 deletion mutants were unable to localize the fluorescent DsRED-SKL protein to peroxisomal punctate structures, in contrast to wild-type cells. pex1 and pex6 single mutants and a pex1 pex6 double mutant exhibit identical phenotypes, including abolished growth on fatty acids but no growth difference on acetate. Because both icl1 and mls1 mutants are unable to grow on acetate as the sole carbon source, these findings demonstrate that the glyoxylate pathway can function efficiently outside the peroxisome in C. neoformans. The pex1 mutant exhibits wild-type virulence in a murine inhalation model and in an insect host, demonstrating that peroxisomes are not required for virulence under these conditions. An unusual phenotype of the pex1 and pex6 mutants was that they grew poorly with glucose as the carbon source, but nearly wild type with galactose, which suggested impaired hexokinase function and that C. neoformans peroxisomes might function analogously to the glycosomes of the trypanosomid parasites. Deletion of the hexokinase HXK2 gene reduced growth in the presence of glucose and suppressed the growth defect of the pex1 mutant on glucose. The hexokinase 2 protein of C. neoformans contains a predicted peroxisome targeting signal (type 2) motif; however, Hxk2 fused to fluorescent proteins was not localized to peroxisomes. Thus, we hypothesize that glucose or glycolytic metabolites are utilized in the peroxisome by an as yet unidentified enzyme or regulate a pathway required by the fungus in the absence of peroxisomes.

Indexed as

AcetatesAnimalsBacterial ProteinsCryptococcus neoformansGlucoseGlyoxylatesHexokinaseMalate SynthaseMicePeroxisomal DisordersPeroxisomesVirulenceAcetatesBacterial ProteinsGlucoseGlyoxylatesglyoxylic acidHexokinaseMalate SynthasePex protein, Synechococcus

Identifiers

PMID17041184
PMCPMC1800366
OpenAlexW2138220484

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.