Evidence map›Paper›PMID 10224251›Full record

ArticleGenetics1999

Topoisomerase I is essential in Cryptococcus neoformans: role In pathobiology and as an antifungal target.

M Del Poeta, D L Toffaletti, T H Rude, C C Dykstra, J Heitman, J R Perfect

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
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  4. 'Acridines' as New Horizons in Antifungal Treatment.Molecules (Basel, Switzerland) · 2020
    Review
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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

6 authors at 4 institutions in 2 countries.

M Del PoetaDepartment of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.
D L Toffaletti
T H Rude
C C Dykstra
J Heitman
J R Perfect
Duke Medical Center · USAuburn University · USDuke University Hospital · USHoward Hughes Medical Institute · US

Funding

GENTIC &MOLECULAR BIOLOGY OF VIRULENCE IN C. NEOFORMANSR01AI028388 · NIAID · DUKE UNIVERSITY · PI PERFECT, JOHN R. · 1991 to 2004
$1.9M
Combined Peanut Oral Immunotherapy and Anti-IgE: Mechanistic StudiesR21AI094014 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BURKS, A. WESLEY · 2011 to 2012
$415k
Genetic molecular biology of virulence in C. neoformansR56AI028388 · NIAID · DUKE UNIVERSITY · PI PERFECT, JOHN R. · 2006 to 2006
$389k
NOVEL ANTIFUNGAL DRUG TARGETS IN CRYPTOCOCCUS NEOFORMANSR01AI041937 · NIAID · DUKE UNIVERSITY · PI HEITMAN, JOSEPH · 1997 to 1999
–
NIAID NIH HHS AI28388NIAID NIH HHS AI41937NIAID NIH HHS AI-94-014
6 · The paper itself

Abstract

Topisomerase I is the target of several toxins and chemotherapy agents, and the enzyme is essential for viability in some organisms, including mice and drosophila. We have cloned the TOP1 gene encoding topoisomerase I from the opportunistic fungal pathogen Cryptococcus neoformans. The C. neoformans topoisomerase I contains a fungal insert also found in topoisomerase I from Candida albicans and Saccharomyces cerevisiae that is not present in the mammalian enzyme. We were unable to disrupt the topoisomerase I gene in this haploid organism by homologous recombination in over 8000 transformants analyzed. When a second functional copy of the TOP1 gene was introduced into the genome, the topoisomerase I gene could be readily disrupted by homologous recombination (at 7% efficiency). Thus, topoisomerase I is essential in C. neoformans. This new molecular strategy with C. neoformans may also be useful in identifying essential genes in other pathogenic fungi. To address the physiological and pathobiological functions of the enzyme, the TOP1 gene was fused to the GAL7 gene promoter. The resulting GAL7::TOP1 fusion gene was modestly regulated by carbon source in a serotype A strain of C. neoformans. Modest overexpression of topoisomerase I conferred sensitivity to heat shock, gamma-rays, and camptothecin. In contrast, alterations in topoisomerase I levels had no effect on the toxicity of a novel class of antifungal agents, the dicationic aromatic compounds (DACs), indicating that topoisomerase I is not the target of DACs. In an animal model of cryptococcal meningitis, topoisomerase I regulation was not critically important to established infection, but may impact on the initial stress response to infection. In summary, our studies reveal that topoisomerase I is essential in the human pathogen C. neoformans and represents a novel target for antifungal agents.

Indexed as

Amino Acid SequenceAnimalsBiotransformationCamptothecinCell SurvivalCloning, MolecularCryptococcusDNA Topoisomerases, Type IEnzyme InhibitorsGene ExpressionModels, GeneticMolecular Sequence DataPlasmidsRabbitsRadiation, IonizingReverse Transcriptase Polymerase Chain ReactionCamptothecinDNA Topoisomerases, Type IEnzyme Inhibitors

Identifiers

PMID10224251
PMCPMC1460578
OpenAlexW2121897520

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.