Evidence map›Paper›PMID 23950731›Full record

ArticlePLoS genetics2013

Ras1 acts through duplicated Cdc42 and Rac proteins to regulate morphogenesis and pathogenesis in the human fungal pathogen Cryptococcus neoformans.

Elizabeth Ripley Ballou, Lukasz Kozubowski, Connie B Nichols, J Andrew Alspaugh

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Is Cryptococcus neoformans a pleomorphic fungus?Current opinion in microbiology · 2024
    Review
  3. Roles of Different Signaling Pathways inJournal of fungi (Basel, Switzerland) · 2024
    Review
  4. Determination of Ploidy Levels and Nuclear DNA Content inJournal of fungi (Basel, Switzerland) · 2024
    Article
  5. Article
  6. Article
  7. Measuring Stress Phenotypes in Cryptococcus neoformans.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  8. Article
  9. CryptoCEN: A Co-Expression Network forbioRxiv : the preprint server for biology · 2023
    Article
  10. Article
  11. Epistatic genetic interactions govern morphogenesis during sexual reproduction and infection in a global human fungal pathogen.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Article
  13. Article
  14. Overexpression of theJournal of fungi (Basel, Switzerland) · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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.

Elizabeth Ripley BallouDepartment of Medicine, Duke University School of Medicine, Durham, North Carolina, USA.
Lukasz Kozubowski
Connie B Nichols
J Andrew Alspaugh
Duke University · US

Funding

Ras Signaling in C. neoformans virulence and developmentR01AI050128 · NIAID · DUKE UNIVERSITY · PI ALSPAUGH, ANDREW · 2003 to 2012
$3.0M
C. neoformans cAMP signaling and pathogenesisR56AI063242 · NIAID · DUKE UNIVERSITY · PI ALSPAUGH, J. ANDREW · 2006 to 2006
$311k
Ras signaling in C.neoformans virulence and developmentR21AI050128 · NIAID · DUKE UNIVERSITY · PI ALSPAUGH, J. ANDREW · 2002 to 2002
$305k
NIAID NIH HHS AI050128NIAID NIH HHS AI063242NIAID NIH HHS R01 AI050128NIAID NIH HHS R21 AI050128NIAID NIH HHS R56 AI063242
6 · The paper itself

Abstract

Proliferation and morphogenesis in eukaryotic cells depend on the concerted activity of Rho-type GTPases, including Ras, Cdc42, and Rac. The sexually dimorphic fungus Cryptococcus neoformans, which encodes paralogous, non-essential copies of all three, provides a unique model in which to examine the interactions of these conserved proteins. Previously, we demonstrated that RAS1 mediates C. neoformans virulence by acting as a central regulator of both thermotolerance and mating. We report here that ras1Δ mutants accumulate defects in polarized growth, cytokinesis, and cell cycle progression. We demonstrate that the ras1Δ defects in thermotolerance and mating can be largely explained by the compromised activity of four downstream Rho-GTPases: the Cdc42 paralogs, Cdc42 and Cdc420; and the Rac paralogs, Rac1 and Rac2. Further, we demonstrate that the separate GTPase classes play distinct Ras-dependent roles in C. neoformans morphogenesis and pathogenesis. Cdc42 paralogs primarily control septin localization and cytokinesis, while Rac paralogs play a primary role in polarized cell growth. Together, these duplicate, related signaling proteins provide a robust system to allow microbial proliferation in the presence of host-derived cell stresses.

Indexed as

cdc42 GTP-Binding ProteinCryptococcus neoformansCytokinesisFungal ProteinsGene Expression Regulation, FungalHumansMorphogenesisMutationrac GTP-Binding ProteinsSignal Transductioncdc42 GTP-Binding ProteinFungal Proteinsrac GTP-Binding Proteins

Identifiers

PMID23950731
PMCPMC3738472
OpenAlexW2029192414

What OpenQuestion holds

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LicenceCC BY
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.