Evidence map›Paper›PMID 18515753›Full record

ArticleEukaryotic cell2008

SSD1 is integral to host defense peptide resistance in Candida albicans.

Kimberly D Gank, Michael R Yeaman, Satoshi Kojima, Nannette Y Yount, Hyunsook Park, John E Edwards, Scott G Filler, Yue Fu

Open access · diamondAbstract read
In one paragraph

Article in Eukaryotic cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

30 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. The mRNA stability factor Khd4 defines a specific mRNA regulon for membrane trafficking in the pathogenProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Post-transcriptional control of fungal cell wall synthesis.Cell surface (Amsterdam, Netherlands) · 2022
    Article
  4. Article
  5. Article
  6. Membrane-Interacting Antifungal Peptides.Frontiers in cell and developmental biology · 2021
    Review
  7. Medical mycology case reports · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Unifying structural signature of eukaryotic α-helical host defense peptides.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  13. Article
  14. Methodologies forMicrobial cell (Graz, Austria) · 2018
    Review
  15. Review
  16. Fungal Strategies to Evade the Host Immune Recognition.Journal of fungi (Basel, Switzerland) · 2017
    Review
  17. Review
  18. Review
  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

8 authors at 3 institutions in 1 country.

Kimberly D GankDivision of Infectious Diseases, LAC-Harbor UCLA Medical Center, Torrance, California 90509, USA.
Michael R Yeaman
Satoshi Kojima
Nannette Y Yount
Hyunsook Park
John E Edwards
Scott G Filler
Yue Fu
UCLA Medical Center · USHarbor–UCLA Medical Center · USUniversity of California, Los Angeles · US

Funding

Staphylococcal Adaptations to Platelet Microbicidal ProteinR01AI039108 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI BAYER, ARNOLD S · 1997 to 2016
$5.1M
Candida albicans Epithelial Cell Interactions and Oropharyngeal DiseaseR01DE017088 · NIDCR · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI FILLER, SCOTT G · 2005 to 2014
$3.4M
Candida Invasion of Endothelium and VirulenceR01AI054928 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI FILLER, SCOTT G · 2004 to 2013
$2.9M
DETERMINANTS IN PLATELET MICROBICIDAL PROTEINSR01AI048031 · NIAID · LA BIOMED RES INST/ HARBOR UCLA MED CTR · PI YEAMAN, MICHAEL R · 2000 to 2004
$1.6M
Optimizing Measurement Of Hiv-1 Neutralization Using A FZ01AI005010 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI MASCOLA, JOHN R · 2002 to 2008
$538k
Functional Screening for Candida Virulence GPI-proteinsR21AI066010 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI FU, YUE · 2007 to 2008
$378k
Intramural NIH HHS Z01 AI005010NIAID NIH HHS AI039108NIAID NIH HHS AI048031NIAID NIH HHS AI054928NIAID NIH HHS AI066010NIAID NIH HHS R01 AI039108NIAID NIH HHS R01 AI048031NIAID NIH HHS R01 AI054928NIAID NIH HHS R21 AI066010NIDCR NIH HHS R01 DE017088
6 · The paper itself

Abstract

Candida albicans is usually a harmless human commensal. Because inflammatory responses are not normally induced by colonization, antimicrobial peptides are likely integral to first-line host defense against invasive candidiasis. Thus, C. albicans must have mechanisms to tolerate or circumvent molecular effectors of innate immunity and thereby colonize human tissues. Prior studies demonstrated that an antimicrobial peptide-resistant strain of C. albicans, 36082(R), is hypervirulent in animal models versus its susceptible counterpart (36082(S)). The current study aimed to identify a genetic basis for antimicrobial peptide resistance in C. albicans. Screening of a C. albicans genomic library identified SSD1 as capable of conferring peptide resistance to a susceptible surrogate, Saccharomyces cerevisiae. Sequencing confirmed that the predicted translation products of 36082(S) and 36082(R) SSD1 genes were identical. However, Northern analyses corroborated that SSD1 is expressed at higher levels in 36082(R) than in 36082(S). In isogenic backgrounds, ssd1Delta/ssd1Delta null mutants were significantly more susceptible to antimicrobial peptides than parental strains but had equivalent susceptibilities to nonpeptide stressors. Moreover, SSD1 complementation of ssd1Delta/ssd1Delta mutants restored parental antimicrobial peptide resistance phenotypes, and overexpression of SSD1 conferred enhanced peptide resistance. Consistent with these in vitro findings, ssd1 null mutants were significantly less virulent in a murine model of disseminated candidiasis than were their parental or complemented strains. Collectively, these results indicate that SSD1 is integral to C. albicans resistance to host defense peptides, a phenotype that appears to enhance the virulence of this organism in vivo.

Indexed as

AnimalsAntimicrobial Cationic PeptidesCandida albicansCandidiasisDisease Models, AnimalGene Expression Regulation, FungalHost-Pathogen InteractionsImmunity, InnateMaleMiceMice, Inbred BALB CMutationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsVirulenceAntimicrobial Cationic PeptidesSaccharomyces cerevisiae ProteinsSsd1 protein, S cerevisiae

Identifiers

PMID18515753
PMCPMC2519774
OpenAlexW2132265773

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.