Eukaryotic Cell Journal Impact Factor & Information

Publisher: American Society for Microbiology, American Society for Microbiology

Journal description

Eukaryotic Cell (EC) focuses on eukaryotic microbiology and presents reports of basic research on simple eukaryotic microorganisms such as yeasts, fungi, algae, protozoa, and social amoebae. The journal also covers viruses of these organisms and their organelles and their interactions with other living systems, where the focus is on the eukaryotic cell.

Current impact factor: 3.18

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2013 / 2014 Impact Factor 3.179
2012 Impact Factor 3.586
2011 Impact Factor 3.604
2010 Impact Factor 3.395
2009 Impact Factor 3.806
2008 Impact Factor 3.83
2007 Impact Factor 3.399
2006 Impact Factor 3.707
2005 Impact Factor 4.303
2004 Impact Factor 3.954
2003 Impact Factor 3.267

Impact factor over time

Impact factor

Additional details

5-year impact 3.77
Cited half-life 5.40
Immediacy index 0.65
Eigenfactor 0.02
Article influence 1.32
Website Eukaryotic Cell website
Other titles Eukaryotic cell (Online), Eukaryotic cell
ISSN 1535-9786
OCLC 47259667
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

American Society for Microbiology

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Author's pre-print on recognised non profit pre-print archives
    • Author's post-print on funder's repositories, institutional repository or subject-based repositories
    • Non-commercial
    • Publisher's version/PDF may be used
    • Publisher's version/PDF may be used on author's personal website or employers website
    • Recommended that author's post-prints submitted to PubMed or institutional repositories are made available 6 months after publication
    • Publisher last contacted on 21/05/2015
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Candida albicans and Candida dubliniensis are highly related species that share the same main developmental programs. In C. albicans it has been demonstrated that the biofilms formed by strains heterozygous and homozygous at the mating type locus (MTL) differ functionally, but studies rarely identify the MTL configuration. This becomes a particular problem in studies of C. dubliniensis given that one third of natural strains are MTL-homozygous. For that reason, we have analyzed MTL-homozygous strains of C. dubliniensis for their capacity to switch from white to opaque, for the stability of the opaque phenotype, CO2 induction of switching, pheromone induction of adhesion, the effects of minority opaque cells on biofilm thickness and dry weight, and biofilm architecture, by comparison with C. albicans. Our results reveal that C. dubliniensis strains switch to opaque at lower average frequencies, exhibit far lower level of opaque phase stability, are not stimulated to switch by high CO2, exhibit more variability in biofilm architecture, and most notably, form mature biofilm composed predominately of pseudohyphae rather than true hyphae. Therefore, while several traits of MTL-homozygous strains of C. dubliniensis appear to be degenerating or have been lost, others, most notably several related to biofilm formation, have been conserved. Within this context, the possibility is considered that C. dubliniensis is transitioning from a hypha-dominated to pseudohyphae-dominated biofilm and that aspects of C. dubliniensis colonization may provide insights into the selective pressures that are involved.
    Eukaryotic Cell 10/2015; DOI:10.1128/EC.00146-15
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    ABSTRACT: In the light of multidrug resistance (MDR) among pathogenic microbes and cancer cells, membrane transporters have gained profound clinical significance. Chemotherapeutic failure, by far has been mainly attributed to the robust and diverse array of these proteins, omnipresent in every stratum of the living world. Candida albicans, one of the major fungal pathogen affecting immune-compromised patients, too develops MDR during the course of chemotherapy. The pivotal membrane transporters which C. albicans has exploited for the purpose as one of the strategies to develop MDR belongs either to ATP Binding Cassette (ABC) or Major Facilitator Superfamily (MFS) proteins. ABC transporter Candida drug resistance 1 protein (Cdr1p) is a major player among these transporters which enables the pathogen to outplay the battery of antifungals encountered by it. The promiscuous Cdr1 protein fulfils the quintessential need of a model to study molecular mechanisms of multidrug transporter regulation and structure-function analyses of asymmetric ABC transporters. Herein, with this review, we highlight the research of two decades with Cdr1p which has provided a platform to study its structure-function and regulatory circuitry for a better understanding of MDR not only in yeast but also in other organisms.
    Eukaryotic Cell 09/2015; DOI:10.1128/EC.00137-15
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    ABSTRACT: Entamoeba histolytica, a microaerophilic protozoan parasite, possesses mitosomes. Mitosomes are mitochondrion-related organelles that have largely lost typical mitochondrial functions, such as the tricarboxylic acid cycle, and oxidative phosphorylation. The biological roles of Entamoeba mitosomes have been a long-standing enigma. We previously demonstrated that sulfate activation, which is not generally compartmentalized to mitochondria, is a major function of E. histolytica mitosomes. Sulfate activation cooperates with cytosolic enzymes, sulfotransferases (SULTs), for the synthesis of sulfolipids, one of which is cholesteryl sulfate. Notably, cholesteryl sulfate plays an important role in encystation, an essential process in the Entamoeba life cycle. These findings provided a biological role for Entamoeba mitosomes; however, they simultaneously raised a new question of how the reactions of the pathway, separated by the mitosomal membranes, cooperate. Here, we demonstrated that E. histolytica mitochondrial carrier family (EhMCF) has the capacity to exchange 3' -phosphoadenosine 5' -phosphosulfate (PAPS) with ATP. We also confirmed the cytosolic localization of all the E. histolytica SULTs, suggesting that in Entamoeba, PAPS, which is produced through mitosomal sulfate activation, is translocated to the cytosol and becomes a substrate for SULTs. Conversely, ATP, which is produced through cytosolic pathways, is translocated into the mitosomes and is a necessary substrate for sulfate activation. Collectively, we suggest that EhMCF functions as a PAPS/ATP antiporter and plays a crucial role in linking the mitosomal sulfate-activation pathway to cytosolic SULTs for the production of sulfolipids.
    Eukaryotic Cell 09/2015; DOI:10.1128/EC.00130-15
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    ABSTRACT: As a successful commensal and pathogen of humans, Candida albicans encounters a wide range of environmental conditions. Among them, ambient pH, which changes frequently and affects many biological processes in this species, is an important factor, and the ability to adapt to pH changes is tightly linked with pathogenesis and morphogenesis. In this study, we report that pH has a profound effect on white-opaque switching and sexual mating in C. albicans. Acidic pH promotes white-to-opaque switching under certain culture conditions but represses sexual mating. The Rim101-mediated pH sensing pathway is involved in the control of pH-regulated white-opaque switching and mating response. Phr2 and Rim101 could play a major role in acidic pH-induced opaque cell formation. Despite the fact that the cAMP signaling pathway does not play a major role in pH-regulated white-opaque switching and mating, white and opaque cells of the cyr1/cyr1 mutant, which is defective in producing cAMP, show distinct growth defects under acidic and alkaline conditions. We further discover that acidic pH conditions repress sexual mating due to the failure of activation of the Ste2-mediated α-pheromone response pathway in opaque " A: " cells. The effects of pH changes on phenotypic switching and sexual mating could involve a balance of host adaptation and sexual reproduction in C. albicans. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 09/2015; DOI:10.1128/EC.00123-15
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    ABSTRACT: Candida albicans is associated with humans as both a harmless commensal organism and a pathogen. Cph2 is a transcription factor whose DNA binding domain is similar to mammalian sterol response element binding proteins (SREBPs). SREBPs are master regulators of cellular cholesterol levels, and are highly conserved from fungi to mammals. However, ergosterol biosynthesis is regulated by the zinc finger transcription factor Upc2 in C. albicans and several other yeasts. Cph2 is not necessary for ergosterol biosynthesis, but important for colonization in the murine gastrointestinal tract. Here we demonstrate that Cph2 is a membrane-associated transcription factor that is processed to release the N-terminal DNA binding domain like SREBPs; but its cleavage is not regulated by cellular levels of ergosterol or oxygen. ChIP-Seq shows that Cph2 binds to the promoters of HMS1 and other components of the regulatory circuit for GI tract colonization. In addition, 50% of Cph2 targets are also bound by Hms1 and other factors of the regulatory circuit. Several common targets function at the head of the glycolysis pathway. Thus, Cph2 is an integral part of the regulatory circuit for GI colonization that regulates glycolytic flux. RNA-seq shows a significant overlap in genes differentially regulated by Cph2 and hypoxia, and Cph2 is important for optimal expression of some hypoxia-responsive genes in glycolysis and the citric acid cycle. We suggest that Cph2 and Upc2 regulate hypoxia-responsive expression in different pathways, consistent with a synthetic lethal defect of the cph2 upc2 double mutant in hypoxia. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 09/2015; DOI:10.1128/EC.00102-15
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    ABSTRACT: Low rates of homologous recombination have broadly encumbered genetic studies in the fungal pathogen Aspergillus fumigatus. The CRISPR/Cas9 system of bacteria has recently been developed for targeted mutagenesis of eukaryotic genomes with high efficiency and, importantly, through a mechanism independent of homologous repair machinery. As this new technology has not been developed for use in A. fumigatus, we sought to test its feasibility for targeted gene disruption in this organism. As a proof-of-principle, we first demonstrate that CRISPR/Cas9 can indeed be used for high-efficiency (25-53%) targeting of the A. fumigatus polyketide synthase gene (pksP), as evidenced by the generation of colorless (albino) mutants harboring the expected genomic alteration. We further demonstrate that the constitutive expression of the Cas9 nuclease by itself is not deleterious with respect to A. fumigatus growth or virulence, thus making the CRISPR system compatible with studies involved in pathogenesis. Taken together, these data demonstrate that CRISPR can be utilized for loss-of-function studies in A. fumigatus and has the potential to bolster the genetic toolbox of this important pathogen.
    Eukaryotic Cell 08/2015; DOI:10.1128/EC.00107-15
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    ABSTRACT: Candida albicans is the leading cause of fungal infections; but it is also a member of the human microbiome, an ecosystem of thousands of microbial species potentially influencing the outcome of host-fungal interactions. Accordingly, antibacterial therapy raises the risk of candidiasis, yet the underlying mechanism is currently not fully understood. We hypothesize the existence of bacterial-derived metabolites that normally control C. albicans growth and of fungal resistance mechanisms against these metabolites. Among the most abundant microbiota-derived metabolites found on human mucosal surfaces are weak organic acids (WOAs), such as acetic, propionic, butyric and lactic acid. Here we used quantitative growth assays to investigate the dose-dependent fungistatic property of WOAs on C. albicans growth and found it to occur at physiologically relevant concentrations and pH. This effect was conserved across distantly related fungal species both inside and outside the CTG clade. We next screened a library of transcription factor mutants and identified several genes required for resistance of C. albicans to one or more WOAs. A single gene, MIG1, previously known for its role in glucose repression, conferred resistance against all four tested acids. Consistent with glucose being an upstream activator of Mig1p, presence of this carbon source was required for WOA resistance in wild-type C. albicans. Conversely, a MIG1-complemented strain completely restored the glucose-dependent resistance against WOAs. We conclude that Mig1p plays a central role in orchestrating a transcriptional programme to fight against the fungistatic effect of this class of highly abundant metabolites produced by the GI microbiota. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 08/2015; DOI:10.1128/EC.00129-15
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    ABSTRACT: Eisosomes are among the few remaining eukaryotic cellular differentiations that lack defined function(s). These trough-shaped invaginations of the plasma membrane have been largely studied in Saccharomyces cerevisiae, where their associated proteins, including two BAR-domain proteins, have been identified and homologues have been found throughout the fungal radiation. Using quick-freeze deep-etch electron-microscopy to generate high-resolution replicas of membrane fracture faces without the use of chemical fixation, we report that eisosomes are also present in a subset of red and green microalgae as well as in the cysts of the ciliate Euplotes. Eisosome assembly is closely correlated with both the presence and the nature of cell walls. Microalgal eisosomes vary extensively in topology and internal organization. Unlike fungi, their convex fracture faces can carry lineage-specific arrays of intramembranous particles, and their concave fracture faces usually display fine striations, also seen in fungi, that are pitched at lineage-specific angles and, in some cases, adopt a broader banded patterning. The conserved genes that encode fungal eisosome-associated proteins are not found in sequenced algal genomes, but we have identified genes encoding two algal lineage-specific families of predicted BAR-domain proteins, called Green-BAR and Red-BAR, that are candidate eisosome organizers. We propose a model for eisosome formation wherein 1) positively-charged recognition patches first establish contact with target membrane regions and 2) a (partial) unwinding of the coiled-coil conformation of the BAR domains then allows interactions between the hydrophobic faces of their amphipathic helices and the lipid phase of the inner membrane leaflet, generating the striated patterns. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 08/2015; DOI:10.1128/EC.00106-15
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    ABSTRACT: Several important classes of antifungal agents including the azoles, act by blocking ergosterol biosynthesis. It was recently reported that the azoles cause massive disruption of the fungal vacuole in the prevalent human pathogen Candida albicans. This is significant as normal vacuolar function is required to support C. albicans pathogenicity. This study examined the impact of the morpholine antifungals, which inhibit latter steps of ergosterol biosynthesis, upon C. albicans vacuolar integrity. It was found that overexpression of either the ERG2 or ERG24 genes, encoding C-8 sterol isomerase and C-14 sterol reductase respectively, suppresses C. albicans sensitivity to the morpholines. In addition, both erg2Δ/Δ and erg24Δ/Δ mutants are hypersensitive to the morpholines. These data are consistent with the antifungal activity of the morpholines depending upon the simultaneous inhibition of both Erg2p and Erg24p. The vacuoles within both erg2Δ/Δ and erg24Δ/Δ C. albicans strains exhibit an aberrant morphology and accumulate large quantities of the weak base quinacrine, indicating enhanced vacuolar acidification compared with the control strains. Both erg mutants exhibit significant defects in polarized hyphal growth and are avirulent in a mouse model of disseminated candidiasis. Surprisingly, in a mouse model of vaginal candidiasis, both mutants colonize at high levels and induce a pathogenic response similar to the controls. Thus while targeting Erg2p or Erg24p alone could provide a potentially efficacious therapy for disseminated candidiasis, it may not be an effective strategy to treat vaginal infections. The potential value of drugs targeting these enzymes as adjunctive therapies is discussed. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 07/2015; DOI:10.1128/EC.00116-15
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    ABSTRACT: The global regulatory veA gene governs development and secondary metabolism in numerous fungal species, including Aspergillus flavus. This is especially relevant since A. flavus infects crops of agricultural importance worldwide, contaminating them with potent mycotoxins. The most well-known are aflatoxins, cytotoxic and carcinogenic polyketide compounds. The production of aflatoxins, and the expression of genes implicated in the production of these mycotoxins, are veA-dependent. The genes responsible for the synthesis of aflatoxins are clustered, a signature common for genes involved in fungal secondary metabolism. Studies of the A. flavus genome revealed many gene clusters possibly connected to the synthesis of secondary metabolites. Many of these metabolites are still unknown, or the association between a known metabolite with a particular gene cluster has not yet been established. In the present transcriptome study we show that veA is necessary for the expression of a large number of genes. Twenty-eight out of the predicted 56 secondary metabolite gene clusters include at least one gene that is differentially expressed depending on presence or absence of veA. One of the clusters under the influence of veA is cluster 39. Absence of veA results in a down-regulation of the five genes found within this cluster. Interestingly, our results indicate that the cluster is mainly expressed in sclerotia. Chemical analysis of sclerotial extracts revealed that cluster 39 is responsible for the production of aflavarin. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 07/2015; 14(10). DOI:10.1128/EC.00092-15
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    ABSTRACT: Candida species cause a variety of mucosal and invasive infections and are, collectively, the most important human fungal pathogens in the developed world. The majority of these infections result from a handful of related species within the "CUG clade," so named because they use a non-standard translation for that codon. Some members of the CUG clade, like C. albicans, are significant clinical problems while others, such as Candida (Meyerozyma) guilliermondii, are uncommon in patients. The differences in incidence rates are imperfectly correlated with virulence in animal models of infection, but comparative analyses that might provide an explanation for why some species are effective pathogens and others are not have been rare or incomplete. To better understand the phenotypic basis for these differences, we have characterized eight CUG clade species, C. albicans, C. dubliniensis, C. tropicalis, C. parapsilosis, Clavispora lusitaniae, M. guilliermondii, Debaryomyces hansenii, and Lodderomyces elongisporus for host-relevant phenotypes including nutrient utilization, stress tolerance, morphogenesis, interactions with phagocytes, and biofilm formation. Two species deviated from expectations based on animal studies and human incidence. C. dubliniensis was quite robust, grouping in nearly all assays with the most virulent species, C. albicans and C. tropicalis, while C. parapsilosis was substantially less fit than might be expected from its clinical importance. These findings confirm the utility of in vitro measures of virulence and provide insight into the evolution of virulence in the CUG clade. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 07/2015; 14(9). DOI:10.1128/EC.00062-15
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    ABSTRACT: Mechanistic studies on gliotoxin biosynthesis and self-protection, both of which require the gliotoxin oxidoreductase, GliT, in Aspergillus fumigatus have revealed a rich landscape of highly novel biochemistries, yet key aspects of this complex molecular architecture remain obscure. Here we show that A. fumigatus ΔgliA is completely deficient in gliotoxin secretion but still retains the ability to efflux bisdethiobis(methylthio)gliotoxin (BmGT). This correlates with a significant increase in sensitivity to exogenous gliotoxin because gliotoxin trapped inside the cell leads to (i) Activation of the gli cluster. Disabling gli cluster activation, via gliZ deletion, attenuates the sensitivity of A. fumigatus ΔgliT to gliotoxin, thus implicating cluster activation as a factor in gliotoxin sensitivity. (ii) Increased methylation activity due to excess substrate (dithiol gliotoxin) for gliotoxin bis-thiomethyltransferase GtmA. Intracellular dithiol gliotoxin is oxidized by GliT and subsequently effluxed by GliA. In the absence of GliA, gliotoxin persists in the cell, and is converted to BmGT, with levels significantly higher than the wild-type. Similarly, in ΔgliT, gliotoxin oxidation is impeded, and methylation occurs unchecked, leading to significant S-adenosylmethionine (SAM) depletion and S-adenosylhomocysteine (SAH) overproduction. This in turn significantly contributes to the observed hypersensitivity to gliotoxin in gliT-deficient A. fumigatus. Our observations reveal a key role for GliT in preventing dysregulation of the methyl/methionine cycle, to control intracellular SAM and SAH homeostasis during gliotoxin biosynthesis and exposure. Moreover, we reveal attenuated GliT abundance in A. fumigatus ΔgliK, but not ΔgliG, following exposure to gliotoxin, correlating with relative sensitivities. Overall, we illuminate new systems interactions which have evolved in gliotoxin-producing, compared to gliotoxin-naïve, fungi to facilitate its cellular presence.
    Eukaryotic Cell 07/2015; 14(9). DOI:10.1128/EC.00055-15
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    ABSTRACT: Yeast Bro1 and Rim20 belong to a family of proteins, which possess a common architecture of Bro1- and V-domains. Alix and HD-PTP, mammalian Bro1 family proteins, bind YP(X)nL (n = 1 ∼ 3) motifs in their target proteins through their V domains. In Alix, the Phe residue, which is located in the hydrophobic groove of the V domain, is critical for binding to the YP(X)nL motif. Although the overall sequences are not highly conserved between mammalian and yeast V domains, we show that the conserved Phe residue in the yeast Bro1 V domain is important for binding to its YP(X)nL-containing target protein, Rfu1. Furthermore, we show that Rim20 binds to its target protein Rim101 through the interaction between the V domain of Rim20 and the YPIKL motif of Rim101. The mutation of either the critical Phe residue in the Rim20 V domain or the YPIKL motif of Rim101 affected the Rim20-mediated processing of Rim101. These results suggest that the interactions between V domains and YP(X)nL motif-containing proteins are conserved from yeast to mammalian cells. Moreover, the specificities of each V domain to their target protein suggest that unidentified elements determine the binding specificity. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 07/2015; DOI:10.1128/EC.00091-15