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 2015
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
Year

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 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: Coccidioides immitis and C. posadasii are soil-dwelling fungi and the causative agents of coccidioidomycosis, a mycosis endemic to certain semi-arid regions within the Americas. The most common route of infection is by inhalation of airborne Coccidioides arthroconidia. Once a susceptible host inhales the conidia, a transition into mature endosporulated spherules can occur within the first five days of infection. For this study, we examined the host response in a murine model of coccidioidomycosis during a time-period of infection that has not been well characterized. We collected lung tissue and bronchoalveolar lavage fluids (BALF) from BALB/c mice that were infected with a C. immitis pure strain, a C. immitis hybrid strain, or a C. posadasii strain as well as uninfected mice. We compared the host response to each of the Coccidioides strains used in this study by assessing the level of transcription of select cytokine genes in lung tissues and characterized host and fungal proteins present in BALF. Host response varied depending on the Coccidioides strain that was used and did not appear to be overly robust. This study provides a foundation to begin to dissect the host immune response early in infection, to detect abundant Coccidioides proteins, and to develop diagnostics that target these early time points of infection. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 08/2015; DOI:10.1128/EC.00122-15
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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; 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; 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; 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
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    ABSTRACT: When treated with a hyperosmotic stimulus, K. lactis cells respond by activating the MAPK KlHog1 protein via two conserved branches, SLN1 and SHO1. Mutants affected only in one branch can cope with external hyperosmolarity by activating KlHog1p by phosphorylation, except for single ΔKlste11 and ΔKlste50 mutants, which showed high sensitivity to osmotic stress, even though the other branch (SLN1) is intact. Inactivation of both branches by deletion of KlSHO1 and KlSSK2 also produced sensitivity to high salt. Interestingly we have observed that in mutants ΔKlste11 and ΔKlsho1ΔKlssk2, which exhibit sensitivity to hyperosmotic stress and contrary to what would be expected, KlHog1p becomes phosphorylated. Additionally, in mutants lacking both MAPKKKs present in K. lactis (KlSte11p and KlSsk2p), the hyperosmotic stress induces phosphorylation and nuclear internalization of KlHog1p but it fails to induce transcriptional expression of KlSTL1 and the cell is unable to growth in high osmotic medium. KlHog1p phosphorylation via the canonical HOG pathway or in mutants where the SHO1 and SLN1 branches have been inactivated requires not only the presence of KlPbs2p but also its kinase activity. This indicates that when the SHO1 and SLN1 branches are inactivated, high osmotic conditions activate an independent input that yields active KlPbs2p, which in turn, renders ineffective KlHog1p phosphorylation. Finally, we found that KlSte11p can alleviate the sensitivity to hyperosmotic stress displayed by a ΔKlsho1ΔKlssk2 when is anchored to the plasma membrane by adding the KlSho1p transmembrane segments, indicating that this chimeric protein can substitute for KlSho1p and KlSsk2p. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 07/2015; DOI:10.1128/EC.00048-15
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    ABSTRACT: Polarized growth in filamentous fungi needs a continuous supply of proteins and lipids to the growing hyphal tip. One of the important membrane compounds in fungi is ergosterol. At the apical plasma membrane ergosterol accumulations, which are called sterol-rich plasma membrane domains (SRDs). The exact roles and formation mechanism of the SRDs remained unclear, although the importance has been recognized for hyphal growth. Transport of ergosterol to hyphal tips is thought to be important for the organization of the SRDs. Oxysterol binding proteins, which are conserved from yeast to human, are involved in non-vesicular sterol transport. In Saccharomyces cerevisiae seven oxysterol-binding proteins homologues (OSH1-7) play a role in ergosterol distribution between closely located membranes independent of vesicle transport. We found five homologous genes (oshA-E) in the filamentous fungi Aspergillus nidulans. The functions of OshA-E were characterized by gene deletion and subcellular localization. Each gene-deletion strain showed characteristic phenotypes and different sensitivities to ergosterol-associated drugs. GFP tagged Osh proteins showed specific localization at late Golgi, puncta associated with the ER, or diffusely in the cytoplasm. The genes expression and regulation were investigated in a medically important species Aspergillus fumigatus as well as A. nidulans. Our results suggest that each Osh protein plays a role in ergosterol distribution at distinct sites and contributes to proper fungal growth. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 06/2015; DOI:10.1128/EC.00027-15
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    ABSTRACT: Filamentous growth is a microbial differentiation response that involves the concerted action of multiple signaling pathways. In budding yeast, one pathway that regulates filamentous growth is a Cdc42p-dependent mitogen activated protein kinase (MAPK) pathway. Several transmembrane (TM) proteins regulate the filamentous growth pathway, including the signaling mucin, Msb2p, the tetraspan osmosensor, Sho1p, and an adaptor, Opy2p. The TM proteins were compared to identify common and unique features. Msb2p, Sho1p, and Opy2p associated by co-immunoprecipitation analysis but showed predominately different localization patterns. The different localization patterns of the proteins resulted, in part, from different rates of turnover from the PM. In particular, Msb2p (and Opy2p) were turned over rapidly compared to Sho1p. Msb2p signaled from the PM and its turnover was a rate-limiting step in MAPK signaling. Genetic analysis identified unique phenotypes of cells overexpressing the TM proteins. Therefore, each TM regulator of the filamentous growth pathway has a unique regulatory pattern and specific function in regulating filamentous growth. This specialization may be important for fine-tuning and potentially diversifying the filamentation response. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 06/2015; DOI:10.1128/EC.00085-15
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    ABSTRACT: The centriole in eukaryotes functions as the cell's microtubule-organizing center (MTOC) to nucleate spindle assembly, and its biogenesis requires an evolutionarily conserved protein, SAS-6, which assembles the centriole cartwheel. Trypanosoma brucei, an early branching protozoan, possesses the basal body as its MTOC to nucleate flagellum biogenesis. However, little is known about the components of the basal body and their roles in basal body biogenesis and flagellum assembly. Here we report that the T. brucei SAS-6 homolog, TbSAS-6, is localized to the mature basal body and the pro-basal body throughout the cell cycle. RNAi of TbSAS-6 inhibited pro-basal body biogenesis, compromised flagellum assembly, and caused cytokinesis arrest. Surprisingly, overexpression of TbSAS-6 in T. brucei also impaired pro-basal body duplication and flagellum assembly, contrary to SAS-6 overexpression in humans which produces supernumerary centrioles. Furthermore, we showed that depletion of Polo-like kinase, TbPLK, or inhibition of TbPLK activity did not abolish TbSAS-6 localization to the basal body, in contrast to the essential role of Polo-like kinase in recruiting SAS-6 to centrioles in animals. Altogether, these results identified the essential role of TbSAS-6 in pro-basal body biogenesis and flagellum assembly, and suggest the presence of a TbPLK-independent pathway governing basal body duplication in T. brucei. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 06/2015; DOI:10.1128/EC.00083-15
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    ABSTRACT: The gametogenesis program of the budding yeast Saccharomyces cerevisiae, also known as sporulation, employs an unusual internal meiotic division, following which all four meiotic products differentiate within the parental cell. We showed previously that sporulation is typically accompanied by the destruction of discarded immature meiotic products through their exposure to proteases released from the mother cell vacuole, which undergoes an apparent programmed rupture. Here we demonstrate that vacuolar rupture contributes to a de facto programmed cell death (PCD) of the meiotic mother cell itself. Meiotic mother PCD is accompanied by an accumulation of depolarized mitochondria, organelle swelling, altered plasma membrane characteristics, and cytoplasmic clearance. To ensure that the gametes survive the destructive consequences of developing within a cell that is executing PCD, we hypothesized that PCD is restrained from occurring until spores have attained a threshold degree of differentiation. Consistent with this hypothesis, gene deletions that perturb all but the most terminal post-meiotic spore developmental stages are associated with altered PCD. In these mutants, meiotic mother cells exhibit a delay in vacuolar rupture, and then appear to undergo an alternative form of PCD associated with catastrophic consequences for the under-developed spores. Our findings reveal yeast sporulation as a context of bona fide PCD that is developmentally coordinated with gamete differentiation. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Eukaryotic Cell 06/2015; DOI:10.1128/EC.00068-15