Eukaryotic Cell (Eukaryot Cell )

Publisher: American Society for Microbiology, American Society for Microbiology

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.

  • Impact factor
    3.59
  • 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 cannot archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Cannot archive before publication
    • Author's version
    • 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
    • Reviewed on 30th June 2014
  • Classification
    ​ blue

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Toxoplasma gondii is an obligate intracellular parasite that causes serious opportunistic infections, birth defects and blindness in humans. Microtubules are critically important components of diverse structures that are used throughout the Toxoplasma life cycle. As in other eukaryotes, spindle microtubules are required for chromosome segregation during replication. Additionally, a set of membrane-associated microtubules is essential for the elongated shape of invasive zoites and motility follows a spiral trajectory that reflects the path of these microtubules. Toxoplasma zoites also construct an intricate, tubulin-based apical structure termed the conoid which is important for host cell invasion and associates with proteins typically found in the flagellar apparatus. Lastly, microgametes specifically construct a microtubule-containing flagellar axoneme in order to fertilize macrogametes, permitting genetic recombination. The specialized roles of these microtubule populations are mediated by distinct sets of associated proteins. This review summarizes our current understanding of the role of tubulin, microtubule populations, and associated proteins in Toxoplasma; these components are used for both novel and broadly conserved processes that are essential for parasite survival.
    Eukaryotic Cell 11/2014;
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    ABSTRACT: The utilization of silicon by diatoms has both global and small scale implications, from oceanic primary productivity to nanotechnological applications of their silica cell walls. The sensing and transport of silicic acid is a key aspect of understanding diatom silicon utilization. At low silicic acid concentrations (<30 μM) transport mainly occurs through silicic acid transport proteins (SITs), and at higher concentrations through diffusion. Previous analyses of the SITs were done either in heterologous systems or without distinction between individual SITs. Herein, we examine individual SITs in Thalassiosira pseudonana in terms of transcript and protein abundance in response to different silicic acid regimes and examine knockdown lines to evaluate the role of the SITs in transport, silica incorporation, and lipid accumulation resulting from silicon starvation. SIT1 and 2 were localized in the plasma membrane, and protein levels were generally inversely correlated with cellular silicon needs, with a distinct response comparing the two SITs. We developed highly effective approaches for RNAi and antisense knockdowns - the first such for a centric diatom. SIT knockdown differentially affected the uptake of silicon and incorporation of silicic acid, and resulted in the induction of lipid accumulation under silicon starvation far earlier than in wild type, suggesting that the cells were artificially sensing silicon limitation. The data suggest that the transport role of the SITs is relatively minor under sufficient silicic acid - their primary role is to sense silicic acid levels to evaluate whether the cell can proceed with its cell wall formation and division processes.
    Eukaryotic Cell 11/2014;
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    ABSTRACT: The abundant molecular chaperone Hsp90 is essential for the folding and stabilization of hundreds of distinct client proteins. Hsp90 is assisted by multiple co-chaperones that modulate Hsp90's ATPase activity and/or promote client interaction, but the in vivo functions of many of these co-chaperones are largely unknown. We found that Cpr6, Cpr7 and Cns1 interact with the intact ribosome and that yeast lacking CPR7 or containing mutations in CNS1 exhibited sensitivity to the translation inhibitor hygromycin. Cpr6 contains a peptidyl-prolyl isomerase (PPIase) domain and a tetratricopeptide repeat (TPR) domain flanked by charged regions. Truncation or alteration of basic residues near the carboxy-terminus of Cpr6 disrupted ribosome interaction. Cns1 contains an amino-terminal TPR domain and a poorly characterized carboxy-terminal domain. The isolated carboxy-terminal domain was able to interact with the ribosome. Although loss of CPR6 does not cause noticeable growth defects, overexpression of CPR6 results in enhanced growth defects in cells expressing the temperature-sensitive cns1-G90D mutation. Cpr6 mutants that exhibit reduced ribosome interaction failed to cause growth defects, indicating that ribosome interaction is required for in vivo functions of Cpr6. Together these results represent a novel link between the Hsp90 molecular chaperone machine and protein synthesis.
    Eukaryotic Cell 11/2014;
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    ABSTRACT: The cullin 4 complex DCDC (DIM-5/-7/-9/CUL4/DDB1 Complex) is essential for DNA methylation and heterochromatin formation in Neurospora crassa. Cullins form the scaffold of Cullin RING E3 ubiquitin ligases (CRLs) and are modified by covalent attachment of NEDD8, a ubiquitin-like protein that regulates the stability and activity of CRLs. We report that neddylation is not required for CUL4-dependent DNA methylation and heterochromatin formation but is required for the DNA repair functions. Moreover, the RING-domain protein RBX1 and a segment of the CUL-4 C-terminus that normally interacts with RBX1, the E2 ligase, CAND-1 and CSN are dispensible for DNA methylation and heterochromatin formation by DCDC. Our study provides evidence for noncannonical functions of core CRL components.
    Eukaryotic Cell 10/2014;
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    ABSTRACT: Candida albicans is a commensal in heathy people, but has the potential to become an opportunistic pathogen, responsible for half of all clinical infections in immunocompromised patients. Central to understanding C. albicans behavior is the white-opaque phenotypic switch, in which cells can undergo an epigenetic transition between the white state and the opaque state. The phenotypic switch regulates multiple properties including biofilm formation, virulence, mating, and fungus-host interactions. Switching between white and opaque is associated with many external stimuli, such as oxidative stress, pH and N-acetylglucosamine, and is directly regulated by the Wor1 transcriptional circuit. The Hog1 SAPK pathway is recognized as the main pathway for adapting to environmental stress in C. albicans. In this work, we first show that loss of the HOG1 gene in A/A: and α/α cells, but not A: /α cells, results in 100% white-to-opaque switching when grown on synthetic medium, indicating that switching is repressed by the A1: /α2 heterodimer that represses WOR1 gene expression. Indeed, switching in the hog1Δ was dependent on WOR1, as a hog1Δ wor1Δ strain did not show switching to the opaque state. Deletion of PBS2 and SSK2 also resulted in C. albicans cells switching from white to opaque with 100% efficiency, indicating that the entire Hog1 SAPK pathway is involved in regulating this unique phenotypic transition. Interestingly, all Hog1 pathway mutants also caused defects in shmoo formation and mating efficiencies. Overall, this work reveals a novel role for the Hog1 SAPK pathway in regulating white-opaque switching and sexual behavior in C. albicans.
    Eukaryotic Cell 10/2014;
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    ABSTRACT: The cAMP-protein kinase A (PKA) signaling activates virulence expression during hyphal development in the fungal human pathogen Candida albicans. The hyphal growth is characterized by Golgi polarization towards the hyphal tips, which is thought to enhance directional vesicle transport. However, how the hypha-induction signal regulates Golgi polarization is unknown. Gyp1, a Golgi-associated protein and the first GTPase-activating protein (GAP) in the Rab GAP cascade, critically regulates membrane trafficking from the endoplasmic reticulum to the plasma membrane. Here, we report a novel pathway by which the cAMP-PKA signaling triggers Golgi polarization during hyphal growth. We demonstrate that Gyp1 plays a crucial role in actin-dependent Golgi polarization. Hyphal induction activates PKA which in turn phosphorylates Gyp1. Phosphomimetic mutation of four PKA sites identified by mass spectrometry (Gyp1(4E)) caused strong Gyp1 polarization to hyphal tips, whereas non-phosphorylatable mutations (Gyp1(4A)) abolished it. Gyp1(4E) exhibited enhanced association with the actin motor Myo2, while Gyp1(4A) had the opposite effect, providing a possible mechanism for Golgi polarization. A GAP-dead Gyp1 (Gyp1(R292K)) showed a strong polarization like Gyp1(4E), indicating a role for the GAP activity. Mutating the PKA sites on Gyp1 also impaired the recruitment of a late Golgi marker, Sec7. Furthermore, proper PKA phosphorylation and GAP activity of Gyp1 are required for virulence in mice. We propose that the cAMP-PKA signaling directly targets Gyp1 to promote Golgi polarization in the yeast-to-hyphal transition, an event crucial for C. albicans infection.
    Eukaryotic Cell 10/2014;
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    ABSTRACT: Candida albicans, a major human fungal pathogen, is the primary cause of invasive candidiasis in a wide array of immunocompromised patients. C. albicans virulence requires the ability to undergo a reversible morphological transition from yeast to filaments in response to a variety of host environmental cues. These cues are sensed by the pathogen and activate multiple signal transduction pathways to induce filamentation. Reversible phosphorylation events are critical for regulation of many of these pathways. While a variety of protein kinases are known to function as components of C. albicans filamentous growth signal transduction pathways, considerably little is known about the role of phosphatases. Here we demonstrate that PPG1, encoding a putative type 2A-related protein phosphatase, is important for C. albicans filament extension, invasion and virulence in a mouse model of systemic candidiasis. PPG1 is also important for down-regulation of NRG1, a key transcriptional repressor of C. albicans filamentous growth, and is shown to affect the expression of several filament-specific target genes. An epistasis analysis suggests that PPG1 controls C. albicans filamentation via the cAMP-PKA signaling pathway. We demonstrate that Ppg1 possesses phosphatase activity and that a ppg1 catalytic mutant shows nearly equivalent filamentation, invasion and virulence defects when compared to those of a ppg1Δ/Δ strain. Overall, our results suggest that phosphatases, such as Ppg1, play critical roles in controlling and fine-tuning C. albicans filament extension and virulence as well as signal transduction pathways, transcriptional regulators and target genes associated with these processes.
    Eukaryotic Cell 10/2014;
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    ABSTRACT: Cells sense and appropriately respond to the physical conditions and availability of nutrients in their environment. This sensing of the environment and consequent cellular responses are orchestrated by a multitude of signaling pathways and typically involve changes in transcription and metabolism. Recent discoveries suggest that the signaling and transcription machineries are regulated by signals which are derived from metabolism and reflect the metabolic state of the cell. Acetyl-CoA is a key metabolite linking metabolism with signaling, chromatin structure, and transcription. Acetyl-CoA is produced by glycolysis as well as other catabolic pathways and used as a substrate for the citric acid cycle and as a precursor for synthesis of fatty acids, steroids, and in other anabolic pathways. This central position in metabolism endows acetyl-CoA with an important regulatory role. Acetyl-CoA serves as a substrate for lysine acetyltransferases (KATs) that catalyze the transfer of acetyl groups to the epsilon amino groups of lysines in histones and many other proteins. Fluctuations in the concentration of acetyl-CoA, reflecting metabolic state of the cell, are translated into dynamic protein acetylations that regulate variety of cell functions, including transcription, replication, DNA repair, cell cycle progression, and aging. This review highlights the synthesis and homeostasis of acetyl-CoA, and the regulation of transcriptional and signaling machineries in yeast by acetylation.
    Eukaryotic Cell 10/2014;
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    ABSTRACT: Entamoeba histolytica, an amitochondriate protozoan parasite that relies on glycolysis as a key pathway for ATP generation, has developed an unique extended PPi-dependent glycolytic pathway in which ADP-forming acetyl-CoA synthetase (ACD; Acetate:CoA ligase (ADP-forming) [EC 6.2.1.13]) converts acetyl-CoA to acetate to produce additional ATP and recycle CoA. We have characterized the recombinant E. histolytica ACD and have shown that the enzyme is bidirectional, allowing it to potentially play a role in ATP production or in utilization of acetate. In the acetate-forming direction, acetyl-CoA is the preferred substrate and propionyl-CoA was used with lower efficiency. In the acetyl-CoA forming direction, acetate is the preferred substrate, with a lower efficiency observed with propionate. The enzyme can utilize both ADP/ATP and GDP/GTP in the respective directions of the reaction. ATP and PPi were found to inhibit the acetate-forming direction of the reaction with IC50 values of 0.81 ± 0.17 mM and 0.75 ± 0.20 mM, respectively, which are both in the range of their physiological concentrations. ATP and PPi displayed mixed inhibition versus each of the three substrates, acetyl-CoA, ADP, and phosphate. This is the first example of regulation of ACD enzymatic activity, and possible roles for this are discussed.
    Eukaryotic Cell 10/2014;
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    ABSTRACT: Tetrahymena telomeres are protected by a protein complex composed of Pot1, Tpt1, Pat1 and Pat2. Pot1 binds the 3' overhang and serves multiple roles in telomere maintenance. Here we describe Pot2, a paralog of Pot1, which has evolved a novel function during Tetrahymena sexual reproduction. Pot2 is unnecessary for telomere maintenance during vegetative growth as telomere structure is unaffected by POT2 macronuclear gene disruption. Pot2 is expressed only in mated cells where it accumulates in developing macronuclei around the time of two chromosome processing events: Internal Eliminated Sequence (IES) excision and chromosome breakage. Chromatin immunoprecipitation (ChIP) demonstrated Pot2 localization to regions of chromosome breakage but not to telomeres or IESs. Pot2 association with Chromosome Breakage Sites (CBSs) occurs slightly before chromosome breakage. Pot2 did not bind CBS or telomeric DNA in vitro suggesting that it is recruited to CBSs by another factor. The telomere proteins Pot1, Pat1 and Tpt1 and the IES binding factor Pdd1 fail to co-localize with Pot2. Thus, Pot2 is the first protein found to associate specifically with CBSs. The selective association of Pot2 versus Pdd1 with CBSs or IESs indicates a mechanistic difference between the chromosome processing events at these two sites. Moreover, ChIP revealed that histone marks characteristic of IES processing, H3K9me3 and H3K27me3, are absent from CBSs. Thus, the mechanisms of chromosome breakage and IES excision must be fundamentally different. Our results lead to a model where Pot2 directs chromosome breakage by recruiting telomerase and/or the endonuclease responsible for DNA cleavage to CBSs.
    Eukaryotic Cell 10/2014;
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    ABSTRACT: Toxoplasma gondii and its nearest extant relative, Hammondia hammondi, are phenotypically distinct despite their remarkable similarity in gene content, synteny and functionality. To begin to identify genetic differences that might drive distinct infection phenotypes of T. gondii and H. hammondi, in the present study we 1) determined whether two known host-interacting proteins, dense granule protein 15 (GRA15) and rhoptry protein 16 (ROP16), were functionally conserved in H. hammondi, and 2) performed the first comparative transcriptional analysis of H. hammondi and T. gondii sporulated oocysts. We found that GRA15 and ROP16 from H. hammondi (HhGRA15; HhROP16) modulate the host NF-κB and STAT6 pathways, respectively, when expressed heterologously in T. gondii. We also found the transcriptomes of H. hammondi and T. gondii to be highly distinct. Consistent with the spontaneous conversion of H. hammondi tachyzoites into bradyzoites both in vitro and in vivo, H. hammondi high-abundance transcripts are enriched for genes that are of greater abundance in T. gondii bradyzoites. We also identified genes that are of high transcript abundance in H. hammondi, but are poorly expressed in multiple T. gondii life stages, suggesting that these genes are uniquely expressed in H. hammondi. Taken together these data confirm the functional conservation of known T. gondii virulence effectors in H. hammondi, and point to transcriptional differences as a potential source of the phenotypic differences between these species.
    Eukaryotic Cell 10/2014;
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    ABSTRACT: Protein phosphatase 2A (PP2A) is a major intracellular protein phosphatase that regulates multiple aspects of cell growth and metabolism. Different activities of PP2A and subcellular localization are determined by its regulatory subunits. Here, we identified and characterized the function of two protein phosphatase regulatory subunit homologs parA and pabA in Aspergillus nidulans. Our results demonstrate that ParA locates to the septum site and deletion of parA causes hyper-septation, while over-expression of parA abolishes septum formation; this suggests that ParA may function as a negative regulator of septation. In comparison, PabA displays a clear co-localization pattern with DAPI stained nuclei and deletion of pabA induces a remarkable delayed septation phenotype. Both parA and pabA are required for hyphal growth, conidiation, and self-fertilization likely to maintain normal levels of PP2A activities. Most interestingly, parA deletion is capable of suppressing septation defects in pabA mutants, suggesting that ParA counteracts PabA during the septation process. By contrast, double mutants of parA and pabA led to synthetic defects in colony growth, indicating that ParA functions synthetically with PabA during hyphal growth. Moreover, unlike PP2A-Par1 and PP2A-Pab1 in yeast (which are negative regulators that inactivate the Septation Initiation Network [SIN]), loss of ParA or PabA fails to suppress defects of the temperature-sensitive mutants of the SEPH kinase of the SIN components. Thus, our findings support the previously unrealized evidence that the B-family subunits of PP2A have comprehensive functions as the partners of heterotrimeric enzyme complexes of PP2A spatially and temporally in A. nidulans.
    Eukaryotic Cell 10/2014;
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    ABSTRACT: The CRISPR/Cas9 system has become a powerful and precise tool for targeted gene modification (e.g., gene knockout and gene replacement) in numerous eukaryotic organisms. Initial attempts to apply this technology to the model, single cell alga, Chlamydomonas reinhardtii failed to yield cells containing edited genes. To determine if the Cas9 and single guide RNA (sgRNA) genes were functional in C. reinhardtii, we tested the ability of a codon-optimized Cas9 gene along with one of four different sgRNAs to cause targeted gene disruption during a 24-hour period immediately following transformation. All three exogenously supplied gene targets as well as the endogenous FKB12 (rapamycin sensitivity) gene of C. reinhardtii displayed distinct Cas9/sgRNA-mediated target site modifications as determined by DNA sequencing of cloned PCR amplicons of the target site region. Success in transient expression of Cas9 and sgRNA genes contrasted with the recovery of only a single rapamycin resistant colony bearing an appropriately modified FKB12 target site in 16 independent transformation experiments involving >10(9) cells. Failure to recover transformants with intact or expressed Cas9 genes following transformation with the Cas9 gene alone (or even with a gene encoding a Cas9 lacking nuclease activity) provided strong suggestive evidence for Cas9 toxicity when produced constitutively in C. reinhardtii. The present results provide compelling evidence that Cas9 and sgRNA genes function properly in C. reinhardtii to cause targeted gene modifications and point to the need for focus on development of methods to properly stem Cas9 production and/or activity following gene editing.
    Eukaryotic Cell 09/2014;
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    ABSTRACT: The regulatory circuits during infection of dinoflagellates by their parasites are largely unknown on the molecular level. Here we provide molecular insights into these infection dynamics. Alexandrium tamarense is one of the most prominent Harmful Algal Bloom dinoflagellate. Its pathogen, the dinoflagellate parasitoid Amoebophrya spp., has been observed to infect and control the blooms of this species. We generated a dataset of transcripts from three time points during the infection of this parasite-host system (0, 6 and 96 hours). Assembly of all transcript data from the parasitoid (>900.000 reads/313MBp with 454/Roche NGS) yielded 14,455 contigs, to which we mapped the raw transcript reads of each time point of the infection cycle. We show that particular surface lectins are expressed at the beginning of the infection cycle, which likely mediate the attachment to the host cell. In a later phase signal transduction related genes together with transmembrane transport and cytoskeleton proteins point to a high integration of processes involved in host recognition, adhesion, and invasion. At the final maturation stage, cell division and proliferation related genes were highly expressed, reflecting the fast cell growth and nuclear division of the parasitoid. Our molecular insights in dinoflagellate parasitoid interaction point to general mechanisms also known from other eukaryotic parasites, especially from the Alveolata. These similarities indicate the presence of fundamental processes of parasitoid infection that have remained stable throughout evolution within different phyla.
    Eukaryotic Cell 09/2014;
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    ABSTRACT: Marine algae of the genus Nannochloropsis are promising producers of biofuel precursors and nutraceuticals, and are also commercially harvested for aquaculture feed. We have used quick-freeze, deep-etch electron microscopy, Fourier transform-infrared spectroscopy, and carbohydrate analyses to characterize the architecture of the Nannochloropsis gaditana (CCMP 526) cell wall, whose recalcitrance presents a significant barrier to biocommodity extraction. The data indicate a bilayer structure consisting of a cellulosic inner wall (∼75% of the mass balance) protected by an outer hydrophobic algaenan layer. Cellulase treatment of walls purified after cell lysis generates highly enriched algaenan preparations without using the harsh chemical treatments typically used in algaenan isolation and characterization. Nannochloropsis algaenan was determined to comprise long, straight-chain, saturated aliphatics with ether cross-links, which closely resembles the cutan of vascular plants. Chemical identification of >85% of the isolated cell wall mass is detailed, and genome analysis is used to identify candidate biosynthetic enzymes.
    Eukaryotic Cell 09/2014;
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    ABSTRACT: Most freshwater flagellates use contractile vacuoles (CVs) to expel excess water. We have used Chlamydomonas reinhardtii as a green model system to investigate CV function during adaptation to osmotic changes in culture medium. We show that the contractile vacuole in Chlamydomonas is regulated in two different ways. The size of the contractile vacuoles increases during cell growth, with the contraction interval strongly depending on the osmotic strength of the medium. In contrast, there are only small fluctuations in cytosolic osmolarity and plasma membrane permeability. Modeling of the CV membrane permeability indicates that only a small osmotic gradient is necessary for water flux into the CV, which is most likely facilitated by the aquaporin major intrinsic protein 1 (MIP1). We show that MIP1 is localized to the contractile vacuole, and that the expression rate and protein level of MIP1 exhibit only minor fluctuations under different osmotic conditions. In contrast, SEC6, a protein of the exocyst complex that is required for the water expulsion step, and a dynamin-like protein are upregulated under strong hypotonic conditions. Overexpression of a CreMIP1-GFP construct did not change the physiology of the CV. The functional implications of these results are discussed.
    Eukaryotic Cell 09/2014;
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    ABSTRACT: Septin proteins are conserved structural proteins that often demarcate regions of cell division. The essential nature of the septin ring, composed of several septin proteins, complicates investigation of the functions of the ring, although careful analysis in the model yeast Saccharomyces cerevisiae has elucidated the role that septins play in the cell cycle. Mutation analysis of non-essential septins in the pathogenic fungus Candida albicans has shown that septins also have vital roles in CWR, hyphal formation, and pathogenesis. While mutations in non-essential septins have been useful in establishing phenotypes, the septin defect is so slight that identifying causative associations between septins and downstream effectors has been difficult. In this work, we describe Decreased Abundance by mRNA Perturbation (DAmP) alleles of essential septins, which display a more severe septin defect than the defect observed in deletions of non-essential septins. The septin-DAmP alleles have allowed us to genetically separate the role of septins in hyphal growth and CWR and to identify the cyclic AMP pathway as a pathway that likely acts in a parallel manner with septins in hyphal morphogenesis.
    Eukaryotic Cell 09/2014;
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    ABSTRACT: Malaria kills nearly one million people each year, and the protozoan parasite Plasmodium falciparum has become increasingly resistant to current therapies. Isoprenoid synthesis via the methylerythritol phosphate (MEP) pathway represents an attractive target for the development of new antimalarials. The phosphonic acid antibiotic fosmidomycin is a specific inhibitor of isoprenoid synthesis and has been a helpful tool to outline the essential functions of isoprenoid biosynthesis in P. falciparum. Isoprenoids are a large, diverse class of hydrocarbons that function in a variety of essential cellular processes in eukaryotes. In P. falciparum, isoprenoids are used for tRNA isopentenylation and protein prenylation, as well as synthesis of vitamin E, carotenoids, ubiquinone, and dolichols. Recently, isoprenoid synthesis in P. falciparum has been shown to be regulated by a sugar phosphatase. We outline what is known about isoprenoid function and regulation of isoprenoid synthesis in P. falciparum, in order to identify valuable directions for future research.
    Eukaryotic Cell 09/2014;