Svetlana Moskalenko

Russian Academy of Sciences, Moskva, Moscow, Russia

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Publications (16)17.46 Total impact

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    ABSTRACT: The major part of existing models of belowground competition in mixed forest stands is limited in explaining the spatial distribution of roots as a response to competitive pressure from neighbours and heterogeneity of soil properties. We are presenting a new spatially explicit and multi-layered discrete model of belowground competition, RootInt (ROOTs INTake). It describes spatial distribution of belowground biomass and allows simulation of competition between trees for soil nutrients. The tree-specific area of root zone is calculated on the basis of stem diameter, with site-specific modifiers to account for the effect of soil fertility and moisture. The shape of root zone is dependent on the amount of available nitrogen in the current cell, distance between this cell and the stem base, and the mass of roots of other plants. RootInt was incorporated into ecosystem model EFIMOD to refine the existing description of belowground competition in forest stands with multiple cohorts and tree species. The results of simulation showed that bringing more complexity into structure of stand (including initial spatial locations of trees, species composition and age structure, vertical structure of canopy) resulted in higher spatial variation in competition intensity, as well as in higher rates of resource uptake. This indicates that stands with complex canopy structure had high plasticity in their root systems and were adapted to intensive competition for soil resources.
    No preview · Article · Nov 2015 · European Journal of Forest Research
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    ABSTRACT: Mutations in the essential genes SUP45 and SUP35, encoding yeast translation termination factors eRF1 and eRF3, respectively, lead to a wide range of phenotypes and affect various cell processes. In this work we show that nonsense and missense mutations in the SUP45, but not the SUP35, gene abolish diploid pseudohyphal and haploid invasive growth. Missense mutations that change phosphorylation sites of Sup45 protein do not affect the ability of yeast strains to form pseudohyphae. Deletion of the C-terminal part of eRF1 did not lead to impairment of filamentation. We show a correlation between the filamentation defect and the budding pattern in sup45 strains. Inhibition of translation with specific antibiotics causes a significant reduction in pseudohyphal growth in the wild type strain, suggesting a strong correlation between translation and ability for filamentous growth. Partial restoration of pseudohyphal growth by addition of exogenous cAMP assumes that sup45 mutants are defective in the cAMP-dependent pathway that control filament formation. © FEMS 2015. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
    Full-text · Article · Jun 2015 · FEMS Yeast Research
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    ABSTRACT: Aims 1. Structure of model must be understandable by biologists and ecologists which are not experienced in modelling. 2. Model must be of simulation type, being based on simple set of relationships and rules. 3. Model must have small amount of parameters which are easily calculated. 4. Model operates on small grid, divided into homogenous cells. This simplifies simulation of small-scale processes, such as growth of root tips, water and nutrients uptake, mycorrhizal relationships, etc. 5. We try to avoid high level of details since all possible roughness and uncertainties will be eliminated when calculating the average dynamics for a set of interacting individuals. Model concepts I. Defining zone of nutrition: Average and maximal distance of lateral spreading ; ; , , are species-specific Modifying and according to environmental conditions ;; , are site-specific Calculating square of the nutrition zone Adding new cells to the nutrition zone , where are the probability functions (return values of corresponding parameters normalized by the maximal one among all cells to be between 0 and 1) -distance from the rooting cell, (inverse relationship) -amount of nutrients (direct relationship) -mass of roots of other species (inverse relationship) Including cells with highest until total square = II. Distribute biomass of fine and coarse roots Horizontal distribution -of fine roots -according to value of -of coarse roots -according to value of Vertical distribution -function of soil layer depth: ; is the cumulative portion of total biomass of roots above the given depth is species-specific III. Simulate uptake The uptake rate is proportional to the biomass of fine roots, nutrient content, and distance from stem in given cell +Age-specific modifier ; are species-specific IV. Simulate mortality of roots and corresponding in-soil litter income Regular mortality (portion of biomass on each step) -defined by the ratio between costs necessary to maintain the biomass of roots and benefits (amount of nutrients) provided by the roots -c*DBH -c*DBH l_max=a/(1+b*exp) l_avg=a/(1+b*exp) abc l_avg l_max l_max=l_max*m *m l_avg=l_avg*m *mm m moist fert moist fert moist fert 2 S =Pi*l_avg n_zone p=f(d)*f(m)*f(n) f() dd <=l_max n m p S n_zone f(d)*f(n)*f(m) f(d) -a_ms*d m_ms=1-exp m_ms d a_ms -b_ur*age u =a_ur*exp a_ur b_ur a and Graphical abstract: l_avg l_max Square of the nutrition zone Cells potentially to be included into the nutrition zone Actual nutrition zone = Acknowledgements:
    Full-text · Conference Paper · Oct 2014
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    S. E. Moskalenko · O. A. Murina · O. L. Askinazi · G. A. Zhuravleva
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    ABSTRACT: A search for proteins which interact with the eRF1 termination translation factor encoded by SUP45 gene in yeast Saccharomyces cerevisiae was carried out by screening yeast genes located on a multicopy plasmid. This approach allowed finding the ECM23 gene whose increased expression led to lower viability of the sup45 nonsense mutants. Overexpression ECM23 gene led also to an antisuppressor effect, although the amount of the eRF1protein was not changed. Possible mechanisms of how ECM23 can affect the viability of the sup45 nonsense mutants are discussed.
    Full-text · Article · Mar 2014 · Russian Journal of Genetics: Applied Research
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    O. A. Murina · S. E. Moskalenko · G. A. Zhouravleva
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    ABSTRACT: At present, the machinery supporting the viability of organisms possessing nonsense mutations in essential genes is not entirely understood. Nonsense mutants of Saccharomyces cerevisiae yeast containing a premature translation termination codon in the essential SUP45 gene are known. These strains are viable in the absence of mutant suppressor tRNAs; hence, the existence of alternative mechanisms providing nonsense suppression and mutant viability is conjectured. Analysis of clones obtained by transformation of a strain bearing a nonsense-mutant allele of SUP45 with a multicopy yeast genomic library revealed three genes encoding wild-type tRNATyr and four genes encoding wild-type tRNAGln, which increased nonsense mutant viability. Moreover, overexpression of these genes leads to an increase in the amount of the full-length eRF1 protein in cells and compensates for heat sensitivity in the nonsense mutants. Probable ways of tRNATyr and tRNAGln influence on the increase in the viability of strains with nonsense mutations in SUP45 are discussed. Key wordstranslation termination-yeast-nonsense suppression- SUP45 - sup45 nonsense mutants-eRF1-tRNA
    Full-text · Article · Apr 2010 · Molecular Biology
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    O. A. Murina · S. E. Moskalenko · G. A. Zhouravleva
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    ABSTRACT: 301 *Ключевыми компонентами терминации трансс ляции у эукариот являются факторы eRF1 и eRF3 (см. обзор [1]). Белок eRF1 распознает любой из трех стоппкодонов (UAA, UAG или UGA) при его попадании в ААсайт рибосомы, что приводит к гидролизу связи пептидиллтРНК [2]. Фактор eRF3 – это GTPаза, которая стимулирует фактор eRF1, обеспечивая высвобождение новосинтезии рованной полипептидной цепи с рибосомы [3, 4]. Для терминации трансляции необходимо взаимоо * Эл. почта: zhouravleva@rambler.ru действие белков eRF1 и eRF3 [3, 5]. У дрожжей Saccharomyces сerevisiae фактор терминации трансс ляции eRF1 кодируется геном SUP45 [6, 7], а факк тор eRF3 – геном SUP35 [8–10]. Несмотря на то что гены SUP35 и SUP45 жизненно важны для клетки, показана возможность возникновения в них нонсенссмутаций [11–15]. Не будучи летальь ными, такие мутации приводят к нарушению терр минации трансляции. Впервые дрожжи с нонсенссмутацией в гене SUP45 получили на фоне доминантного супресс
    Full-text · Dataset · Jan 2010
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    ABSTRACT: The mechanisms leading to non-lethality of nonsense mutations in essential genes are poorly understood. Here, we focus on the factors influencing viability of yeast cells bearing premature termination codons (PTCs) in the essential gene SUP45 encoding translation termination factor eRF1. Using a dual reporter system we compared readthrough efficiency of the natural termination codon of SUP45 gene, spontaneous sup45-n (nonsense) mutations, nonsense mutations obtained by site-directed mutagenesis (76Q --> TAA, 242R --> TGA, 317L --> TAG). The nonsense mutations in SUP45 gene were shown to be situated in moderate contexts for readthrough efficiency. We showed that readthrough efficiency of some of the mutations present in the sup45 mutants is not correlated with full-length Sup45 protein amount. This resulted from modification of both sup45 mRNA stability which varies 3-fold among sup45-n mutants and degradation rate of mutant Sup45 proteins. Our results demonstrate that some substitutions in the place of PTCs decrease Sup45 stability. The viability of sup45 nonsense mutants is therefore supported by diverse mechanisms that control the final amount of functional Sup45 in cells.
    Full-text · Article · Apr 2009 · MGG Molecular & General Genetics
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    ABSTRACT: Proteins eRF1 and eRF3 are key components of translation termination in eukaryotes. The highly conserved translation termination factor eRF1 decodes stop codons, while another eukaryotic release factor (RF) eRF3 stimulates eRF1 in GTP-dependent manner. Functional C-terminal domain of eRF3 is necessary for cell viability and reveals high degree of similarity between all known eRF3 and elongation factor eEF1A. Unlike the C-terminal part, the N-terminal region of eRF3 proteins is not conserved and contains ‘prion forming domain’ (PFD). In mammals, eRF3 homologous proteins can be divided into two subfamilies based on the sequence of their N termini, GSPT1 (eRF3a) and GSPT2 (eRF3b). In our work we hypothesize that GSPT2 gene originated through retrotransposition of processed GSPT1 transcript after divergence between placental and marsupial mammals. Data obtained on the order Rodentia indicate that nucleotide sequence encoding N-terminal part of GSPT2 maybe used as a new marker for philogenetic analysis to distinguish between families.
    Full-text · Chapter · Dec 2007
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    G A Zhuravleva · S E Moskalenko · O A Murina · S G Inge-Vechtomov
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    ABSTRACT: Nonlethal nonsense mutations obtained earlier in the essential gene SUP45 encoding the translation termination eRFI factor in the yeast Saccharomyces cerevisiae were further characterized. Strains carrying these mutations retain the viability, since the full-length eRF1 protein is present in these strains, although in decreased amounts as compared to wild-type cells, together with a truncated eRF1. All nonsense mutations are likely to be located in a weak termination context, because a change in the stop codon UGAA (in the case of mutation sup45-107) to UAGA (sup45-107.2) led to the alteration of the local context from a weak to strong and to the lethality of the strain carrying sup45-107.2. All nonsense mutations studied are characterized by thermosensitivity expressed as cell mortality after cultivation at 37 degrees C. When grown under nonpermissive conditions (37 degrees C), cells of nonsense mutants sup45-104, sup45-105. and sup45-107 display a decrease in the amount of the truncated eRF1 protein without reduction in the amount of the full-length eRF1 protein. The results of this study suggest that the N-terminal eRF1 fragment is indispensable for cell viability of nonsense mutants due to the involvement in termination of translation.
    Full-text · Article · Nov 2007 · Genetika
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    ABSTRACT: Nonlethal nonsense mutations obtained earlier in the essential gene SUP45 encoding the translation termination factor eRF1 in the yeast Saccharomyces cerevisiae were further characterized. Strains carrying these mutations retain the viability, since the full-length eRF1 protein is present in these strains, although in decreased amounts as compared to wild-type cells, together with a trucated eRF1. All nonsense mutations are likely to be located in a weak termination context, because a change in the stop codon UGAA (in the case of mutation sup45-107) to UAGA (sup45-107.2) led to the alteration of the local context from a weak to strong and to the lethality of the strain carrying sup45-107.2. All nonsense mutations studied are characterized by thermosensitivity expressed as cell mortality after cultivation at 37°C. When grown under nonpermissive conditions (37°C), cells of nonsense mutants sup45-104, sup45-105, and sup45-107 display a decrease in the amount of the truncated eRF1 protein without reduction in the amount of the full-length eRF1 protein. The results of this study suggest that the N-terminal eRF1 fragment is indispensable for cell viability of nonsense mutants due to the involvement in termination of translation.
    Full-text · Article · Oct 2007 · Russian Journal of Genetics
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    ABSTRACT: The nonsense-mediated mRNA decay (NMD) pathway promotes the rapid degradation of mRNAs containing premature termination codons (PTCs). In yeast Saccharomyces cerevisiae, the activity of the NMD pathway depends on the recognition of the PTC by the translational machinery. Translation termination factors eRF1 (Sup45) and eRF3 (Sup35) participate not only in the last step of protein synthesis but also in mRNA degradation and translation initiation via interaction with such proteins as Pab1, Upf1, Upf2 and Upf3. In this work we have used previously isolated sup45 mutants of S. cerevisiae to characterize degradation of aberrant mRNA in conditions when translation termination is impaired. We have sequenced his7-1, lys9-A21 and trp1-289 alleles which are frequently used for analysis of nonsense suppression. We have established that sup45 nonsense and missense mutations lead to accumulation of his7-1 mRNA and CYH2 pre-mRNA. Remarkably, deletion of the UPF1 gene suppresses some sup45 phenotypes. In particular, sup45-n upf1Delta double mutants were less temperature sensitive, and more resistant to paromomycin than sup45 single mutants. In addition, deletion of either UPF2 or UPF3 restored viability of sup45-n double mutants. This is the first demonstration that sup45 mutations do not only change translation fidelity but also acts by causing a change in mRNA stability.
    Full-text · Article · Feb 2007 · BMC Molecular Biology
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    ABSTRACT: We have earlier characterized Saccharomyces cerevisiae strains with mutations of essential SUP45 and SUP35, which code for translation termination factors eRF1 and eRF3, respectively. In this work, the sup45 and sup35 nonsense mutants were compared with respect to the levels of eight tRNAs: tRNATyr, tRNAGln, tRNATrp, tRNALeu, tRNAArg (described as potential suppressor tRNAs), tRNAPro, tRNAHis, and tRNAGly. The mutants did not display a selective increase in tRNAs, capable of a noncanonical read-through at stop codons. Most of the mutations increased the level of all tRNAs under study. The mechanisms providing for the viability of the sup45 and sup35 nonsense mutants are discussed.
    Full-text · Article · Jun 2006 · Molecular Biology
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    ABSTRACT: Earlier we have characterized strains bearing mutations in essential genes SUP45 and SUP35 of yeast S. cerevisiae, encoding translation termination factors eRF1 and eRF3 respectively. In the present work nonsense-mutants on genes SUP45 and SUP35 have been compared by a level of eight tRNA: tRNATyr, tRNAGln, tRNATrp, tRNALeu and tRNAArg (previously described as potentially suppressor tRNA), and also tRNAPro, tRNAHis and tRNAGly. We have not revealed preferable increase in amount of natural suppressor tRNA. The majority of the investigated mutations leads to increase in a level of all investigated tRNA. The mechanisms providing viability of nonsense-mutants on essential genes SUP45 and SUP35 are discussed.
    Full-text · Article · Jan 2006 · Molekuliarnaia biologiia
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    ABSTRACT: Collection of missense mutations in the SUP45 gene of Saccharomyces cerevisiae encoding translation termination factor eRF1 has been obtained by different approaches. It has been shown that most of isolated mutations cause amino acid substitutions in the N-terminal part of eRF1 and do not decrease the eRF1 amount. Most of mutations studied do not abolish eRF1-eRF3 interaction. The role of the N-terminal part of eRF1 in stop codon recognition is discussed.
    Full-text · Article · Jun 2004 · Genetika
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    ABSTRACT: Background Termination of protein synthesis in eukaryotes involves at least two polypeptide release factors (eRFs) – eRF1 and eRF3. The highly conserved translation termination factor eRF1 in Saccharomyces cerevisiae is encoded by the essential gene SUP45. Results We have isolated five sup45-n (n from nonsense) mutations that cause nonsense substitutions in the following amino acid positions of eRF1: Y53 → UAA, E266 → UAA, L283 → UAA, L317 → UGA, E385 → UAA. We found that full-length eRF1 protein is present in all mutants, although in decreased amounts. All mutations are situated in a weak termination context. All these sup45-n mutations are viable in different genetic backgrounds, however their viability increases after growth in the absence of wild-type allele. Any of sup45-n mutations result in temperature sensitivity (37°C). Most of the sup45-n mutations lead to decreased spore viability and spores bearing sup45-n mutations are characterized by limited budding after germination leading to formation of microcolonies of 4–20 cells. Conclusions Nonsense mutations in the essential gene SUP45 can be isolated in the absence of tRNA nonsense suppressors.
    Full-text · Article · Feb 2003 · BMC Molecular Biology
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    ABSTRACT: The termination of protein synthesis in eukaryotes involves at least two polypeptide release factors (eRFs), eRF1 and eRF3. In mammals two genes encoding eRF3 structural homologues were identified and named GSPT1 and GSPT2. In the present study, we demonstrate that mouse mGSPT2 but not mGSPT1 could functionally substitute the essential yeast gene SUP35. However, we show that the complementation property of mGSPT1 protein is modified when NH2-tagged by GST. Since mGSPT1 and mGSPT2 differ mainly in their N-terminal regions, we developed a series of N-terminal deleted constructs and tested them for complementation in yeast. We found that at least amino acids spanning 84-120 of mGSPT1 prevent the complementation of sup35 mutation. The fact that chimeras between mGSPT1, mGSPT2 and yeast Sup35 complement the disruption of the SUP35 gene indicates that the N-terminal region of mGSPT1 is not sufficient by itself to prevent complementation. Complementation of the mutant with a double disruption of SUP35 and SUP45 genes is obtained when mGSPT2 and human eRF1 are co-expressed but not by co-expression of mGSPT1 and human eRF1. Our results strongly suggest that the two proteins (mGSPT1 and mGSPT2) are different. We hypothesize that the full length mGSPT1 does not have the properties expected for eRF3.
    Full-text · Article · Nov 2002 · Genes to Cells

Publication Stats

109 Citations
17.46 Total Impact Points

Institutions

  • 2015
    • Russian Academy of Sciences
      Moskva, Moscow, Russia
  • 2004-2015
    • Saint Petersburg State University
      • Department of Genetics and Biotechnology
      Sankt-Peterburg, St.-Petersburg, Russia
  • 2014
    • Vavilov Institute of General Genetics
      Moskva, Moscow, Russia
  • 2002-2007
    • Université de Rennes 1
      • Faculty of Medicine
      Roazhon, Brittany, France