Ökotoxikologie

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Dr. Doris Pester

Wissenschaftliche Mitarbeiterin (PostDoc)

Tel.: 07531-884664

doris.pester[at]uni-konstanz.de

Raum M1004

Publikationen

Journalartikel

  1. Pester D, Milčevičová R, Schaffer J, Wilhelm E, Blümel S. 2012. Erwinia amylovora expresses fast and simultaneously hrp/dsp virulence genes during flower infection on apple trees. PLoS One 7(3):e32583. doi: 10.1371/journal.pone.0032583.

  2. Schirawski J, Mannhaupt G, Münch K, Brefort T, Schipper K, Doehlemann G, Di Stasio M, Rössel N, Mendoza-Mendoza A, Pester D, Müller O, Winterberg B, Meyer E, Ghareeb H, Wollenberg T, Münsterkötter M, Wong P, Walter M, Stukenbrock E, Güldener U, Kahma. 2010. Pathogenicity determinants in smut fungi revealed by genome comparison.Science 330(6010):1546-8.

  3. Kämper J, Kahmann R, Bölker M, Ma LJ, Brefort T, Saville BJ, Banuett F, Kronstad JW, Gold SE, Müller O, Perlin MH, Wösten HA, de Vries R, Ruiz-Herrera J, Reynaga-Peña CG, Snetselaar K, McCann M, Pérez-Martín J, Feldbrügge M, Basse CW, Steinberg G, Ibeas JI, Holloman W, Guzman P, Farman M, Stajich JE, Sentandreu R, González-Prieto JM, Kennell JC, Molina L, Schirawski J, Mendoza-Mendoza A, Greilinger D, Münch K, Rössel N, Scherer M, Vranes M, Ladendorf O, Vincon V, Fuchs U, Sandrock B, Meng S, Ho EC, Cahill MJ, Boyce KJ, Klose J, Klosterman SJ, Deelstra HJ, Ortiz-Castellanos L, Li W, Sanchez-Alonso P, Schreier PH, Häuser-Hahn I, Vaupel M, Koopmann E, Friedrich G, Voss H, Schlüter T, Margolis J, Platt D, Swimmer C, Gnirke A, Chen F, Vysotskaia V, Mannhaupt G, Güldener U, Münsterkötter M, Haase D, Oesterheld M, Mewes HW, Mauceli EW, DeCaprio D, Wade CM, Butler J, Young S, Jaffe DB, Calvo S, Nusbaum C, Galagan J, Birren BW. 2006. Insights from the genome of the biotrophic fungal plant pathogen Ustilago maydis. Nature 444(7115):97-101.

  4. Zauner S, Greilinger D, Laatsch T, Kowallik KV, Maier UG. 2004. Substitutional editing of transcripts from genes of cyanobacterial origin in the dinoflagellate Ceratium horridum. FEBS Lett. 577(3):535-8.

Populärwissenschaftliche Artikel

  1. Pester, D. 2011. Gene expression in the quarantine pest Erwinia amylovora during apple flower-infection. Acta Hort. (ISHS) 896.

  2. Persen, U und Pester, D. 2010. Gemeinsam gegen Feurbrand: Bericht vom 12. Interantionalen Feuerbrand.-Workshop in Polen. Besseres Obst, Heft 12.

  3. Pester, D. 2010. Langfristige Feuerbrandbekämpfung: Erforschung effektiver umweltverträglicher Strategien. Besseres Obst, Heft 2.

Curriculum vitae

  • 06/2013 - heute: Wissenschaftliche Mitarbeiterin (Post-Doc), Universität Konstanz, AG Umwelt- und Ökotoxikologie
  • 12/2011-04/2013: Elternzeit
  • 12/2007-12/2011: Institut für Pflanzengesundheit, Österreichische Agentur für Gesundheit und Ernährungssicherheit, Wien, Österreich
  • 06/2004-09/2007: Promotion, Max-Planck-Institut für terrestrische Mikrobiologie, Institut für Organismische Interaktionen/ Genetik (Charaktersierung von frphen Komponenten der Signaltransduktion in Ustilago maydis)
  • 10/2003-05/2004: wissenschaftliche Mitarbeiterin, Universität Marburg
  • 01/2003-09/2003: wissenschaftliche Mitarbeiterin, Universität Konstanz
  • 12/2002: Diplom, Biologie, Limnologisches Institut, Universität Konstanz (Charakterisierung bioaktiver Fischerelline in benthischen Cyanobakterien der Gattung Fischerella)

 

Fortbildung

Konferenzen

Forschung

Projekt: Early deleterious effects of L-BMAA in human neuronal cells

L-methylamino-β-alanine (L-BMAA), a non-protein amino acid naturally produced by cyanobacteria, acts as a neurotoxin in eukaryotic nervous systems. In humans chronic exposure to L-BMAA is suspected to cause neurodegenerative diseases similar to Alzheimer. The increased incidence of Amyotrophic Lateral Sclerosis/Parkinsonism-Dementia Complex (ALS/ PDC) among people in certain geographical regions points toward exposure via drinking water and/or uptake via terrestrial or maritime food containing L-BMAA [1; 2]. The molecular mechanism underlying L-BMAA neurotoxicity is currently not well understood. Two main hypotheses discuss how L-BMAA acts inside the cell. One hypothesis suggests an excessive overstimulation (excitotoxicity) damaging neuronal cells by L-BMAA acting as neurotransmitter analog [3]. Another hypothesis proposes an incorporation or binding of BMAA into/to proteins [2; 4; 5] disturbing protein homeostasis [6]. In the former a higher L-BMAA concentration is necessary to induce neurotoxicity, whereas in the latter low-dose long-term exposure hypothetically could be causal for the development of the disease. Our goal is to further clarify the low-dose effects of L-BMAA on protein homeostasis in human neuronal cells. Testing putative incorporation of the alanine analog L-BMAA into proteins is a first fundamental step in understanding how protein turnover might be affected. Other chemical properties of L-BMAA, such as dimer formation and metal chelating potency, suggest that enzyme activity might be affected as well [2]. Thus, activity tests with key enzymes for neuronal activity should provide for the mechanistic link between L-BMAA and measured imbalances in the cell, e.g., protein ubiquitination, 20S proteasomal and caspase 12 activity, expression of ER stress markers [6]. Together, these investigations should allow for a better understanding of the early deleterious effects of L-BMAA in human neuronal cells which might cumulate in a later onset of neurodegenerative diseases.

References

[1] Jonasson, S., Eriksson, J., Berntzon, L., Spá, Z. (2010). Transfer of cyanobacterial neurotoxins within a temperate aquatic ecosystem suggests pathways for human exposure. PNAS 107, 9252-9257.

[2] Murch, S. J., Cox, P. A., Banack, S. A. (2004). A mechanism for slow release of biomagnified cyanobacterial neurotoxins and neurodegenerative disease in Guam. PNAS 101, 12228-12231.

[3] Chiu, A. S., Gehringer, M. M., Welch, J. H., Neilan, B. A. (2011). Does α-amino-β-methylaminopropionic acid (BMAA) play a role in neurodegeneration? Int. J. Environ. Res. Public Health 8, 3728-3746.

[4] Banack, S. A., Caller, T. A., and Stommel, E. W. (2010). The cyanobacterial derived toxin beta-N-methylamino-L-alanine and amyotrophic lateral sclerosis. Toxins (Basel) 2, 2837-2850.

[5] Field, N. C., Caller, T. A. and Stommel, E. W. (2011). An explanation for the changes in collagen in sporadic amyotrophic lateral sclerosis. Med. Hypotheses 77, 565-567.

[6] Okle, O., Stemmer, K., Deschl, U., Dietrich, D. R. (2013). L-BMAA induced ER stress and enhanced Caspase 12 cleavage in human neuroblastoma SH-SY5Y cells at low nonexcitotoxic concentrations. Toxicological Sciences 131(1), 217-224.

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