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Integrantes

ALVAREZ, M. Elena

Investigadora Principal de CONICET / Profesora Asociada UNC
Teléfono: +54 351 5353855 x 3422
E-mail: malena@mail.fcq.unc.edu.ar

Tema de Investigación

Bases moleculares de la resistencia a patógenos microbianos en Arabidopsis

Plants activate complex responses upon pathogen perception, using receptors, protein kinases, hormones, transducers and transcription factors to stimulate the plant immune networks. Detection of pathogens at the cell surface or intracellular level induce pattern- or effector- triggered immunity (PTI or ETI), respectively. These pathways involve important cellular alterations, such as a rapid oxidative burst that derives from NADPH oxidase and requires mitochondrial and chloroplastic activities, and changes in gene expression that are sometimes associated to epigenetic modifications.

We are studying two traits of defenses in the Pseudomonas syringae pv. tomato (Pst)- Arabidopsis model.

a) Metabolism of L-proline (Pro): we found that Pro synthesis and catabolism are altered in infected tissues. Proline dehydrogenase (ProDH) is required to mount the oxidative burst that promotes cell death in ETI. This enzyme acts with P5C dehydrogenase (P5CDH) to convert Pro into Glu in mitochondria, having the toxic compound P5C as intermediate. During ROS accumulation, ProDH becomes uncoupled of P5CDH but does generate P5C accumulation. Apparently, P5C is converted back into Pro, through the Pro/P5C cycle suspected to regulate the cellular redox homeostasis. Our current investigations are focused on determine how ProDH increases ROS levels in infected tissues, and how other Pro metabolic changes affect the development of ETI and PTI.

b) Hypomethylation of the plant genome: tissues infected with Pst display a massive demethylation, loosing 5m-C from single copy genes and repetitive sequences. Infected cells also alter chromatin structure producing chromocenter decondensation. These responses occur in the absence of DNA replication suggesting active demethylation leads to chromatin relaxation. We are investigating the mechanisms underlying both genomic alterations, and assessing how DNA demethylation alters the defense responses.

Investigadores Integrantes del Grupo

Becarios Integrantes del Grupo

Publicaciones Seleccionadas

(Ver más publicaciones-CONICET)

Colaboraciones

  • Dr. László Szabados, Biological Research Centre, Hungarian Academy of Sciences, Institute of Plant Biology, Hungary.
  • Dr. Christine Foyer; Centre for Plant Sciences, University of Leeds, UK.
  • Dr. Loreto Holuigue; Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Chile.
  • Dr. Mohammad-Reza Hajirezaei; Institute of Plant Genetics and Crop Plant Research Gatersleben, Germany.

Breve Currículum Vitae

Educación y Formación

  • Bioquímica. Facultad Ciencias Químicas, Universidad Nacional de Córdoba. 1985.
  • Doctora en Ciencias Químicas. Universidad Nacional de Córdoba. 1992.
  • Posdoctorado. Plant Biology Laboratory, Salk Institute, San Diego, USA.1994-1997.

Investigación

Biología Molecular de Plantas. Fitopatología. Estudio de mecanismos de defensa contra patógenos biótrofos y necrótrofos en Arabidopsis.

Publicaciones (últimos 10 años)

  • Fabro G, Kóvácz I, Pavet V, Szabados L and Alvarez ME. “Proline accumulation and AtP5CS2 gene activation induced by plant-pathogen incom-patible interactions in Arabidopsis”. 2004. Molec. Plant-Microbe Interact. 17, 343-350.
  • Temporini ED, Alvarez ME, Mautino MR, Folco DH y Rosa AL. “The Neurospora crassa cfp promoter drives a carbon-source-dependent expression of transgenes in filamentous fungi”. 2004. J. Appl. Microbiol. 96:1256-1264.
  • Monti M, Smania A, Fabro G, Alvarez ME and Argaraña CE. “Engineering Pseudomonas fluorescens for biodegradation of 2,4-dinitrotoluene”. 2005. Appl. Environ. Microbiol. 71: 8864-8872.
  • Pavet V, Olmos E, Kiddle G, Mowla S, Kumar S, Antoniw J, Alvarez ME and Foyer CH. “Ascorbic acid deficiency activates cell death and disease resistance responses in Arabidopsis thaliana”. 2005. Plant Physiol. 139:1291-1303.
  • Pavet V, Quintero C, Cecchini NM, Rosa AL and Alvarez ME. “Arabidopsis displays centromeric DNA hypomethylation and cytological alterations of heterochromatin upon the attack by Pseudomonas syringae”. 2006. Molec. Plant-Microbe Interact. 19: 577-87.
  • Fabro G, Di Rienzo JA, Voigt C, Somerville S, Savchenko T, Dehesh K and Alvarez ME. “Genome-wide expression profiling Arabidopsis thaliana at the stage of Golovinomyces cichoracearum haustorium formation”. 2008. Plant Physiology 146: 1421-39.
  • Cecchini N, Monteoliva M, Blanco F, Holuigue L and Alvarez ME. “Features of basal and race-specific defences in photosynthetic Arabidopsis thaliana suspension cultured cells”. 2009. Mol. Plant Pathol. 10:305-310.
  • Blanco F, Salinas P, Cecchini N, Jordana X, Van Hummelen P, Alvarez ME, Holuigue L.”Early genomic responses to salicylic acid in Arabidopsis” 2009. Plant Mol. Biol. 70:79-102.
  • Alvarez ME, Nota F and Cambiagno D. “Epigenetic control of plant immunity”. 2010. Mol. Plant Pathol. 11, 563–576.
  • Cecchini NM, Monteoliva MI and Alvarez ME. “Proline dehydrogenase contributes to pathogen defence in Arabidopsis”. 2011. Plant Physiology 155, 1947-1959.
  • Cecchini NM, Monteoliva MI and Alvarez ME. “Proline dehydrogenase is a positive regulator of cell death in different kingdoms”. 2011 Plant Signal Behav 6(8).
  • Fabro G and Alvarez ME. “Loss of compatibility might explain resistance of the Arabidopsis thaliana accession Te-0 to Golovinomyces cichoracearum”. 2012. BMC Plant Biology 12(1):143.
  • Armijo G, Salinas P, Monteoliva MI, García C, Seguel A, Song W, van der Krol AR, Alvarez ME and Holuigue L. “A salicylic acid-induced lectin-like protein plays a positive role in the Effector-Triggered Immunity response of Arabidopsis thaliana to Pseudomonas syringae Avr-Rpm1”. 2013. Molec. Plant-Microbe Interact. 26:1395-406.
  • Monteoliva MI, Rizzi YS, Cecchini NM, Hajirezaei MR, Alvarez ME. “Context of action of Proline Dehydrogenase (ProDH) in the Hypersensitive Response of Arabidopsis”. 2014. BMC Plant Biology 14(1):21.

Tesis Doctorales dirigidas

  • Valeria Pavet. “Alteraciones moleculares y estructurales del genoma de Arabidopsis thaliana en el proceso de infección con Pseudomonas syringae”. 2005.
  • Georgina Fabro. “Caracterización molecular de señales de Arabidopsis que modulan la virulencia de patógenos fúngicos”. 2005.
  • Nicolás Cecchini. “Metabolismo de prolina en respuestas de defensa apatógenos en Arabidopsis”. 2010.
  • Mariela Monteoliva. “Contribución del catabolismo de prolina a la Respuesta Hipersensible”. 2012.
  • Florencia Nota. “Caracterización molecular y funcional del gen AtMBD4L, codificante de una nueva DNA glicosilasa de Arabidopsis thaliana”. 2014.
  • Damián Cambiagno. En curso.
  • Yanina Rizzi. En curso.

 

Research Topic

Molecular features of Arabidopsis disease resistance

Plants activate complex responses upon pathogen perception, using receptors, protein kinases, hormones, transducers and transcription factors to stimulate the plant immune networks. Detection of pathogens at the cell surface or intracellular level induce pattern- or effector- triggered immunity (PTI or ETI), respectively. These pathways involve important cellular alterations, such as a rapid oxidative burst that derives from NADPH oxidase and requires mitochondrial and chloroplastic activities, and changes in gene expression that are sometimes associated to epigenetic modifications.

We are studying two traits of defenses in the Pseudomonas syringae pv. tomato (Pst)- Arabidopsis model.

a) Metabolism of L-proline (Pro): we found that Pro synthesis and catabolism are altered in infected tissues. Proline dehydrogenase (ProDH) is required to mount the oxidative burst that promotes cell death in ETI. This enzyme acts with P5C dehydrogenase (P5CDH) to convert Pro into Glu in mitochondria, having the toxic compound P5C as intermediate. During ROS accumulation, ProDH becomes uncoupled of P5CDH but does generate P5C accumulation. Apparently, P5C is converted back into Pro, through the Pro/P5C cycle suspected to regulate the cellular redox homeostasis. Our current investigations are focused on determine how ProDH increases ROS levels in infected tissues, and how other Pro metabolic changes affect the development of ETI and PTI.

b) Hypomethylation of the plant genome: tissues infected with Pst display a massive demethylation, loosing 5m-C from single copy genes and repetitive sequences. Infected cells also alter chromatin structure producing chromocenter decondensation. These responses occur in the absence of DNA replication suggesting active demethylation leads to chromatin relaxation. We are investigating the mechanisms underlying both genomic alterations, and assessing how DNA demethylation alters the defense responses.

Researchers members of the group

Fellows

Selected Publications

(See more publications-CONICET)

Current Grants

  • ANPCyT PICT 2015-2018.
  • ANPCyT PICT 2012-2015.
  • SECyT- UNC.

Brief CV

Academic Formation

  • Biochemist. School of Chemical Sciences, National University of Córdoba. 1985.
  • PhD in Chemical Sciences. School of Chemical Sciences, National University of Córdoba. 1992.
  • Postdoctoral training. Plant Biology Laboratory, Salk Institute, San Diego, USA.1994-1997.

Research Background

  • See publications.

Teaching Background

  • Associate Professor. Dept. of Biological Chemistry, School of Chemical Sciencies, University of Cordoba, Argentina.
  • Undergraduate courses: Biotechnology, Plant Biotechnology.
  • PhD courses in the area of: Phytopathology, Plant Molecular Biology. Plant Biotechnology.

Directed Ph.D. Theses

  • 2005. Valeria Pavet.
  • 2005. Georgina Fabro.
  • 2010. Nicolás Cecchini.
  • 2012. Mariela Monteoliva.
  • 2014. Florencia Nota.