Mariona Nadal

    Research Group: 
    Cell Signaling
    Unit: 
    MECHANISMS OF DISEASE
    Position: 
    Postdoctoral Fellow
    Office: 
    EM01B1314
    Telephone: 
    +34 93 40 39976
    Email: 
    mariona.nadal@irbbarcelona.org

     

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    Selected group publications

    Rapid reversible changes in compartments and local chromatin organization revealed by hyperosmotic shock
    Amat R, Böttcher R, Le Dily F, Vidal E, Quilez J, Cuartero Y, Beato M, de Nadal E and Posas F.
    Genome Res, 29 (1), 18-28 (2019)
    Multiple signaling kinases target Mrc1 to prevent genomic instability triggered by transcription-replication conflicts.
    Duch Aº, Canal Bº, Barroso SI, García-Rubio M, Seisenbacher G, Aguilera A, de Nadal E*, Posas F*.
    Nat Commun., 9(1):379. (25), (2018)
    Interaction Dynamics Determine Signaling and Output Pathway Responses.
    Stojanovski K, Ferrar T, Benisty H, Uschner F, Delgado J, Jimenez J, Solé C, de Nadal E, Klipp E, Posas F, Serrano L, Kiel C
    Cell Rep, (19), -136-49 (2017)
    Regulation of transcription elongation in response to osmostress.
    Silva Aº, Cavero Sº, Begley V, Solé C, Böttcher R, Chávez S, Posas F*, de Nadal E*.
    PLoS Genet, (13), (2017)
    Implementation of Complex Biological Logic Circuits Using Spatially Distributed Multicellular Consortia.
    Macia Jº, Manzoni Rº, Conde Nº, Urrios A, de Nadal E, Solé R*, Posas F*.
    PLoS Comput Biol, (12), (2016)
    Evolution of protein phosphorylation across 18 fungal species.
    Studer RA, Rodriguez-Mias RA, Haas KM, Hsu JI, Viéitez C, Solé C, Swaney DL, Stanford LB, Liachko I, Böttcher R, Dunham MJ, de Nadal E, Posas F, Beltrao P and Villén J.
    Science, (354), -229-32 (2016)
    The N-Terminal Phosphorylation of RB by p38 Bypasses Its Inactivation by CDKs and Prevents Proliferation in Cancer Cells.
    Gubern A, Joaquin M, Marquès M, Maseres P, Garcia-Garcia J, Amat R, González-Nuñez D, Oliva B, Real FX, de Nadal E*, Posas F*.
    Mol. Cell. , (64), -25-36 (2016)
    H3K4 monomethylation dictates nucleosome dynamics and chromatin remodeling at stress-responsive genes.
    Nadal-Ribelles M, Mas G, Millán-Zambrano G, Solé C, Ammerer G, Chávez S, Posas F*, de Nadal E*.
    Nucleic Acids Res, (43), -4937-49 (2015)
    Control of Cdc28 CDK1 by a stress-induced lncRNA.
    Nadal-Ribelles Mº, Solé Cº, Xu Z, Steinmetz LM, de Nadal E*, Posas F*.
    Mol Cell., (53), -546-61 (2014)
    Coordinated control of replication and transcription by a SAPK protects genomic integrity.
    Duch A, Felipe-Abrio I, Barroso S, Yaakov G, García-Rubio M, Aguilera A, de Nadal E and Posas F.
    Nature, (493), -116-9 (2013)
    Distributed biological computation with multicellular engineered networks.
    Regot Sº, Macia Jº, Conde N, Furukawa K, Kjellén T, Peeters T, Hohmann S, de Nadal, Posas F and Solé R.
    Nature, (469), -207-11 (2011)
    Transient activation of the HOG MAPK pathway regulates bimodal gene expression.
    Pelet S, Rudolf F, Nadal-Ribelles, de Nadal, Posas F and Peter M
    Science, (332), -732-5 (2011)
    Controlling gene expression in response to stress.
    de Nadal E, Ammerer G, and Posas F.
    Nat Rev Genet., (469), -207-11 (2011)
    The stress-activated Hog1 kinase is a selective transcriptional elongation factor for genes responding to osmotic stress.
    Proft M, Mas G, de Nadal E, Vendrell A, Noriega N, Struhl K and Posas F.
    Mol Cell., (23), -241-50 (2006)
    The MAPK Hog1 recruits Rpd3 histone deacetylase to activate osmoresponsive genes.
    de Nadal E, Zapater M, Alepuz PM, Sumoy L, Mas G and Posas F.
    Nature, (427), -370-4 (2004)
    Hog1 mediates cell-cycle arrest in G1 phase by the dual targeting of Sic1.
    Escoté X, Zapater M, Clotet J, Posas F.
    Nat Cell Biol., (6), -997-1002 (2004)
    Full publication list