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Research Group
Cellular plasticity and neuropathology
Unit Unit Molecular Neurobiology »

Principal Investigator Graduate students / Research Assistant
Research Fields
Cell identity is a reflection of a cell type-specific transcription factor network that governs complex patterns of gene expression. In eukaryotic cells, these transcriptional profiles are maintained by alterations in chromatin structure that include covalent modifications of the DNA and histone proteins, and nucleosome positioning. More recent evidence suggests that the three-dimensional genome architecture may also be critical for achieving proper spatio-temporal patterns of gene expression during cell differentiation and contributes to the maintenance of cellular memory.

Cells’ ability to change their behaviour in response to internal or external environmental cues is a key feature of development and normal function of cells within most multicellular organisms. One of the most striking naturally occurring transitions in cellular phenotype is observed in the mammalian brain. In the brain, glial cells play fundamental roles in neuronal physiology including regulation of neurotransmission and synapse formation and maintenance. In addition, neuroglia constitutes the intrinsic brain defence system. Stroke, trauma, infection or chronic neurodegeneration trigger a pronounced glial response. This dual role is associated to a profound phenotypic switch from “quiescent” to “activated”. Critically, microglia and astrocytes must orchestrate complex genetic programs in response to a variety of stimuli that dictate the induction of alternations in their phenotype to serve the appropriate functions. However, the mechanisms underlying these phenotypic transitions and their maintenance remain largely unknown.

We combine mouse genetics, genomics and cell biological approaches to explore the boundaries of epigenome plasticity in differentiated cells. We use neuroglia as models to study how gene regulatory interactions control cellular state and identity. Our research may provide direct mechanistic links to neuroinflammatory processes in brain aging and neurodegenerative diseases.

Representative Publications

Lopez-Atalaya JP , Barco A " Can changes in histone acetylation contribute to memory formation? " Trends Genet . 30(12) , 529 - 539 ( 2014 )

Lopez-Atalaya JP , Barco A. " Epigenetic Factors in Intellectual Disability:The Rubinstein–Taybi Syndrome as a Paradigm of Neurodevelopmental Disorder with Epigenetic Origin. " Prog Mol Biol Transl Sci . 128 , 139 - 176 ( 2014 )

Lopez-Atalaya JP , Ito S, Valor LM, Benito E and Barco A " Genomic targets, and histone acetylation and gene expression profiling of neural HDAC inhibition. " Nucleic Acids Res . 41(17) , 8072 - 8084 ( 2013 )

Lopez-Atalaya JP , Gervasini C, Mottadelli F, Spena S, Piccione M, Scarano G, Selicorni A, Barco A, Larizza L " Histone acetylation deficits in lymphoblastoid cell lines from patients with Rubinstein-Taybi syndrome. " J Med Genet . 49(1) , 66 - 74 ( 2012 )

Lopez-Atalaya JP , Ciccarelli A, Viosca J, Valor LM, Jimenez-Minchan M, Canals S, Giustteto M and Barco A " CBP is required for environmental enrichment-induced neurogenesis and cognitive enhancement " EMBO Journal . 30(20) , 4287 - 4298 ( 2011 )
Consejo Superior de Investigaciones Científicas
Universidad Miguel Hernández

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