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Research Group
Transcriptional and epigenetic mechanisms of neuronal plasticity
Unit Unit Molecular Neurobiology and Neuropathology »

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Principal Investigator Ph.D. Investigator Graduate students / Research Assistant Technician
Research Fields
Our research focuses on the molecular bases of neuronal plasticity, learning and memory, and other long-lasting modifications of the animal’s behavior. More precisely, we are investigating the role of specific transcription and epigenetic factors in these processes. We also aim to determine how the malfunction of epigenetic mechanisms leads to different pathological situations in the nervous system. To tackle these questions, we use a multidisciplinary approach that combines mouse genetics, genomics, behavioral and electrophysiological analyses and molecular and cellular biology techniques. From the methodological point of view, we are particularly interested in the application of genomic profiling techniques based on next generation sequencing (NGS) and epigenetic editing approaches in the nervous system.

We currently work on two main lines of research:

• Interplay of transcriptional and epigenetic mechanisms in activity-dependent transcription: Alterations in the patterns of neuronal gene expression are thought to underlie the long-lasting changes in the strength of synaptic connections responsible for the encoding of memories in the nervous system. We are investigating the participation of specific activity-regulated transcription factors, such as CREB and SRF, and epigenetic enzymes, such as CBP and p300, in this process. We are also interested in determining the role of the covalent modification of chromatin in neuroplasticity.

• Contribution of epigenetic mechanisms to intellectual disability (ID) disorders: We investigate the contribution of epigenetic mechanisms, such as histone acetylation and methylation, to the pathoetiology of different neurological conditions associated with cognitive impairments and autism, including Rubinstein-Taybi syndrome and X-linked intellectual disability. Towards this end, we generate and characterize mouse models for these conditions, explore the molecular causes of the disease and tackle new therapies.

Representative Publications

Fernandez-Albert J , Lipinski M, Lopez-Cascales MT, Rowley MJ, Martin-Gonzalez AM, del Blanco B, Corces VG, Barco A. " Immediate and deferred epigenomic signatures of in vivo neuronal activation in mouse hippocampus. " Nat Neurosci . , in press - ( 2019 )

Hutson TH , Kathe, Palmisano, Bartholdi, Hervera, De Virgiliis, McLachlan, Zhou, Kong, Barraud, Danzi, Medrano-Fernandez A, Lopez-Atalaya JP, Boutillier, Sinha, Singh, Chaturbedy, Moon, Kundu, Bixby, Lemmon, Barco A, Courtine G and Di Giovanni S. " Environmental enrichment induces axon regeneration and recovery after peripheral and spinal injuries via activity mediated CBP-dependent histone acetylation: a druggable pathway. " Sci Traslat Med . 11(487) , - ( 2019 )

Lipinski M , del Blanco B and Barco A. " CBP/p300 in brain development and plasticity: Disentangling the KAT’s cradle. " Current Opinion in Neurobiology . 59 , 1 - 8 ( 2019 )

Scandaglia M , and Barco A. " The Contribution of Spurious Transcription to Intellectual Disability Disorders. " J Med Gen . pii: jmedgenet , 2018 - 105668 ( 2019 )

Del Blanco B , Guiretti D, Tomasoni R, Lopez-Cascales MT, Muñoz-Viana R, Lipinski M, Scandaglia M, Coca Y, Olivares R, Valor LM, Herrera E, Barco A . " CBP and SRF co-regulate dendritic growth and synaptic maturation. " Cell Death & Diff . doi , 10.1038/s41418-019-0285 - x ( 2019 )
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Consejo Superior de Investigaciones Científicas
Universidad Miguel Hernández

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