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

Laboratory Web Unit

Principal Investigator Ph.D. Investigator Graduate students / Research Assistant Master Students 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

Scandaglia M , Lopez-Atalaya JP, Medrano-Fernandez A,Lopez-Cascales MT, del Blanco B, Lipinski M, Benito E, Olivares R, Iwase S, Shi Y, Barco A " Loss of Kdm5c causes spurious transcription and prevents the fine-tuning of activity-regulated enhancers in neurons. " Cell Reports . 21 , 47 - 59 ( 2017 )

Fiorenza A , Lopez-Atalaya JP, Rovira V, Scandaglia M, Geijo-Barrientos E, Barco A " Blocking miRNA biogenesis in adult forebrain neurons enhances seizure susceptibility, fear memory and food intake by increasing neuronal responsiveness. " Cereb Cortex . 26(4) , 1619 - 33 ( 2016 )

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

Ito S , Magalska A, Alcaraz-Iborra M, Lopez-Atalaya JP, Rovira V, Contreras-Moreira B, Lipinski M, Olivares R, Martinez-Hernandez J, Ruszczycki B, Lujan R, Geijo-Barrientos E, Wilczynski G, and Barco A " Loss of neuronal 3D chromatin organization causes transcriptional and behavioral deficits related to serotonergic dysfunction " Nat Commun . 5 , - 4450 ( 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 )
Consejo Superior de Investigaciones Científicas
Universidad Miguel Hernández

Campus de San Juan | Sant Joan d’Alacant
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