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Volga Neuroscience School 2016 Astroglial control of rhythm genesis in the brain
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hp1 and Endogenous Retroviruses in the Brain
Andrew Newman*
Charité Universitätsmedizin Berlin, Germany. * Presenting e-mail: [email protected]
Heterochromatin Protein 1 (HP1), a structural protein found in the nucleus, is highly conserved across plants and animals and has a mechanism of action that has remained enigmatic since it was first observed 20 years ago. Known for binding to the repressive histone mark H3K9me3 or H3K9me2 (tri- or di-methylated Lysine 9 of Histone 3 respectively), HP1 has naturally emerged to be an essential component in a host of epigenetic systems essential for survival. Briefly, HP1 proteins have been implicated in retrotransposon silencing and heterochromatin spreading, proviral HIV silencing, chromosome stability and mitosis, cell cycle exit, spermatogenesis, DNA methylation, transcription, and embryonic stem cell maintenance. However, whatever the essential interaction is between HP1, H3K9 and respective Lysine methyltransferases remains elusive due to conflicting evidence. Concomitant to this, a growing body of evidence now implicates HP1 proteins as important components of various transcriptionary regulatory systems important in tissue specification during development. Differential interactions have been observed between distinct HP1 proteins and specific members of Nucleosome remodelling histone deacetylase (NuRD) complexes, BRG1 associated factor (BAF) (also called SWI/SNF) complexes, Polycomb (PcG) complexes, as well interacting with Kruppel-associated box (KRAB) containing zinc finger family, including the neuronal specific REST/ CoREST complex.
Presented here are two novel findings: 1) Class II endogenous retrovirus (ERVs) are de-repressed in HP1ß and HP1y double knockouts, and 2) this is due to two independent mechanisms that are synergistic. Here we report the mechanisms responsible for Class II ERV repression, the effects of de-repression on behaviour and aging, and test occurrences of retrotransposition due to neuronal stimulation and DNA damage.
Greating of Adenoassotiated Viral Vector for Expressing of Neurotrophic Factor BDNF in Neuronal Cells
E.A. Epifanova *, E.V. Mitroshina, A.A. Babaev
Lobachevsky State University of Nizhny Novgorod, Nizhny Novgorod, Russia. * Presenting e-mail: [email protected]
Brain-derived neurotrophic factor (BDNF) is important signaling molecule which takes part in regulation of neurogenesis, growth and survival of neurons in central nervous system. BDNF participates not only in neuronal differentiation and in formation of synaptic contacts during neurogenesis but also can correct the metabolism of mature neurons. According data from recent studies BDNF has strong neuroprotective properties, depresses cell apoptosis, stimulates growth and prevent neuronal death. In rehabilitation period after injuries, ischemic and neurodegenerative diseases it is important to stimulate endogenic reparation of functional neuronal nets. One of the approaches may be therapeutically rising of the BDNF level.
Recombinant adeno-associated virus is one of the most promising delivery vectors for gene therapy due to its nonpathogenic property, nonimmunogenecity to host and broad cell and tissue tropisms.
OM&P
86 Opera Med Physiol 2016 Vol. 2 (S1)
