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UID:DSC-14354
DTSTART;TZID=Europe/Berlin:20180420T160000
SEQUENCE:1524210497
TRANSP:OPAQUE
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URL:https://dresden-science-calendar.de/calendar/en/detail/14354
LOCATION:TUD CRTD\, Fetscherstraße 10501307 Dresden
SUMMARY:Karl: Deciphering regulators of reactive gliosis and barriers of ne
 uronal regeneration in the mouse retina // Symmetrical H3K4 trimethylation
  is conveyed by the dimeric Set1 complex and demethylation
CLASS:PUBLIC
DESCRIPTION:Speaker: Mike O. Karl\, Patrick Schäfer // Francis Stewart\, R
 upam Choudhury\nInstitute of Speaker: Predoc\; Postdoc\nTopics:\nBiologie\
 , Medizin\n Location:\n  Name: TUD CRTD (CRTD\, auditorium left)\n  Street
 : Fetscherstraße 105\n  City: 01307 Dresden\n  Phone: +49 (0)351 458 8205
 2\n  Fax: +49 (0)351 458 82059 \nDescription: Abstract 1st talk:  Reactive
  gliosis is an umbrella term for various incompletely understood glia cell
  functions in neurodegenerative diseases and upon injury\, which may have 
 beneficial and detrimental consequences. Indeed\, in fish\, the Müller gl
 ia (MG) in the retina readily regenerate lost neurons\, but not in mammals
 . Limited MG-derived neurogenesis had been stimulated experimentally in ro
 dents\, which is a potential future therapeutic approach. Further\, there 
 is a pressing unmet clinical need to prevent glial proliferative disorders
  and scar formation. Using a powerful mouse retina ex vivo assay we sought
  to stimulate and determine specific glial functions. Our assay recapitula
 tes different damage-induced processes to compensate neuronal cell loss: S
 o far\, there were no mouse models available\, which facilitated studies o
 f three potential modes of reactive gliosis - cell hypertrophy\, hyperplas
 ia and regeneration - in one assay. Our lab identified different means to 
 stimulate glial proliferation\, which is a major limitation for neuronal r
 egeneration and studies of proliferative gliosis. A phenotypic screen reve
 aled that combined application of two factors\, each alone induced regener
 ation in fish\, led to massive proliferative gliosis in mouse retina ex vi
 vo. Gene expression studies of isolated MG suggested regulated and timed p
 rograms of reactive gliosis. Comparative RNASeq studies of MG from defined
  experimental paradigms with embryonic retinal progenitor cells are aimed 
 at discovering molecular programs regulating distinct glial functions and 
 neuronal regeneration.  Abstract 2nd talk:  Epigenetic modifications may m
 aintain or break the inherent symmetry of the nucleosome however the mecha
 nisms that deposit and/or propagate symmetry or asymmetry are poorly under
 stood. The enzyme that methylates histone 3 lysine 4 is inherently dimeric
  and this relates to symmetrical methylation of nucleosomes on both histon
 e 3 tails.
DTSTAMP:20261020T174821Z
CREATED:20180419T075833Z
LAST-MODIFIED:20180420T074817Z
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