Deciphering regulators of reactive gliosis and barriers of neuronal regeneration in the mouse retina // Symmetrical H3K4 trimethylation is conveyed by the dimeric Set1 complex and demethylation

Date

Apr 20, 2018

Time

4:00 PM - 5:00 PM

Speaker

Mike O. Karl, Patrick Schäfer // Francis Stewart, Rupam Choudhury

Affiliation

Predoc; Postdoc

Language

en

Main Topic

Biologie

Other Topics

Biologie, Medizin

Description

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 glia (MG) in the retina readily regenerate lost neurons, but not in mammals. Limited MG-derived neurogenesis had been stimulated experimentally in rodents, 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 recapitulates different damage-induced processes to compensate neuronal cell loss: So far, there were no mouse models available, which facilitated studies of three potential modes of reactive gliosis - cell hypertrophy, hyperplasia and regeneration - in one assay. Our lab identified different means to stimulate glial proliferation, which is a major limitation for neuronal regeneration and studies of proliferative gliosis. A phenotypic screen revealed that combined application of two factors, each alone induced regeneration in fish, led to massive proliferative gliosis in mouse retina ex vivo. Gene expression studies of isolated MG suggested regulated and timed programs 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 maintain or break the inherent symmetry of the nucleosome however the mechanisms that deposit and/or propagate symmetry or asymmetry are poorly understood. The enzyme that methylates histone 3 lysine 4 is inherently dimeric and this relates to symmetrical methylation of nucleosomes on both histone 3 tails.

Links

• to announcement of the organizer

Last modified: Apr 20, 2018, 9:48:17 AM