BiMe

What it takes to be a MAP & Overcoming limitations of retinal regeneration in mammals: Deciphering key players in glial reactivation and proliferation

Datum
01.02.2019 
Zeit
16:00 Uhr - 17:00 Uhr 
Sprecher
Hauke Drechsler, Robert Münch 
Institut
Postdoc; Predoc 
Sprache
en 
Hauptthema
Biologie: Allgemein
Subthemen
Medizin: Regeneration
Ansprechpartner
Prof. Stefan Diez (B CUBE) & Dr. Mike O'Karl (CRTD / DZNE) 
Zusammenfassung

Hauke Drechsler (Postdoc): What it takes to be a MAP
Abstract
The eukaryotic microtubule cytoskeleton is key to vital cellular processes like intracellular transport, cell migration or mitosis. During these, altogether, highly dynamic events, the shape and functionality of the microtubule cytoskeleton have to be constantly adjusted. In addition to molecular motors, this task is carried out by a multitude of microtubule associated proteins (MAPs). MAPs are a structurally and functionally diverse class of proteins that structurally support microtubule structures, regulate the intrinsic dynamicity of microtubules or govern microtubule-dependent transport. Surprisingly, the capacity to bind microtubules is not associated with a particular protein structure or sequence, raising the question what (minimal) properties define a microtubule-binding domain or a MAP. To answer this question we have chosen a bottom-up approach to reconstitute basic MAP-like behaviour using simple synthetic peptides. We identified a multivalent, positively charged peptide that shows complex MAP-like behaviour on dynamic microtubules as it is capable to bundle microtubules, modify their dynamics and mediate force coupling to depolymerising microtubules. Based on this artificial MAP, we aim to develop an easy manipulatable modular system that yields tailored MAPs with a defined functional spectrum for basic research on MAPs and biotechnical applications.
Robert Münch (Predoc): Overcoming limitations of retinal regeneration in mammals: Deciphering key players in glial reactivation and proliferation
Abstract
Vision mediates the highest percentage of our perception but is on the other hand affected in over the half of all neurological impaired patients. Some types of lower vertebrates can regenerate neuronal cell loss in the retina: The Müller glia (MG) reactivate upon retinal damage, reprogram into a stem-cell like state and produce cell progeny that can dedifferentiate into new neurons to restore vision loss. Unfortunately, this process does not naturally occur in mammals, but a limited regeneration response can be experimentally stimulated in rodents. Thus, the underlying mechanisms and limitations are not yet solved. In this talk, we will discuss recent findings in our well established mouse retina regeneration assay: We could show that activation of EGFR and its downstream targets is necessary for MG proliferation. Further, correlative studies of neuronal cell death and MG proliferation revealed a retinal damage dependence and suggested that additional factors might be required to induce MG proliferation. Thus, we discovered a new marker to monitor MG reactivation and new ways to more effectively stimulate MG proliferation. Finally, we started to transfer some of our findings in the ex vivo assay to mice in vivo, which revealed new avenues and roadblocks for retina regeneration research.

 

Letzte Aktualisierung: 01.02.2019 00:09.

Vortragsort 

DFG Center for Regenerative Therapies Dresden (CRTD, auditorium left) 
Fetscherstraße 105
01307 Dresden
Telefon
+49 (0)351 458 82064 
Fax
+49 (0)351 458 82059  
E-Mail
DFG Center for Regenerative Therapies Dresden 
Homepage
http://www.crt-dresden.de 

Veranstalter 

DFG Center for Regenerative Therapies Dresden (CRTD)
Fetscherstraße 105
01307 Dresden
Telefon
+49 (0)351 458 82064 
Fax
+49 (0)351 458 82059 
E-Mail
DFG Center for Regenerative Therapies Dresden (CRTD) 
Homepage
http://www.crt-dresden.de 
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