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

CMCB PhD/Postdoc Seminar

Date:01.02.2019, 16:00 - 17:00
Speaker: Hauke Drechsler (Postdoc), Robert Münch (Predoc)
Location: CRTD, auditorium left
Host: Prof. Stefan Diez (B CUBE) & Dr. Mike O'Karl (CRTD / DZNE)

Hauke Drechsler (Postdoc): "What it takes to be a MAP"


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"


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.

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