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Dissection of Arp2/3 complex function and regulation in actin-based protrusion

Termin: 
Mo, 14.06.2021 - 17:15 Uhr
Treffpunkt: 
Online-Lecture via Zoom (Zugangs-Link erhältlich bei: vonderemde@uni-bonn.de
Veranstaltungsart: 
Vortrag
Veranstaltungsreihe: 
Biologisches/Evolutionsbiologisches Kolloquium
Zielgruppe: 
Erwachsene
Vortragende / Vortragender: 
Prof. Dr. Klemens Rottner Vortrag am 16.11.20 Division of Molecular Cell Biology Zoological Institute Technische Universität Braunschweig

In higher eukaryotes, the formation of branched actin filament networks generated by Arp2/3 complex is crucial to a plethora of cellular processes, like cell edge protrusion, cell-cell adhesion, phagocytosis or membrane trafficking. We are dissecting the molecular regulation of these and related processes such as host-pathogen interaction using CRISPR/Cas9-mediated genome editing. We are characterizing derived, mutant cell lines with respect to essential, functional parameters and including various, advanced imaging approaches.

In this talk, I will focus on the molecular regulation of lamellipodium protrusion, and provide examples for how CRISPR/Cas9-edited cell lines can be employed to study the biochemistry, individual mutations or the gene dose of selected, Arp2/3 complex-dependent actin assembly complexes.

In higher eukaryotes, the formation of branched actin filament networks generated by Arp2/3 complex is crucial to a plethora of cellular processes, like cell edge protrusion, cell-cell adhesion, phagocytosis or membrane trafficking. We are dissecting the molecular regulation of these and related processes such as host-pathogen interaction using CRISPR/Cas9-mediated genome editing. We are characterizing derived, mutant cell lines with respect to essential, functional parameters and including various, advanced imaging approaches.

In this talk, I will focus on the molecular regulation of lamellipodium protrusion, and provide examples for how CRISPR/Cas9-edited cell lines can be employed to study the biochemistry, individual mutations or the gene dose of selected, Arp2/3 complex-dependent actin assembly complexes.

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