KINE 1000 Lecture Notes - Lecture 12: Protein Kinase, Formins, Cdc42
4 Jun 2018
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Laellipodia Cotai all Machiey
euied fo cell Motility
• Lamellipodia are in epithelial cells
• Unidirectional motion by lamellipodia requires cooperation & mechanical integration of
several factors.
• Filament nucleation is localizated at leading edge, w/new actin filament growth
occurring in front. Most filament depolymerization occurs at site located at back
• As filament ages & ATP hydrolysis proceeds, cofilin disassembles older filament. Coflin
binds to actin filaments containing ADP. Delay in ATP hydrolysis by filamentaneous actin
provides basis for mechanisms that maintains an efficient unidirectional threadmilling
process in lamellipoium
• Figure: Model of Protrusion. Nucleation is mediated by Arp 2/3 Complex at Front.
Filaments elongate pusing membrane fwd. At steady rate, actin filaments plus end
become capped. After newly polymerized subunits hydrolyze ATP, they become
susceptible to depolymerization by coflin. Results in net filament assembly at front &
dissasebly at rear. At the rear of lamellipodium, actin works w/ myosin to migrate by
contraction
• ARP proteins activated at front to nucleate; inactive ARP & active cofilin at rear allows
disassembly. Pushs cell fwd
Myosin Contraction & Cell Adhesion allows Cell to pull themselves forward
• Contraction & de-adhesion at rear of cell
Cell Polarization is Controlled by Members of Rho Protein Families
• Cell Migration requires long-distance communication & coordination b/t one end of cell
& other. Front different from back
• Protrusion at front, retraction at rear. Cytoskeleton is responsible for coordinatin cell
shape, organization & mechanical properties
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Document Summary
Most filament depolymerization occurs at site located at back: as filament ages & atp hydrolysis proceeds, cofilin disassembles older filament. Delay in atp hydrolysis by filamentaneous actin provides basis for mechanisms that maintains an efficient unidirectional threadmilling process in lamellipoium: figure: model of protrusion. Nucleation is mediated by arp 2/3 complex at front. At steady rate, actin filaments plus end become capped. After newly polymerized subunits hydrolyze atp, they become susceptible to depolymerization by coflin. Results in net filament assembly at front & dissasebly at rear. At the rear of lamellipodium, actin works w/ myosin to migrate by contraction: arp proteins activated at front to nucleate; inactive arp & active cofilin at rear allows disassembly. Myosin contraction & cell adhesion allows cell to pull themselves forward: contraction & de-adhesion at rear of cell. Cell polarization is controlled by members of rho protein families: cell migration requires long-distance communication & coordination b/t one end of cell.
