Slide 11: Cytoskeleton
Lecture 11: Cytoskeleton in Action
Slide 2: Mysoin V can walk a lot faster than Myosin 2. Saccharomyces Cerevesiae is a type of yeast. Myosin V interacts with one end of the nucleus, and another binds to the other side to orient the nucleus.
Slide 3: The entire cytoplasm moves in one side: “streaming”, what happens is that very close to the membrane, the chloroplast are not moving and close to it are the actin filaments that are not moving. Then everything else is on the Myosin V which is moving since Myosin V moves around. Evidence: we have EM data.
Animated movie: how does actin filaments involve itself in the movement of cells?
Slide 5: When cells want to move, they need to polarize. A leading edge (the direction they’re moving), …show more content…
Rho GTPase can activate the protein “formin” which is on the plus end (or was it minus end..). GEF often localizes to different cell positions – in this case, it’s close to the receptor and then activate Rho GTPase which activates formin. Ran GTPase also uses GEF which is localized in the membrane and the cytoplasm.
Slide 9: Rho GTPase gives rise to stress fibers. Rho GTPase can also be isolated so that it can be active the entire time. Researchers isolated mutant Cdc42, Rac, and Rho – in a dominant mutation so active all the time. Dominant active Rac gave ruffles which are folded membranes that move around and contains a lot of branched actin structures that are more similar to lamellipodia. Dominant mutant Cdc42 didn’t have a lot of stress fibers but something about the filopodia. The dominant active Rho has a lot of stress fibers. Dominant active/dominant mutation = over expressed. This is a type of “gain-of-function” study (as opposed to loss-of-function).
Slide 10: I fell asleep. Something about… signals. Cdc 42 has a little branch that activates Par 6. Par 6 regulates cell …show more content…
This movement allows us to study the cell. When the dominant negative mutations of Rac, Cdc42 and Rho were studied – the wound didn’t close. Shows that they’re important.
Slide 12: Cdc42 activates in the front. Stabilizes the polarity and controls the regulation of microtubules. Rac is active in the front (pushes membrane forward); when Rac is controlled, very little ruffling. Rho GTPase is active in the back and makes a lot of stress fibers. When cells move, you must localize small GTPases to control the different bits of the cell. They’re all carefully regulated.
Slide 13: How does the signal work and where does it come from? Chemotaxis (attraction toward chemicals). An example is dictostellium – organisms that live in two states: individual cells or as an aggregation. The aggregation happens when there’s not enough nutrients available – they aggregate together and look almost like a multicellular organism and move. When enough nutrients reappear, they separate.
Slide 13: He’s talking about some signaling stuff – it’s very confusing.
PI-3Kinase, when activated, activates other downstream pathways. Once the PI-3K is activated, PTEN is activated, which activates
Slide 2: Mysoin V can walk a lot faster than Myosin 2. Saccharomyces Cerevesiae is a type of yeast. Myosin V interacts with one end of the nucleus, and another binds to the other side to orient the nucleus.
Slide 3: The entire cytoplasm moves in one side: “streaming”, what happens is that very close to the membrane, the chloroplast are not moving and close to it are the actin filaments that are not moving. Then everything else is on the Myosin V which is moving since Myosin V moves around. Evidence: we have EM data.
Animated movie: how does actin filaments involve itself in the movement of cells?
Slide 5: When cells want to move, they need to polarize. A leading edge (the direction they’re moving), …show more content…
Rho GTPase can activate the protein “formin” which is on the plus end (or was it minus end..). GEF often localizes to different cell positions – in this case, it’s close to the receptor and then activate Rho GTPase which activates formin. Ran GTPase also uses GEF which is localized in the membrane and the cytoplasm.
Slide 9: Rho GTPase gives rise to stress fibers. Rho GTPase can also be isolated so that it can be active the entire time. Researchers isolated mutant Cdc42, Rac, and Rho – in a dominant mutation so active all the time. Dominant active Rac gave ruffles which are folded membranes that move around and contains a lot of branched actin structures that are more similar to lamellipodia. Dominant mutant Cdc42 didn’t have a lot of stress fibers but something about the filopodia. The dominant active Rho has a lot of stress fibers. Dominant active/dominant mutation = over expressed. This is a type of “gain-of-function” study (as opposed to loss-of-function).
Slide 10: I fell asleep. Something about… signals. Cdc 42 has a little branch that activates Par 6. Par 6 regulates cell …show more content…
This movement allows us to study the cell. When the dominant negative mutations of Rac, Cdc42 and Rho were studied – the wound didn’t close. Shows that they’re important.
Slide 12: Cdc42 activates in the front. Stabilizes the polarity and controls the regulation of microtubules. Rac is active in the front (pushes membrane forward); when Rac is controlled, very little ruffling. Rho GTPase is active in the back and makes a lot of stress fibers. When cells move, you must localize small GTPases to control the different bits of the cell. They’re all carefully regulated.
Slide 13: How does the signal work and where does it come from? Chemotaxis (attraction toward chemicals). An example is dictostellium – organisms that live in two states: individual cells or as an aggregation. The aggregation happens when there’s not enough nutrients available – they aggregate together and look almost like a multicellular organism and move. When enough nutrients reappear, they separate.
Slide 13: He’s talking about some signaling stuff – it’s very confusing.
PI-3Kinase, when activated, activates other downstream pathways. Once the PI-3K is activated, PTEN is activated, which activates