MasterCobra

Hello everyone, I have homework to do about the cytoskeleton and its use in cell motility and I wanted to confirm some of my answers with you guys. Here's the problem: We have the result of a simple scratch test (cells come into confluence in a Petri dish, we make a scratch and study the cells' ability to close the gap) There is a control test, where we see the normal cell motility and 2 study tests: Group A: there is an evident acceleration of cell motility compared to the control test Group B: there is no cell motility And I must associate a different bunch of conditions to either group A or group B, as the expected results 1) GTP hydrolysis is blocked by a mutated GAP Microtubules use GTP to polymerize at their "+" ends. The hydrolysis of GTP to GDP causes the microtubules to depolymerise. So if we block this process, cell motility should be accelerated. Group A 2) Mutated myosin inactivates ATP hydrolysis: ATP hydrolysis is essential to myosin movement on actin filaments. Without it, cell motility is non present, group B 3) Mutation causes hyperactive Cdc42: Cdc42 induces actin polymerization. A hyperactive Cdc42 will accelerate cell motility, group A Thank you very much, your help is always appreciated!

Thank you very much!

Hello, For my genetics class, I had to subclone LUX ABE into pUC18 in order to make E. coli glow in the dark with the addition of aldehyde. Unfortunately, I had star activity with the digestions, so it made it almost impossible to identify the LUX ABE band on my electrophoresis gel. My question is: if an enzyme produces cohesive ends in optimal conditions, will it continue to produce cohesive ends in star activity conditions? Or, will it turn to blunt ends? Thank you, Julien