Enter Smy1, a myosin-passenger protein.
Goode and his colleagues hypothesized that a passenger protein like Smy1 would provide the perfect mechanism for slowing down formins when roadways are longer and would be carrying more passengers. They tested their theory in yeast cells, where formins construct actin cables that transport building materials essential for cell growth and division. As Goode says, they struck gold.
When they deleted the gene for Smy1, cables grew abnormally fast and hit the back of the cell, buckling and misdirecting transport. When they purified Smy1 and placed it in a test tube with formins they discovered that Smy1 slows down actin filament growth.
To further explore, they tagged Smy1 in living cells and learned that Smy1 molecules are carried on cables by myosin to the formin, where they pause for 1-2 seconds to give formins the message to slow down.
Goode says their working model illustrates that as a cable grows longer, it loads up more and more Smy1 molecules, which are transported on the cable to send a message to the formin to slow down.
"This prevents overgrowth of longer cables that are nearing the back of the cell, but allows rapid growth of the shorter cables," says Goode.
This paper will help scientists understand the general mechanisms that are used for directing cell shape and division. The next challenge says Goode, is "to find out whether related mechanisms are used to control formins in mammalian cells and understand the physiological consequences of disrupting those mechanisms."
|Contact: Susan Chaityn Lebovits|