Touch-induced cell squeezing regulates division

In the hopeless hustle of a crowded train station, it might be tempting to "split." At least, that's what your cells would tell you to do.

In a study published on Sept. 15, a team of Hopkins scientists discovered a sensor that allows cells to recognize disruptions to their natural shapes. These disruptions include collisions, wedges and squeezes, and are inevitable results of the proximity between neighboring cells.

Like any biologist will assert, structure is directly related to function. Out of their proper form, cells are incapable of properly implementing daily tasks. And perhaps most importantly, they are unable to engage in cell division.

Cell division is arguably the key role of a cell. Nearly all the cells in our bodies will eventually die out, but cell division constantly produces new cells to replace them. For instance, skin cells are replaced as often as every 35 days.

Dividing cells usually need to be round and symmetrical so that genetic material splits equally between the two daughters. However, the process of cell division does not rely on the all-or-nothing principle. If pressure from or collisions between neighbors changes a cell's shape, cell division can still occur, albeit improperly. Improper division gives rise to an array of life-threatening ailments, including cancer.

Thankfully, reinforcements in the shape of myosin II and cortexillin I pile in during high-pressure situations (no pun intended). These proteins are "force-sensitive," and can "feel" changes in their form. Like a faithful team of paramedics, myosin II and cortexillin I flock to the site of damage and proceed to restore cell shape.

"What we found is an exquisitely tuned mechanosensory system that keeps the cells shipshape so they can divide properly," Douglas Robinson, one of the conductors of the study, and the associate professor of Cell Biology, Pharmacology and Molecular Studies at the Hopkins School of Medicine said.

These cell-restoring agents were discovered when Hopkins scientists simulated inter-cellular activity on protozoa, or simple one-celled organisms whose cells function similarly to ours. They achi

eved this with the aid of a micropipette. A micropipette is a minuscule instrument that can latch onto the cell wall and suck it in like a vacuum cleaner. They tagged the myosin and cortexillin with a fluorescent green color that helped track their movement throughout the cell, and waited.

Within moments of the micropipette's contact with the cell wall, myosin II and cortexillin I began accumulating at the site of damage.

When the proteins reached a certain level, the cell plucked itself from the micropipette and rebounded to its natural shape. The proteins then moved to the middle of the cell, and caused it to divide.

The scientists then proceeded to test each protein's efficacy when separated from the other. They preformed two experiments in which they engineered cells that lacked either myosin II or cortexillin I. They found that each protein was unable to function without its counterpart.

The information about myosin II and cortexillin I derived in this study is crucial to fully understanding cell division. It brings scientists one step closer to controlling, and ultimately minimizing, the prevalence of diseases that develop when this process goes amiss.