The cell biologists conduct their experiments inside living cells. In normal cell division, chromosomes line up in the center, where two copies of each chromosome are held together with "molecular glue" until signaled to dissolve the glue and divide. To oversimplify, each chromosome copy is then pulled to opposite poles of the cell, escorted in what looks like a taffy pull away from the center as two new daughter cells are formed.
During the split, molecular engines pull the copies apart along microtubule tracks that take an active role in the process that includes shortening microtubules by large, flexible scaffold-like protein structures called kinetochores that assemble on every chromosome during division. Maresca and colleagues say until this study revealed details, PEF's function as a kinetochore regulator has been underappreciated.
Overall, this well orchestrated process prevents serious problems such as aneuploidy, that is, too many chromosomes in daughter cells. Aneuploidy in somatic or body cells leads to cell death and is a hallmark of most cancer cells. But in eggs or sperm, it leads to serious birth defects and miscarriages.
In properly aligned division, microtubules from opposite spindle poles tug chromosome copies toward opposite poles, but they stick together with molecular glue until the proper moment. This creates tension at the kinetochores and stabilizes their interactions with microtubules. However, if attachments are bad, or syntelic, both copies attach to the same pole, leading to chromosome mis-segregation and aneuploidy if uncorrected. "Cells have a surveillance mechanism that allows them to wait for each for every chromosome to properly align before divvying up the chromosomes," Maresca says. "It's clear in our movies that the cell waits for the last kinetochores to corre
|Contact: Janet Lathrop|
University of Massachusetts at Amherst