Researchers uncovered the pulses of external signaling factors that push resting cells to divide. In one phase, dialing up the levels of the signaling molecule p53 keeps cells from dividing, while another pathway increases expression of EGR1 and initiates cell division.
Y. Zwang et al., “Two phases of mitogenic signaling unveil roles for p53 and EGR1 in elimination of inconsistent growth signals,” Mol Cell, doi: 10.1016/j.molcel.2011.04.017, 2011. Free F1000 Evaluation
Just before cells divide, chromosomes must duplicate and separate in a coordinated dance. This study showed that after the chromosomes double, a ring molecule called cohesion forms a tight band around them, then a molecule called separase cleaves the cohesion to allow the sister chromatids to synchronously drift apart.
While many tissue types stop growing when nutrients are scarce, Drosophila brain tissue continues to grow, even when starved for food. Anaplastic lymphomakinase (Alk) allows brain tissue to grow under caloric restriction by bypassing the need to activate insulin receptor and target of rapamycin (TOR) pathways. The study may explain why Alk mutations are more common in certain brain cancers.
Researchers showed that the septin cytoskeleton, a network of filamentous proteins, plays a critical role in directing microtubules reorganization. Septins allow the microtubules to keep growing and keep the proper ends of the microtubules aligned.
In budding yeast, it was known that the kinetochores—the spots on chromosomes where spindle fibers separate chromosomes during cell division—rely on methylation of a protein called DAM1. This new study showed that a histone protein must be modified before this methylation can occur.
During mitosis, if even a single kinetochore is not attached before chromosomes segregate, the cell division process is frozen by a mitotic checkpoint complex that binds to a protein called anaphase promoting complex or cyclosome (APC/C), which normally initiates the next stage in cell division. Here, researchers showed that to turn off that halt signal once all the kinetochores are attached, a protein subunit called APC15 continuously and quickly removes the mitotic checkpoint complex from the APC/C, allowing for quick activation.
J. Mansfeld et al., “APC15 drives the turnover of MCC-CDC20 to make the spindle assembly checkpoint responsive to kinetochore attachment,” Nat Cell Biol, doi:10.1038/ncb2347, 2011. Free F1000 Evaluation
Before chromosomes can separate, a checkpoint in mitosis ensures that the next stage doesn’t proceed until all the chromosomes are properly bound to kinetochores. The new study revealed a previously unknown protein CUEDC2 (CUE-domain-containing protein 2) plays a role in silencing this checkpoint and allowing cell division to enter its next phase.
The F1000 Top 7 is a snapshot of the highest ranked articles from a 30-day period on Faculty of 1000 Cancer Biology, as calculated on October 2, 2011. Faculty Members evaluate and rate the most important papers in their field. To see the latest rankings, search the database, and read daily evaluations, visit http://f1000.com.