Sammendrag:
Cell division (mitosis) is one of the most fundamental processes in life as it allows one cell to give rise to two daughter cells with exactly the same sets of chromosomes. It is important that this transmission of chromosomes is as accurate as possible to prevent any loss or modification of the information carried by the chromosomes, as this typically can give rise to cancer cells. To prevent such errors in transmission of the genetic material from happening, cells have developed exquisite surveillance mechanisms that monitor whether chromosomes are equally distributed between the two daughter cells.
In a recent paper (Lopez-Soop et al., 2017, Cell Cycle), the group of Associate Professor Thomas Küntziger (Department of Oral Biology, Faculty of Dentistry) has implicated the protein AKAP95 in such a surveillance mechanism called the spindle assembly checkpoint. The authors uncover a dysfunctional spindle assembly checkpoint in cells where the function of AKAP95 has been invalidated, with as a result the apparition of so called “lagging chromosomes” corresponding to improperly distributed chromosomes. Lagging chromosomes from defects in surveillance mechanisms are a hallmark of chromosomal instability and are known to be one of the factors leading to aneuploidy (gain or loss of whole chromosomes), a situation often found in cancer cells.
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