Universitat Autònoma de Barcelona researchers have identified for the first time the triple mechanism that stops chromosome separation in response to situations that compromise the integrity of the genetic information. The loss of this response capacity is characteristic of cancerous cells.
Cell proliferation requires the chromosomes to be copied (replicated) and distributed (segregated) to the two future daughter cells. Cells continually undergo spontaneous alterations (injuries) to the DNA that makes up the chromosomes, because of their aqueous (reactive) environment, for example. In response to DNA injuries, cells put a stop to the cell division cycle, in order to allow time for the injuries to be repaired and prevent the transmission of damaged, incompletely replicated chromosomes. The loss of this capacity leads to the onset of chromosomal instability, a driver of cancerous transformation.
Studies at other laboratories had already determined that cells from the model organism Schizosaccharomyces pombe, a yeast used in the laboratory to investigate cell behaviour, stop the cell division cycle by means of a process that was thought to be universal (in scientific terms, phosphorylation of a conserved tyrosine residue in cyclin-dependent kinase CDK1, the driver of the cell cycle).
Detail of the cell interior during the cell division process
Source: PLOS Genetics/UAB