When a strand of DNA breaks in the body's cells, it normally does not take long until it has been repaired. Now researchers at the Swedish medical university Karolinska Institutet have discovered a new mechanism that helps to explain how the cell performs these repairs. The results are presented in Science.
The new results are concerned with a phenomenon called cohesion, whereby two copies of a chromosome in the cell nucleus are held tightly together by a protein complex called cohesin.
Cohesion fulfils an important function during cell division as the newly copied chromosomes, the sister chromatids, have to stay together until the right moment of separation. If the chromatids come apart too early, there is a risk of the daughter cells getting the wrong number of chromosomes, something that is often observed in tumour cells.
Dr Camilla Sjögren and her research team have now shown that the cell also employs cohesion to repair damaged sister chromatids. Their results show that DNA damage can reactivate cohesin, which runs counter to the commonly held view that cohesion only arises during the DNA copying that takes place before cell division.
Scientists have long been fascinated by the way in which the duplicated chromosomes are separated before cell division so that exactly half the copied genetic material ends up in each daughter cell. Another large research question is how cells repair damaged DNA and consequently prevent cancer, for example.
"We have shown that chromosome segregation and DNA repair are partly dealt with by the same machinery. These findings provide new understanding of two fundamental cellular mechanisms and may also be of value to cancer research," says Dr Sjögren.
Source: Karolinska Institutet
Related stories:
Mechanisms of cardiovascular disease and cancer give clues to new therapies
Cardiovascular conditions leading to heart attacks and strokes are treated quite separately from common cancers of the prostate, breast or lung, but now turn out to involve some of the same critical mechanisms at the molecular level. This in turn provides clues to more effective therapies for both cancer and cardiovascular diseases, but requires researchers in these distinct fields to come together. The seeds were sown for closer cooperation between these two groups at a recent workshop organised by the European Science Foundation (ESF), which also highlighted the striking progress already made in understanding key common mechanisms underlying both disease categories.
Misreading of damaged DNA may spur tumor formation
The DNA in our cells is constantly under assault from oxygen, the sun's radiation and environmental stresses. Most of the time, our cells can repair the damage before it gets copied into a permanent mutation that could lead to cancer.
Researchers Shed Light on Evolution of Gene Regulation
(PhysOrg.com) -- Scientists at Penn State have shed light on some of the processes that regulate genes -- such as the processes that ensure that proteins are produced at the correct time, place, and amount in an organism -- and they also have shed light on the evolution of the DNA regions that regulate genes. The team focused on regulatory regions that, when bound to the protein GATA1, are thought to turn on genes that play an important role in the development of red blood cells.
New imaging technique tracks cancer-killing cells over prolonged period
Coaxing a patient's own cells to hunt down and tackle infected or diseased cells is a promising therapeutic approach for many disorders. But until now, efforts to follow these specially modified cells after their reintroduction to the body have relied on short-term monitoring techniques that don't give a complete picture of the cells' status.
Gut check reveals vast multicultural community of bugs in bowels
Mention the phrase "diverse ecosystem," and it conjures images of tropical rainforests and endangered coral reefs. It also describes the human colon.
Why only some former smokers develop lung cancer
Canadian researchers are trying to answer why some smokers develop lung cancer while others remain disease free, despite similar lifestyle changes.
New study bolsters beliefs about DNA repair
Aucott et al. report the first in vivo experiments on the heterochromatin protein 1 (HP1) family, which sidles up to silent DNA. The results, to be published in the Nov. 17 issue of the
Journal of Cell Biology, add to the evidence that the different versions of the proteins help cells fix broken DNA.
Breakthrough in cell-type analysis offers new ways to study development and disease
(PhysOrg.com) -- Like skilled assassins, many diseases seem to know exactly what types of cells to attack. While decimating one cadre of cells, diseases will inexplicably spare a seemingly identical group of neighbors. What makes cells vulnerable or not depends largely on the kinds and amounts of proteins they produce — their “translational profile,” in the lingo of molecular biology. For this reason, scientists have struggled to parse the subtle molecular differences among the hundreds of specialized cell types that are tangled together in tissues like the brain.