Researchers identify protein that improves DNA repair under stress

Cells in the human body are constantly being exposed to stress from environmental chemicals or errors in routine cellular processes. While stress can cause damage, it can also provide the stimulus for undoing the damage.

Cells in the human body are constantly being exposed to stress from environmental chemicals or errors in routine cellular processes. While stress can cause damage, it can also provide the stimulus for undoing the damage.

New research by a team of scientists at the University of Rochester has unveiled an important new mechanism that allows cells to recognize when they are under stress and prime the DNA repair machinery to respond to the threat of damage.

Their findings will be published Friday in journal Science.

The scientists, led by biologists Vera Gorbunova and Andrei Seluanov, focused on the most dangerous type of DNA damage -- double strand breaks. Unrepaired, this type of damage can lead to premature aging and cancer. They studied how oxidative stress affects efficiency of DNA repair. Oxidative stress occurs when the body is unable to neutralize the highly-reactive molecules, which are typically produced during routine cellular activities.

The research team found that human cells undergoing oxidative stress synthesized more of a protein called SIRT6. By increasing SIRT6 levels, cells were able to stimulate their ability to repair double strand breaks. When the cells were treated with a drug that inactivated SIRT6, DNA repair came to a halt, thus confirming the role of SIRT6 in DNA repair. Gorbunova notes that the SIRT6 protein is structurally related to another protein, SIR2, which has been shown to extend lifespan in multiple model organisms.

"SIRT6 also affects DNA repair when there is no oxidative stress," explains Gorbunova. "It's just that the effect is magnified when the cells are challenged with even small amounts of oxidative stress."

SIRT6 allows the cells to be economical with their resources, priming the repair enzymes only when there is damage that needs to be repaired. Thus SIRT6 may be a master regulator that coordinates stress and DNA repair activities, according to Gorbunova.

Unsolved Celebrity Murders (1)

Fourteen years ago today, hip-hop lost an icon when the Notorious B.I.G. (See photos of him) also known by his real name, or other aliases — was killed in an L.A. drive-by shooting (see where). Some believed the murder was linked to a growing feud. A new investigation was recently launched.

The case remains unsolved, as do the mysterious murders of these stars:

Bob Crane

Elizabeth Short

David Carradine

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Harlem rapper Big L (this is his given name) was shot and killed on February 15, 1999, at the age of 24. The main suspect was released due to insufficient charges.

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Telomeres at the end of chromosomes shorten during aging

Genes reveal 'biological ageing'

Gene variants that might show how fast people's bodies are actually ageing have been pinpointed by scientists.

Researchers from the University of Leicester and Kings College London say the finding could help spot people at higher risk of age-related illnesses.

People carrying the variant had differences in the "biological clock" within all their cells.

The British Heart Foundation said the findings could offer a clue to ways of preventing heart disease.

While doctors know that as people age they are more at risk from diseases such as Alzheimer's, Parkinson's and heart disease, some people fall prey to these at an earlier age than expected.

Telomeres

One theory suggests that biological timers called "telomeres", part of the chromosomes in every cell that carry genetic code, may be a factor in this.

From birth, every time a cell divides, the telomeres get shorter and there is some evidence that people with shorter telomeres, either because they diminish more quickly or because they were born with shorter versions, may be at higher risk from age-related illness.

The researchers say in the journal, Nature Genetics, that they looked at more than 500,000 genetic variations across the entire human genome to see which variants cropped up more frequently in people known to have shorter telomeres.

They eventually located a number of variants located near a gene called TERC which, in people carrying them, seemed to be equivalent to an extra three or four years of "biological ageing".

Bad lifestyles

Professor Tim Spector, from King's College London, said: "What our study suggests is that some people are genetically programmed to age at a faster rate.

"Alternatively, genetically susceptible people may age even faster when exposed to proven 'bad' environments for telomeres such as smoking, obesity or lack of exercise - and end up several years biologically older or succumbing to more age-related diseases."

Professor Jeremy Pearson, associate medical director at the British Heart Foundation, which part-funded the study, said it was not yet clear whether telomeres did contribute to an increased risk of disease.

He said: "Understanding how our cells age is an important step in our quest for better ways to prevent and treat heart disease.

"Perhaps in the future one of the ways we try to reduce the risk of, or treat, heart disease would be to use an 'anti-ageing' approach for our arteries."

Smoking causes genetic damage in minutes, rather than months

A recent study found that certain substances in tobacco can cause genetic damage within a few minutes -- rather than months, according to media reports Wednesday.

The long term impact of smoking, from heart disease to a range of cancers, is well known.

This study suggests the damage begins just moments after the first cigarette is smoked.

The study shows that the DNA damage associated with lung and other types of cancer become apparent within 15-30 minutes of inhaling cigarette smoke. It is a time frame that surprise even the researchers.

Smoking is to blame for about 90 percent of lung cancers and is linked to at least 18 other types of cancer.

Lung cancer claims 3,000 lives worldwide each day, mostly as a result of cigarette smoking.

Anti-smoking charity Ash described the research as "chilling" and as a warning that it is never too early to quit.

Int'l study finds new genetic loci associated with menopause onset

WASHINGTON, Jan. 23 -- An international team of researchers from the Boston University and other institutions has uncovered 13 genetic loci, linked to immune function and DNA repair, that are factors in the age of onset of menopause.

Menopause -- the cessation of reproductive function of the ovaries -- is a major hormonal change that affects most women when they are in their early 50s. Most prior studies of the age of onset of menopause have focused on genes from the estrogen-production pathway or vascular components.

In the new study, published online Jan. 22 in Nature Genetics, the research team identified 13 novel loci associated with menopause onset, while confirming four previously established loci. Most of the 17 loci are associated with genes related to DNA damage repair or auto-immune disease; others are linked to hormonal regulation.

The authors said they expected further research to identify "a substantial number of additional common variants" that impact age of menopause, and that many of them will be located in genes identified in their study. The study examined more than 50,000 women of European descent who had experienced menopause between the ages of 40 and 60.

The research team noted that a large-scale study of menopause onset in African-American women is underway, which will help to determine whether the genetic variations that affect menopause onset in African-American women are similar or substantially different for women of primarily European descent.

Colourful coral could pave way for cancer cure

The vividly fluorescent cluster was found in waters off Lord Howe Island, 600km east of the Australian mainland, with some displaying rich reds that were difficult to find and in high demand for studies of cancer cells.