The flow of weekly news items related to telomeres and telomerase has grown from a trickle to a steady stream.  Here is a selection of some recent items. 

• Centenarian Ashkenazi Jews

A recent study of centenarian Ashkenazi Jews found that they and their descendents have a mutant gene which results in higher levels of telomerase, longer telomeres, greater health at old age and – well – and ability to live very long healthy lives.  The study looked at “blood samples from 86 very old, but generally healthy, people with an average age of 97; 175 of their offspring; and 93 other people who were the offspring of parents who had lived a normal lifespan and could therefore make up a control group, with which the results could be compared. — Yousin Suh, associate professor of medicine and genetics at Einstein and a lead author on the paper, said: “Our findings suggest that telomere length and variants of telomerase genes combine to help people live very long lives, perhaps by protecting them from the diseases of old age(ref).”  My own comment is “no kidding, that’s what we’ve been talking about for years now.”  Here is the original November 11 news release from the Albert Einstein College of medicine.  The story was picked up by dozens of publications worldwide.

·         Childhood emotional trauma

Another study reported in the press last Friday indicates that a history of childhood emotional trauma such as having been beaten or sexually abused is strongly correlated with shorter telomere lengths in grown adults(ref).  “– researchers Audrey Tyrka of Brown University in Providence, Rhode Island measured DNA extracted from blood samples of 31 18-to-64 year old adults, including 22 women and nine men. — They found more rapid shortening of telomeres only in those who said they had suffered severe mistreatment as children.”  Again, this tends to confirm what we already know about telomere lengths: they respond negatively to stress, apparently due to repeated over-expression of cortisol.   Again, the story was picked up widely in the press and an interview on the social ramifications of the study with Dr. Audrey R. Tyrka the team leader can be found here.

• The oyster fungus

For those of you who have a passionate interest in the oyster fungus (Pleurotus ostreatus), fungus of the month in October 1998, there is more telomerase news.  A Nov 21 news report describes a study that, interestingly enough, indicates that the ‘telomere sequence of P. ostreatus is identical to that of human telomeres.”  How fascinating that we and some mushrooms could enjoy this same genetic feature, and how indicative this is of how fundamental telomeres are to most life forms!  These oyster mushrooms (so-called because of their appearance), by the way, are good to eat and great for the environment “The oyster fungus, together with the common mushroom, is the fungus with the greatest production and consumption worldwide. Likewise this fungus is of great biotechnological interest for its capacity to produce enzymes and degrade industrial and agricultural waste(ref).”

·         The Arabidopsis weed

There is an October 28 report in ScienceDaily about a common weed (the Arabidopsis plant) and about what studies of its telomeres may mean for us. The story’s headline and lead lines are: “Common Weed Could Provide Clues On Aging And Cancer —— A common weed and human cancer cells could provide some very uncommon details about DNA structure and its relationship with telomeres and how they affect cellular aging and cancer, according to a team led by scientists from Texas A&M University and the University of Cincinnati (UC). — “We found that removal of the plant telomere proteins caused rampant end-to-end joining of chromosomes and dramatic defects in plant development,” explains Shippen.” — “The Cincinnati team then showed that removal of one of the human proteins from human cancer cells caused wide-spread DNA damage and complete loss of some telomeres.”Going back in history a slight bit, I found two recent stories relating to the protein structure and replication of telomeres. 

·         TRF1 and telomere fragility

The first, a July 2009 story deals with the protein makeup of telomeres.  A protein TRF1 that was discovered in 1995 plays a very important role in assuring the structural integrity of telomeres and protecting them from what otherwise would be fragility.  “Using a conditional mouse knockout, de Lange and Sfeir (Titia de Lange  and Agnel Sfeir, researchers at Rockerfeller University)  have now revealed that TRF1, which is part of a six-protein complex called shelterin, enables DNA replication to drive smoothly through telomeres with the aid of two other proteins. — Telomeric DNA has a repetitive sequence that can form unusual DNA structures when the DNA is unwound during DNA replication,” says de Lange. “Our data suggest that TRF1 brings in two proteins that can take out these structures in the telomeric DNA. In other words, TRF1 and its helpers remove the bumps in the road so that the replication fork can drive through. — Sfeir deleted TRF1 and saw that the telomeres resembled common fragile sites, suggesting that TRF1 protects telomeres from becoming fragile. Instead of a continuous string of DNA, the telomeres were broken into fragments of twos and threes. — the researchers observed the dynamics of replication across individual DNA molecules — the first time this technique has been used to study telomeres. In the absence of TRF1, the fork often stalled for a considerable amount of time.”

·         hRAP1 and telomere DNA breaks

The second story relating to the structure of telomeres, September 2009 is entitled “Protein Helps Distinguish Chromosome Ends From DNA Breaks.”  The lead line is “The Stowers Institute’s Baumann Lab has demonstrated how human cells protect chromosome ends from misguided repairs that can lead to cancer. The work, published in The EMBO Journal, a publication of the European Molecular Biology Organization, follows the team’s 2007 in vitro demonstration of the role of the hRAP1 protein in preventing chromosome ends from being fused to new DNA breaks.” – “—in this work, the team demonstrated that the human RAP1 protein plays a key role in preventing chromosome ends from being fused to new DNA breaks. Chromosome end fusions result in genomic instability, which can cause cancer. These findings suggest that RAP1 plays a critical role in cancer prevention in humans.”

There are also several recent stories related to development of anti-cancer drugs that work by inhibiting telomerase, b ut I won’t bother listing those.  It probably won’t be long before telomeres and telomerase – things once known only to a handful of distant researchers and geeky anti-aging aficionados – may be familiar to hundreds of millions.