Can a genetic switch spice up supermarket tomato?

WASHINGTON (AP) — Using genetics, scientists have been able to dig up the dirt on why homegrown tomatoes taste so much sweeter than the ones in the supermarket.

Researchers found a genetic switch responsible for some of the sugar production within a tomato. A new study in Friday's edition of Science found that the common type of tomato bred for firmness and good shipping also inadvertently turns off the sugar-producing switch. That makes it less sweet and blander than garden varieties.

University of California Davis plant scientist Ann Powell said knowing the genetics behind the sugar-making could lead someday to development of sweeter tomatoes that also travel well.

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Scientists crack Black Death's genetic code

A Wayson stain of the Yersinia pestis bacterium, responsible for the plague that ravaged Europe between 1347 and 1351.

Credit: Reuters/CDC

By Kate Kelland

LONDON | Thu Oct 13, 2011 10:28am EDT

LONDON (Reuters) - Scientists have mapped out the entire genetic map of the Black Death, a 14th century bubonic plague that killed 50 million Europeans in one of the most devastating epidemics in history.

The work, which involved extracting and purifying DNA from the remains of Black death victims buried in London's "plague pits," is the first time scientists have been able to draft a reconstructed genome of any ancient pathogen.

Their result -- a full draft of the entire Black Death genome -- should allow researchers to track changes in the disease's evolution and virulence, and lead to better understanding of modern-day infectious diseases.

Building on previous research which showed that a specific variant of the Yersinia pestis (Y. pestis) bacterium was responsible for the plague that ravaged Europe between 1347 and 1351, a team of German, Canadian and American scientists went on to "capture" and sequence the entire genome of the disease.

"The genomic data show that this bacterial strain, or variant, is the ancestor of all modern plagues we have today worldwide. Every outbreak across the globe today stems from a descendant of the medieval plague," said Hendrik Poinar, of Canada's McMaster University, who worked with the team.

"With a better understanding of the evolution of this deadly pathogen, we are entering a new era of research into infectious disease."

Major technical advances in DNA recovery and sequencing have dramatically expanded the scope of genetic analysis of ancient specimens, opening up new ways of trying to understand emerging and re-emerging infections.

Experts say the direct descendants of the same bubonic plague still exist today, killing around 2,000 people a year.

A virulent strain of E. coli bacteria which caused a deadly outbreak of infections in Germany and France earlier this year was also found to contain DNA sequences from plague bacteria.

For this study Poinar's team analysed skeletal remains from Black Death victims buried in London's East Smithfield "plague pits," which are located under what is now the Royal Mint.

By focusing on promising specimens from the dental pulp of five bodies, which had already been pre-screened for the presence of Y. pestis, they were able to extract, purify and enrich the disease's DNA and at the same time reduce the amount of background non-plague DNA which might interfere.

Linking the 1349 to 1350 dates of the skeletal remains to the genetic data allowed the researchers to calculate the age of the ancestor of Y. pestis that caused the mediaeval plague.

Poinar, whose work was published in the journal Nature, said the team found that in 660 years of evolution, the genetic map of the ancient organism had only barely changed. "The next step is to determine why this was so deadly," he said.

Johannes Krause Of Germany's University of Tubingen, who also worked on the study, said the same approach could now be used to study the genomes of all sorts of historic pathogens.

"This will provide us with direct insights into the evolution of human pathogens and historical pandemics," he said in a statement.

(Editing by Paul Casciato)

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Scientists unravel genetic clues to multiple sclerosis

Multiple sclerosis patient Sue Sutton (L) embraces Dare, a two-legged Sheltie dog used in therapy for disabled people in Denver, Colorado July 15, 2009.

Credit: Reuters/Rick Wilking

By Kate Kelland

LONDON | Wed Aug 10, 2011 3:55pm EDT

LONDON (Reuters) - Scientists have found 29 new genetic variants linked to multiple sclerosis (MS) and say the findings should help drugmakers focus treatment research on precise areas of the immune system.

In a study published in the journal Nature on Wednesday, researchers said the newly-found links point to the idea that T-cells -- a type of white blood cell responsible for mounting an immune response -- and chemicals called interleukins play a key role in the development of the debilitating disease.

Drugs in development that target the immune system include rituximab, sold under the brand name Rituxan by Roche and Biogen to fight leukemia, Tysabri from Biogen and Elan, Lemtrada, sold as Campath by Sanofi's unit Genzyme for cancer, and Abbott and Biogen's Zenapax or daclizumab.

"We have implicated genes that are highly relevant to the actions of those drugs," said Alastair Compston of Cambridge University, who co-led the study. "It is now clear that multiple sclerosis is primarily an immunological disease. This is the way to nail this disease and get on top of it."

Mid-stage trial data for daclizumab released on Tuesday showed the drug on a par with other new medicines for MS, but some of he side-effects were worrisome.

Multiple sclerosis is one of the most common neurological conditions among young adults, affecting around 2.5 million people worldwide.

It occurs when the protective coating, known as the myelin sheath, around nerve fibres in the brain and spinal cord begins to break down, slowing the brain's communication with the rest of the body.

The affected pathways -- responsible for everyday activities such as seeing, walking, feeling, thinking and controlling the bowel and bladder -- lose the ability to function properly and are eventually destroyed.

In a second study in the Public Library of Science journal PLoS Genetics on Wednesday, researchers found that many of the genes linked to MS are also linked to other autoimmune diseases such as Crohn's disease and Type 1 diabetes. This also points to potential new uses for existing drugs in development, they said.

"We have known for some time that many devastating diseases of the immune system must have common genetic causes," said Chris Cotsapas of Yale University in the United States, who led the PLoS study. "Now we have the outline of a map that tells us where we can look for common treatments."

Most people who develop MS experience their first symptoms in their 20s and 30s, but Compston and colleagues told a briefing in London the trigger for the disease could happen in early childhood when genetic risk factors coincide with some as yet unknown environmental factor.

For their study, Compston and Peter Donnelly of Oxford University worked with some 250 other researchers and studied the DNA from 9,772 people with multiple sclerosis and compared it with a control group of more than 17,300 healthy people.

Their analysis confirmed 23 previously known genetic links and identified another 29 new genetic variants.

Experts think both genetic and environmental factors are equally important in determining who is likely to develop MS, and taken together, the known genetic variants probably explain about 20 percent of the genetic links, they said.

Previous research has suggested a link between Vitamin D deficiency and an increased risk of MS. Compston's team said that along with the many genes which play a role in the immune system, they had also found two involved in the metabolism of Vitamin D -- which mostly comes from sunlight -- lending weight to a possible link between genes and the environment.

(Editing by Hans-Juergen Peters)

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