Category Archives: DNA

MADISON, Wis.--(BUSINESS WIRE)--

Forensic DNA professionals confront many challenges: cold case investigations, DNA backlogs and new applications like rapid DNA and kinship DNA testing. The 23rd International Symposium on Human Identification (ISHI) presents forensic professionals with an opportunity to learn about these and other developing forensic DNA technologies alongside fellow scientists, law enforcement professionals and forensic experts. This years ISHI will be held October 15-18 in Nashville, Tennessee at the Gaylord Opryland Resort.

As the largest conference on DNA analysis for human identification, the symposium attracts more than 800 DNA analysts and forensic scientists from around the world, providing these professionals an opportunity to explore and debate the latest research, technologies and ethical issues in the industry today. This years presenters and topics include:

Author and Educator Douglas Starr

Co-director of Boston Universitys graduate program in Science and Medical Journalism and author of Gold Dagger award-winning book The Little Killer of Shepherds: A True Crime Story and the Birth of Forensic Science, Starr is this years keynote speaker. In his latest book, Starr tells the story of forensic sciences 19th century pioneers and the notorious serial killer they caught and convicted using their new scientific techniques. Winner of the Gold Dagger award in the U.K. and a finalist for the Edgar Allen Poe award in the U.S., the book received laudatory reviews, including an Editors Choice listing in the New York Times Book Review and a place on the True Crime Bestseller lists of the Wall Street Journal and Library Journal.

SNA International Founder Amanda Sozer

SNA International lends expertise to forensic labs and mass fatality identification projects. Founder and President Amanda Sozer, who received recognition for her outstanding efforts during 9/11 and Hurricane Katrina, will be leading a workshop on forensic science and human rights at ISHI. The workshop will include speakers who have worked on human rights projects as well as a presentation on the AAAS Guidelines for Scientists and Human Rights Organizations, developed by a group of collaborating scientists and representatives of human right organizations. The guidelines are designed to be helpful to those establishing science and human rights partnerships and to facilitate and promote cooperation between scientists and human rights organizations seeking scientific expertise.

Sequencing the Black Death Genome: Hendrik Poinar

Hendrik Poinar and his colleagues at McMaster University in Hamilton, Ontario, Canada developed a technique to find and sequence the Black Death genome using the skeletal remains of its victims. The possibility of environmental contamination was high. To address this, Poinar and his team extracted the DNA using a molecular probe made from a modern strain of DNA, testing this new technique on approximately 100 samples of teeth and bone excavated from a London plague pit. The result was a strain of Y. pestis unlike any known today: the Black Death. Poinar will share details of this process during his talk at ISHI.

Workshops: DNA Backlog Reduction, Cold Case Investigative Techniques

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2012 International Symposium on Human Identification Features Emerging and Best Practice Forensic DNA Techniques ...

There was an extremely strong chance DNA found inside the underpants of a five-year-old girl came from the man accused of abusing her, a court has heard.

But the ACT Supreme Court has been told tests for saliva turned up nothing, despite the girls allegation her step-grandfather licked her vagina.

And the court has heard tests werent carried out on other items of clothing and bedding because they were likely to be covered in his DNA and have no probative value.

The underpants were also placed in the same bag as another item of clothing, prompting the defence to suggest the DNA might have transferred from one to the other.

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The 61-year-old man, who cannot be named, is on trial in front of Justice Richard Refshauge accused of two counts of having sexual intercourse with a child.

He has pleaded not guilty, and also denies two alternative charges of committing acts of indecency on the girl.

It is alleged he licked the girls vagina twice when he was babysitting her in April 2009.

The allegations came to light after the girls mother picked her up, when the girl asked her mother if she could tell her the secret she shared with poppy.

The accused man entered the witness box this afternoon and denied any wrongdoing, describing his shock when police confronted him with the allegations.

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Court hears DNA findings in child sex case

ScienceDaily (Sep. 11, 2012) DNA is constantly being damaged by environmental agents such as ultraviolet light or certain compounds present in cigarette smoke. Cells unceasingly implement repair mechanisms for this DNA, which are of redoubtable efficacy. A team from Institut Jacques Monod (CNRS/Universit Paris Diderot), in collaboration with scientists from the Universities of Bristol in the UK and Rockefeller in the USA, has for the first time managed to follow real-time the initial steps in one of these hitherto little known DNA repair systems. Working in a bacterial model, and thanks to an innovative technique applied to a single molecule of DNA, the scientists were able to understand how several actors interact to ensure the reliable repair of DNA.

Published in Nature on 9 September 2012, their work aims to better understand the onset of cancers and how they become resistant to chemotherapies.

Ultraviolet light, tobacco smoke or even the benzopyrenes contained in over-cooked meat can cause changes to the DNA in our cells, which may lead to the onset of cancers. These environmental agents deteriorate the actual structure of the DNA, notably causing so-called "bulky" lesions (like the formation of chemical bonds between DNA bases). In order to identify and repair this type of damage, the cell can call on several systems, such as transcription-coupled repair (TCR), whose complex mechanism of action still remains poorly understood today. Abnormalities affecting this TCR mechanism -- which permits permanent monitoring of the genome -- are the cause of some hereditary diseases such as Xeroderma pigmentosum, sufferers from which are hypersensitive to the Sun's ultraviolet rays and are commonly referred to as "children of the night."

For the first time, a team from Institut Jacques Monod (CNRS/Universit Paris Diderot), in collaboration with scientists at the Universities of Bristol in the UK and Rockefeller in the USA, has succeeded in observing the initial stages of TCR repair mechanisms in a bacterial model. To achieve this, they employed a novel technique for the nanomanipulation of individual molecules[1] which allowed them to detect and follow real-time the interactions between the molecules in play in a single damaged DNA molecule. They elucidated the interactions between different actors during the first steps of this TCR process. A first protein, RNA polymerase[2], usually crosses DNA without mishap, but is stalled when it meets a bulky lesion (like a train blocked on its rails by a landslide). A second protein, Mfd, binds to the stalled RNA polymerase and removes it from the damaged "rail" so that it can then replace it with the other proteins necessary to repair the damage. Measurements of the reaction speeds enabled the observation that Mfd acts particularly slowly on RNA polymerase, pushing it out of the way in about twenty seconds. Furthermore, Mfd does indeed displace stalled RNA polymerase, but then remains associated with the DNA for a longer period (of about five minutes), allowing it to coordinate the arrival of other repair proteins at the damaged site.

Although the scientists were able to explain how this system can achieve almost 100% reliability, a even clearer understanding of these repair processes is still essential in order to determine how cancers appear and subsequently may become resistant to chemotherapies.

Notes:

[1] During these nanomanipulation experiments, damaged DNA was grafted onto a glass surface on one side and a magnetic microbead on the other. The bead surface enabled the perpendicular extension of the DNA and measurement of this end-to-end extension using videomicroscopy. The binding to DNA of different proteins, and their action, is identifiable from the modification the protein generates in the structure or conformation of the DNA. This technique enables an extremely detailed structural and kinetic analysis of in vitro biochemical reactions.

[2] RNA polymerase is responsible for the reading of DNA by a gene and its rewriting in an RNA form, a process known as transcription. It has been shown that RNA polymerase does not only transcribe genes, but also the DNA between genes (until recently referred to as "junk" DNA), allowing, for example, polymerase RNA to perform its quality control by TCR on the entire genome of an organism.

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Real-time observation of single DNA molecule repair

The lexicon of science is riddled with catchy yet misleading terms. The god particle is nothing of the sort. Genes cannot really be selfish, and when astronomers talk about metals, they usually mean something else entirely. Now, we must add junk DNA to the list of scientific misnomers.

Last week, the results of the multinational Encode Project were published across 30 papers in the journals Nature, Science, Genome Biology and Genome Research. The five-year collaboration involved some 450 scientists working in 32 institutions and took up 300 years of computer time. The goal was to analyse the vast bulk of human DNA that does not constitute a gene ie, does not directly code for the creation of particular proteins and is seemingly surplus to requirements.

The conclusion? That this DNA is not junk at all, but absolutely vital for the functioning of our cells. It turns out that as much as a fifth of the 98 per cent of our DNA that falls into this category is instead made up, among other things, of switches bits of DNA that turn some genes on and others off. It is now believed that, in order to get to grips with genetic illnesses such as hereditary heart disease, some forms of diabetes and Crohns Disease, we need to understand these regulatory elements as much as the genes themselves.

It has been clear for a long time that there is a lot more to DNA than just genes. Indeed, one of the great scientific surprises in recent decades has been the discovery that the human genome is surprisingly bereft of actual genes. When the first draft of it was published in the summer of 2001, it did not describe the 100,000 or more genes that most biologists assumed we had, but fewer than 20,000 making Homo sapiens not much more well-endowed genetically than a fruit fly or even a lump of yeast. As an editorial in Nature put it, Unless the human genome contains a lot of genes that are opaque to our computers, it is clear we do not gain our undoubted complexity over worms and plants by using many more genes.

Partly as a result, the idea that scanning a persons genome can tell us pretty much everything about them their likely intelligence, the chance of criminal tendencies, their probable age and cause of death is now seen as a simplistic fantasy. Indeed, the more we learn about our genome, the more complex the story becomes. We have genes that tell our bodies to make proteins, genes that affect other genes, genes that are influenced by the environment, segments of DNA that switch certain genes on and off, as well as our RNA, the still-not-fully understood messenger molecule that conveys information from our DNA to protein factories in the cells.

Despite the fanfare with which the Encode findings were greeted last week, biologists have known for years that junk DNA, a term coined in 1972 by the Japanese-American geneticist Susumu Ohno, performs a host of functions, among them gene regulation. Indeed, it was always obvious that much of our DNA must be tasked with the activation or suppression of other parts of itself: genes that make bone tissue are present in all cells but are only switched on in bone cells; heart muscle genes are present but inactive in your teeth and liver and everywhere else.

Furthermore, as Ohno pointed out, a great deal of the genome consists of pseudogenes non-functioning copies of active genes that form the raw material of evolution. Without this spare genetic material, natural selection would have nothing to act upon. We have also known for some time that the dark part of our genome contains what are known as human endogenous retroviruses: bits of the genetic code from viruses that are a legacy of our long battle with these microbes. In millennia to come, it is likely that bits of the genome for HIV will become similarly incorporated into our DNA, as a legacy of the Aids epidemic.

The more we learn, the more the recipe book of life turns out to resemble less a single tome than a well-organised library, complete with a sophisticated index and with the ability to lend and borrow books. Some of the volumes are crucial a mix-up in the code could kill or cripple us while others moulder in the stacks. There is probably a lot of built-in redundancy, which is not surprising considering that the genomes of any species are the result of three billion years of evolution. Perhaps the most amazing thing is that we can make any sense of it at all.

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'Junk DNA' and the mystery of mankind's missing genes

A Massive Research Effort Now Shows How the Genome Works

By Daniel J. DeNoon WebMD Health News

Reviewed by Louise Chang, MD

Sept. 7, 2012 -- In what scientists call the biggest breakthrough in genetics since the unraveling of the human genome, a massive research effort now shows how the genome works.

The human genome contains 3 billion letters of code containing a person's complete genetic makeup.

The biggest surprise is that most of the DNA in the genome -- which had been called "junk DNA" because it didn't seem to do anything -- turns out to play a crucial role. While only 2% of the genome encodes actual genes, at least 80% of the genome contains millions of "switches" that not only turn genes on and off, but also tell them what to do and when to do it.

Eleven years ago, the Human Genome Project discovered the blueprint carried by every cell in the body. The new ENCODE project now has opened the toolbox each cell uses to follow its individual part of the blueprint. The effort is the work of more than 400 researchers who performed more than 1,600 experiments.

The genome, with its 3-billion-letter code, reads from beginning to end like a book. But in real life, the genome isn't read like a book. The ENCODE data shows it's an intricate dance, with each step carefully choreographed.

Ewan Birney, PhD, associate director of the European Molecular Biology Laboratory, was one of the leaders of the Human Genome Project. He also helped lead the ENCODE project.

"The ENCODE data is just amazing. It shows how complex the human genome is," Birney said at a news conference. "This is the science for this century. We are going to be working out how we make humans, starting out from a simple instruction manual."

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Genetics Breakthrough Changes Thinking About DNA

Last week, in response to a media blitz promoting a $288 million DNA project called ENCODE, headlines announced that most of our DNA formerly known as "junk" was actually useful.

A number of scientists both inside the study and out took issue with this claim - which centered on the 98 percent of our DNA that isn't officially part of any gene.

Sorting the workers from the freeloaders in our DNA is crucial to understanding how our genetic code works, how it drives human evolution and influences our traits and health.

Some biologists dislike the term "junk DNA" because they already knew at least part of it is doing something essential - like regulating how the instructions in the genes are carried out.

The genes hold recipes for making proteins - the working parts and scaffolding of the body. Some of the rest of the DNA tells the genes how much of a given protein to make at any given time.

The goal of the ENCODE (Encylopedia of DNA Elements) project was to figure out which parts have those important regulatory jobs.

According to some scientists involved, they succeeded in pinning down where many of those regulators lurked and identified variants in that DNA that other studies have connected to a variety of diseases. Those findings could lead to new targets for drug research and new avenues for predictive genetic testing.

But long before this project was conceived, scientists had begun to explore our jungle of mystery DNA. The question of non-gene DNA came up in 1975, when researchers discovered that humans and chimpanzees were 98 percent genetically identical. That meant we and chimps were more closely related than mice were to rats, or chimps were to gorillas.

The researchers who did the comparison pointed out that some of our differences might stem not from the genes, but from our other DNA that is regulating the genes.

That regulatory role is crucial when animals are developing in the womb. Some stretch of non-gene DNA could, for example, signal the human brain to keep growing long after chimp brain development would have shut off.

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Planet of the Apes: What is that big hunk of 'junk' DNA up to ?

In a milestone for the understanding of human genetics, scientists just announced the results of five years of work in unraveling the secrets of how the genome operates.

The ENCODE project, as it is known, dispensed with the idea that our DNA is largely "junk," repeating sequences with no function, finding instead that at least 80 percent of the genome is important.

The new findings are the latest in a series of increasingly deep looks at the human genome. Here are some of the major milestones scientists have passed along the way.

1. An understanding of heredity, 1866

The realization that traits and certain diseases can be passed from parent to offspring stretches back at least to the ancient Greeks, well before any genome was actually decoded. The Greek physician Hippocrates theorized that "seeds" from different parts of the body were transmitted to newly conceived embryos, a theory known as pangenesis. Charles Darwin would later espouse similar ideas.

What exactly these "seeds" might be was destined to remain a mystery for centuries. But the first person to put heredity to the test was Gregor Mendel, who systematically tracked dominant and recessive traits in his famous pea plants. Mendel published his work on the statistics of genetic dominance in 1866 to little notice. [Genetics by the Numbers: 10 Tantalizing Tales]

2. Chromosomes come to light, 1902

But the painstaking work of cross-breeding pea plants wouldn't languish for long. In 1869, Swiss physician Johannes Friedrich Miescher became the first scientist to isolate nucleic acids, the active ingredient of DNA. Over the next several decades, scientists peering deeper into the cell discovered mitosis and meiosis, the two types of cell division, and chromosomes, the long strands of DNA and protein in cell nuclei.

In 1903, early geneticist Walter Sutton put two and two together, discovering through his work on grasshopper chromosomes that these mysterious filaments occur in pairs and separate during meiosis, providing a vehicle for mom and dad to pass on their genetic material.

"I may finally call attention to the probability that the associations of paternal and maternal chromosomes in pairs and their subsequent separation may constitute the physical basis of the Mendelian law of heredity," Sutton wrote in the journal The Biological Bulletin in 1902. He followed up with a more comprehensive paper, "The Chromosomes in Heredity" in 1903. (German biologist Theodor Boveri came to similar conclusions about chromosomes at the same time Sutton was working on his chromosome discovery.)

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Decoding Human DNA

Don Bishop / Getty Images

Junk. Barren. Non-functioning. Dark matter. Thats how scientists had described the 98% of human genome that lies between our 21,000 genes, ever since our DNA was first sequenced about a decade ago. The disappointment in those descriptors was intentional and palpable.

It had been believed that the human genome the underpinnings of the blueprint for the talking, empire-building, socially evolved species that we are would be stuffed with sophisticated genes, coding for critical proteins of unparalleled complexity. But when all was said and done, and the Human Genome Project finally determined the entire sequence of our DNA in 2001, researchers found that the 3 billion base pairs that comprised our mere 21,000 genes made up a paltry 2% of the entire genome. The rest, geneticists acknowledged with unconcealed embarrassment, was an apparent biological wasteland.

But it turns out they were wrong. In an impressive series of more than 30 papers published in several journals, including Nature, Genome Research, Genome Biology, Science and Cell, scientists now report that these vast stretches of seeming junk DNA are actually the seat of crucial gene-controlling activity changes that contribute to hundreds of common diseases. The new data come from the Encyclopedia of DNA Elements project, or ENCODE, a $123 million endeavor begun by the National Human Genome Research Institute (NHGRI) in 2003, which includes 442 scientists in 32 labs around the world.

(MORE: Decoding Cancer: Scientists Release 520 Tumor Genomes from Pediatric Patients)

ENCODE has revealed that some 80% of the human genome is biochemically active. What is remarkable is how much of [the genome] is doing at least something. It has changed my perception of the genome, says Ewan Birney, ENCODEs lead analysis coordinator from the European Bioinformatics Institute.

Rather than being inert, the portions of DNA that do not code for genes contain about 4 million so-called gene switches, transcription factors that control when our genes turn on and off and how much protein they make, not only affecting all the cells and organs in our body, but doing so at different points in our lifetime. Somewhere amidst that 80% of DNA, for example, lie the instructions that coax an uncommitted cell in a growing embryo to form a brain neuron, or direct a cell in the pancreas to churn out insulin after a meal, or guide a skin cell to bud off and replace a predecessor that has sloughed off.

What we learned from ENCODE is how complicated the human genome is, and the incredible choreography that is going on with the immense number of switches that are choreographing how genes are used, Eric Green, director of NHGRI, told reporters during a teleconference discussing the findings. We are starting to answer fundamental questions like what are the working parts of the human genome, the parts list of the human genome and what those parts do.

(MORE: Why Genetic Tests Dont Help Doctors Predict Your Risk of Disease)

If the Human Genome Project established the letters of the human genome, ENCODE is providing the narrative of the genetic novel by fashioning strings of DNA into meaningful molecular words that together tell the story not just of how we become who we are, but how we get sick as well.

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'Junk' DNA: Not So Useless After All

More than three decades ago, 15-year-old Stacy Knappenberger was found fatally beaten and stabbed multiple times inside her Oxnard home. Investigators also suspected she been sexually assaulted in July 1980 attack.

Time and technology finally caught up with the man Oxnard police detectives say killed the A-grade student in the 5300 block of South J Street.

Thursday afternoon, Oxnard police detectives and members of the Ventura County Cold Case Task Force arrested Thomas Young, 65, in Fairfield, Ala., for the murder of Knappenberger. Young was connected to the crime via DNA evidence collected at the time of the killing.

Young lived in the Oxnard area at the time.

We know this is a very emotional day for the family and we hope that this helps in the healing process. We know that they have thought about Stacy every single day since she was killed in 1980," said Oxnard Police Chief Jeri Williams. "Its also a very rewarding day for law enforcement and a tribute to the good work that was put into this case over the past 32 years.

Despite an extensive investigation in 1980, Oxnard detectives developed no suspect information, but in 2000, due to advances in technology, the evidence in this case was reexamined by Oxnard detectives and the DNA evidence was submitted for testing by the Ventura County Sheriffs crime lab.

Williams said in 2010, a DNA hit was made on a suspect through the Combined DNA Index System (CODIS) that contains DNA profiles of arrested and convicted criminal offenders. That suspect was identified as Young.

Following the DNA hit, the case was assigned to the Ventura County Cold Case Task Force. Young was located with the assistance of the sheriffs office in Jefferson County, Ala., and arrested about 2:30 p.m. Thursday under the authority of a Ventura County murder warrant.

Young was booked into the Jefferson County Jail in Birmingham, Ala., for murder and is awaiting extradition to Ventura County.

-- Richard Winton

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DNA leads to arrest in 1980 murder of Oxnard girl

24-05-2012 17:51 We wanted to try something new with this track, hope you guys enjoy it! On Itunes: 'Like' us on Facebook: Follow us on Twitter: Instagram - ChromeCats52

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Chrome Cats - DNA of a Winner(Official Video) - Video