Category Archives: Genome

Maintaining the stability and the correct sequence of our genetic information is vital to the accurate transmission of our genetic code. However, in the course of replicating, our DNA frequently runs into roadblocks, arising from both internal and external sources, that threaten the fidelity of our genetic information. The accurate processing of these roadblocks is paramount to genome integrity. Defects in this process can lead to cancer, genetic problems and premature aging.

In a research paper published in the Journal of Cell Biology, Alessandro Vindigni, Ph.D., professor in the Edward A. Doisy Department of Biochemistry and Molecular Biology at Saint Louis University, shares a discovery that explains how cells use a process called replication fork reversal in order to deal with these roadblocks and transmit accurate genetic data.

Lesions in DNA can occur as often as 100,000 times per cell per day. They can be the result of normal metabolic activities, like free radicals, as well as exposure to environmental factors such as UV radiation, X-rays and chemical compounds.

Improper repair of DNA lesions can lead to mutations, abnormal chromosome structures, or loss of genetic information that in turn can cause premature aging, cancer, and genetic abnormalities.

Depending on the degree of genome instability, these alterations will determine whether a cell survives, goes into a growth-arrest state, or dies.

If the cell's replication machinery collides with the lesion, a strand break can occur.

"If these strands are not repaired properly, the cell may simply die," Vindigni said. "Or, growth may be permanently interrupted.

"Or, a serious lesion may be tolerated and the cell will continue to replicate. This may or may not be a good decision, as this can lead to cancer. It is the degree of genomic instability caused by the lesion that will determine whether the cell will survive."

While these scenarios pose serious threats, our cells have evolved elegant mechanisms to cope, Vindigni says.

DNA replicates by unzipping its two interwoven strands and making copies of each. As the DNA strands separate and copy, they form a "replication fork." Sometimes, these forks run into obstacles -- like the lesions described above -- that block their progress. When they do, cells often perform a maneuver called fork reversal.

View original post here:
High fidelity: Researcher finds keys to genome

IMAGE:Saint Louis University research team: Shivasankari Gomathinayagam, Alessandro Vindigni, Monica Carron, Megan Fabry, Denisse Carvajal, Galyna Yakymechko, Matteo Berti, Saravanabhavan Thangavel. view more

Credit: Saint Louis University

ST. LOUIS - Maintaining the stability and the correct sequence of our genetic information is vital to the accurate transmission of our genetic code. However, in the course of replicating, our DNA frequently runs into roadblocks, arising from both internal and external sources, that threaten the fidelity of our genetic information. The accurate processing of these roadblocks is paramount to genome integrity. Defects in this process can lead to cancer, genetic problems and premature aging.

In a research paper published in the Journal of Cell Biology, Alessandro Vindigni, Ph.D., professor in the Edward A. Doisy Department of Biochemistry and Molecular Biology at Saint Louis University, shares a discovery that explains how cells use a process called replication fork reversal in order to deal with these roadblocks and transmit accurate genetic data.

Lesions in DNA can occur as often as 100,000 times per cell per day. They can be the result of normal metabolic activities, like free radicals, as well as exposure to environmental factors such as UV radiation, X-rays and chemical compounds.

Improper repair of DNA lesions can lead to mutations, abnormal chromosome structures, or loss of genetic information that in turn can cause premature aging, cancer, and genetic abnormalities.

Depending on the degree of genome instability, these alterations will determine whether a cell survives, goes into a growth-arrest state, or dies.

If the cell's replication machinery collides with the lesion, a strand break can occur.

"If these strands are not repaired properly, the cell may simply die," Vindigni said. "Or, growth may be permanently interrupted.

"Or, a serious lesion may be tolerated and the cell will continue to replicate. This may or may not be a good decision, as this can lead to cancer. It is the degree of genomic instability caused by the lesion that will determine whether the cell will survive."

Go here to read the rest:
High fidelity: SLU researcher finds keys to genome integrity

Kreidezeit 129: Genome Editing
Dank neuer gentechnischer Werkzeuge lassen sich Abschnitte im Erbgut gezielt und przise verndern. Wie genau das funktioniert, erklrt Jan Wolkenhauer in der Kreidezeit-Folge Genome Editing.

By: biotechgermany

View original post here:
Kreidezeit 129: Genome Editing - Video

Genome editing with the CRISPR-Cas9 system
This online module serves as preparation for the FGTB Next-Generation Technologies Bootcamp at the ATVB|PVD 2015 Scientific Sessions on May 8, 2015. This module is a general introduction to...

By: AHAScienceNews

Read this article:
Genome editing with the CRISPR-Cas9 system - Video

Major Scientific Stragies of Human Genome Project

By: Genome Gyan

Read more:
Major Scientific Stragies of Human Genome Project - Video

Lala Daidai Genome
I valued to sing this song, I hope you #39;ll like it ~ ~ Credits ~ Title : (Daidai Genome) Original vocals : Hatsune Miku Append Music, Lyrics : mezame-P Illustration : F*cla Video...

By: Lala

Read more from the original source:
Lala Daidai Genome - Video

Whole genome sequencing should not be confused with DNA profiling. We ofer WGS.
Whole genome sequencing (also known as full genome sequencing, complete genome sequencing, or entire genome sequencing) is a laboratory process that determines the complete DNA sequence ...

By: Torsten Kunert

Read more here:
Whole genome sequencing should not be confused with DNA profiling. We ofer WGS. - Video

Download The Developing Genome An Introduction to Behavioral Epigenetics PDF
Download PDF Here: http://bit.ly/1NWnw78.

By: ozi rohman

More:
Download The Developing Genome An Introduction to Behavioral Epigenetics PDF - Video

Researchers are looking in the wrong place: White people live longer not because of their DNA but because of inequality.

On April 24, 2003, shortly after the completion of the human genome project, its director Francis Collins and his team posed 15 grand challenges to the scientific community. They dared researchers to harness the genome to crack puzzles of biology, health, and society. In particular, they called for genome-based tools to close health disparities. Since then, the United States has pumped more than $1 billion a year into genomics research. What do we have to show for it?

What we found in the literature published from 2007 to 2013 was basically nothing, said Jay Kaufman, the lead author of the first study to examine available genetic data for evidence that explains a major racial health disparity. For many years, researchers speculated that what they couldnt explain about disparities must be the fingerprint of some mysterious genetic component. But since they are now able to scan the entire genome, this speculation appears both lazy and wrong. When it comes to why many black people die earlier than white people in the U.S., Kaufman and his colleagues show we've been looking for answers in the wrong places: We shouldn't be looking in the twists of the double helix, but the grinding inequality of the environment.

It is no secret that a longer life is a white privilege in the U.S. In 2011, the Centers for Disease Control and Prevention (CDC) reported that white men lived more than four years longer than black men, and white women lived more than three years longer than black women. The main reason for the racial mortality gap is heart disease. Theres a huge number of years of life lost because some people have the black life expectancy and not the white life expectancy, Kaufman said. Its killing people prematurely on the basis of race.

To understand if there is any genetic reason for these deaths, Kaufmans team reviewed six years of genome-wide studies of cardiovascular disease. Having crawled across the genome for every possible variant that could trigger deadlier disease, they only found three that fit the billand two of them suggested that whites, not blacks, should be on the suffering side of the disparity. Were spending a huge amount of money on these studies, he said, but if you are interested in understanding disparities, all this money thats been spent has come up with basically nothing.

Maybe this finding isnt entirely earth-shattering. After all, it is almost universally agreed that race is a social construct. In 2005, only two years after the sequencing of the human genome, the editors of Nature Biotechnology put it like this: Pooling people in race silos is akin to zoologists grouping raccoons, tigers, and okapis on the basis that they are all stripey. Perhaps, then, the better question is: Why do we continue to search for a connection between race and genetics to explain health disparities?

One reason has less to do with biology and more to do with finances. Take BiDil, the first race-specific medication, which made a cameo on House, M.D. BiDil is a combination of two generic drugs for heart failure that have been on the scene for decades. In 2005, the Food and Drug Administration approved the old drugs for a new purpose: the treatment of heart failure in a single race, African Americans. Jonathan Kahn, author of Race in a Bottle, has written extensively on the history of this medication. There is no doubt that BiDil works for African Americans. The sleight of hand, Kahn points out, is that the clinical trial for the drugs approvalthe African American Heart-Failure Trialhad no comparison group. Researchers only studied BiDil in African Americans. The drug likely worked not because they are black, but because they are human. But the juicier claim is that NitroMed, the company behind BiDil, was able to extend its patent to 2020, which otherwise would have expired in 2007. The magic touch was the race-specific label, which made the old method new again.

Another reason for the persistence of race and genetics in biomedical research is much more subtle. Certain diseases cluster in populations, such as Tay-Sachs, which is most common in people with an Ashkenazi Jewish background. In such cases, some researchers say we should turn our attention away from race and toward ancestry. If it is true that there are differences in disease risk between human groups, then what we need is a more clever way to dice up humanity. It has nothing to do with race, it has more to do with ancestry, explained Rick Kittles, the director of the Center for Population Genetics at the University of Arizona and co-founder of African Ancestry, Inc. We talk about ancestry, we talk about shared genetic backgrounds. That is a better proxy for biology than race. If someone says theyre of Ashkenazi Jewish ancestry, and they have a family history of Tay-Sachs, thats not because of a race. Thats because of shared ancestry. If a person of West African descent has a family history of prostate cancer, thats a shared genetic background.

But this only takes us in a circle. Even when researchers study ancestry, it is often just race in a phony moustache and glasses. Take the creation of ancestry informative markers (AIMs). They are a collection of genetic variants between four populations: Europeans, West Africans, Indigenous Americans, and East Asians. They are used for both the sort of recreational ancestry mapping that promises to uncover roots and to understand disease risk. In 2007, an article in Science magazine with 14 co-authors, including Kaufman, pointed out some of the problems with this model: People from the Middle East and India are classified as Native American, even though no archaeological, genetic, or historical evidence supports this suggestion, and East Africans are left out of the mix entirely.

Duana Fullwiley, an anthropologist at Stanford, took an even closer look at how AIMs were dreamed up and used in the laboratories of some prominent researchersMark Shriver at Penn State and Esteban Gonzlez Burchard at UCSF. What she found is that this new system is no better than a find-and-replace of race with ancestry. In one striking example, she unearthed a patent application that straight-up defines biogeographical ancestry as simply the heritable component of race. In her 2008 article, The Biologistical Construction of Race, Fullwiley concludes that the very continents and peoples chosen for this product were selected due to their perceived proximity to what we in North America imagine race to be.

The rest is here:
Genes Don't Cause Racial Health Disparities, Society Does

Patenting the Human Genome: A PSA
I created this video with the YouTube Video Editor (http://www.youtube.com/editor)

By: fastrusting2014

View post:
Patenting the Human Genome: A PSA - Video