Category Archives: Genome

8 hours ago by Hayley London

Director of Science at The Genome Analysis Centre (TGAC) Federica Di Palma co-authors new genetic study on the naked mole rat's resistance to cancer, identifying key genomic variations that may have contributed to the evolution of this extraordinary species.

The naked mole rat is an exceptionally long-lived and cancer-resistant rodent native to East Africa. The new study presents a higher-quality assembly of the rodent's genetic structure to previous sequences of the species genome, enabling the research community to benefit from this key data.

The study, led by international scientists from TGAC, University of Liverpool, Broad Institute, Uppsala University and Harvard Medical School, re-analysed the naked mole rat genome using the improved assembly that revealed further candidate genes of potential relevance to adaptive changes in the context of aging and cancer.

With a life span of over thirty years, not only is the naked mole rat (Heterocephalus glaber) the longest-lived rodent, but it is also extremely resistant to neoplasia (tumours), and therefore is an ideal model for research on longevity, cancer and disease resistance.

Senior author from the University of Liverpool's Institute of Integrative Biology, Dr Joao Pedro De Magalhaes, said: "The new study provides a fundamental resource for research on the naked mole rat and its many evolutionary adaptations, including longevity and resistance to diseases, as well as other traits (metabolic regulation, development, pain, and behaviour). We predict that studying a species so long-lived (particularly given its small body size) and with such an astonishing resistance to neoplasia, will help elucidate mechanisms and genes conferring longevity and cancer resistance in mammals that may have human applications."

To help facilitate and encourage further research into this fascinating species, the team of scientists have developed a freely-available online portal, the Naked Mole-Rat Genome Resource (www.naked-mole-rat.org), featuring the new genome sequence and the data results of their analysis.

Federica Di Palma, co-author and Director of Science at TGAC, said: "A high-quality, annotated naked mole rat genome is essential for the research community to develop the sophisticated molecular biology tools necessary to study these amazing animals. By creating a genome resource for the naked mole rat with an advanced genome assembly, we aim to facilitate studies into this fascinating animal and help establish the naked mole rat as the first long-lived model for bioscience research underpinning health."

Explore further: Hope for healthy hearts revealed in naked mole rat studies

More information: Michael Keane, Thomas Craig, Jessica Alfldi, Aaron M. Berlin, Jeremy Johnson, Andrei Seluanov, Vera Gorbunova, Federica Di Palma, Kerstin Lindblad-Toh, George M. Church, and Joo Pedro de Magalhes. "The Naked Mole Rat Genome Resource: facilitating analyses of cancer and longevity-related adaptations." Bioinformatics first published online August 28, 2014 DOI: 10.1093/bioinformatics/btu579

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New sequence of naked mole rat genome facilitates cancer resistance research

Full of Excuses ~ I See You Cry ~ The Human Genome
http://www.fullofexcuses.ca.

By: FOETVROCKS

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Full of Excuses ~ I See You Cry ~ The Human Genome - Video

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Genome comparisons reveal the DNA that distinguishes Homo sapiens from its kin

In 1871 Charles Darwin surmised that humans were evolutionarily closer to the African apes than to any other species alive. The recent sequencing of the gorilla, chimpanzee and bonobo genomes confirms that supposition and provides a clearer view of how we are connected: chimps and bonobos in particular take pride of place as our nearest living relatives, sharing approximately 99 percent of our DNA, with gorillas trailing at 98 percent.

Yet that tiny portion of unshared DNA makes a world of difference: it gives us, for instance, our bipedal stance and the ability to plan missions to Mars. Scientists do not yet know how most of the DNA that is uniquely ours affects gene function. But they can conduct whole-genome analyseswith intriguing results. For example, comparing the 33 percent of our genome that codes for proteins with our relatives' genomes reveals that although the sum total of our genetic differences is small, the individual differences pervade the genome, affecting each of our chromosomes in numerous ways.

More in this article: A Monkey's Blueprint

This article was originally published with the title "The 1 Percent Difference."

2014 Scientific American, a Division of Nature America, Inc.

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Secrets of the Universe: Past, Present, Future

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Tiny Genetic Differences between Humans and Other Primates Pervade the Genome

Can genome-editing technology revive the idea of genetically modified livestock?

Four years ago, Scott Fahrenkrug saw an ABC News segment about the dehorning of dairy cows, a painful procedure that makes the animals safer to handle. The shaky undercover video showed a black-and-white Holstein heifer moaning and bucking as a farmhand burned off its horns with a hot iron.

Fahrenkrug, a molecular geneticist then at the University of Minnesota, thought he had a way to solve the problem. He could create cows without horns. He could save farmers money. And by eliminating the dairy industrys most unpleasant secret, he might even score a public relations success for genetic engineering.

The technology Fahrenkrug believes could do all this is called genome editing (see Genome Surgery and Genome Editing). A fast, precise new way of altering DNA, its been sweeping through biotechnology labs. Researchers have used it to change the genes of mice, zebrafish, and monkeys, and it is being tested as way to treat human diseases like HIV (see Can Gene Therapy Cure HIV?).

With livestock, gene editing offers some extraordinary possibilities. At his startup, Recombinetics, located in St. Paul, Minnesota, Fahrenkrug thinks he can create blue-ribbon dairy bulls possessing traits not normally found in those breeds but present in other cattle, such as lack of horns or resistance to particular diseases. Such molecular breeding, he says, would achieve the same effects as nature might, only much faster. In short, an animal could be edited to have the very best genes its species can offer.

That could upend the global livestock industry. Companies could patent these animals just as they do genetically modified soybeans or corn. Entrepreneurs are also ready to challenge the U.S. Food and Drug Administration, which has never approved a GMO food animal. They say gene editing shouldnt be regulated if its used to merely swap around traits within a species. Were talking about genes that already exist in a species we already eat, says Fahrenkrug.

The use of the technology remains experimental and far from the food chain. But some large breeding companies are starting to invest. There may be an opportunity for a different public acceptance dialogue and different regulations, says Jonathan Lightner, R&D chief of the U.K. company Genus, which is the worlds largest breeder of pigs and cattle and has paid for some of Recombinetics laboratory research. This isnt a glowing fish. Its a cow that doesnt have to have its horns cut off.

GMO Bust

To date, GMO food animals have been a complete bust. After the first mice genetically engineered with viral DNA appeared in the 1970s, a parade of other modified animals followed, including sheep that grow extra wool thanks to a mouse gene, goats whose udders made spider silk, and salmon that mature twice as quickly as normal. But such transgenicsanimals incorporating genes from other speciesmostly never made it off experimental farms.

Opponents of genetically modified organisms (GMOs) gathered millions of signatures to stop frankenfoods, and the FDA has held off approving such animals as food. AquaBounty Technologies, the company that made the fast-growing transgenic salmon, has spent 18 years and $70 million trying to get the fish cleared. Two years ago, the University of Guelph, in Ontario, euthanized its herd of enviropigs, engineered with an E. coli gene so they pooped less phosphorus, after giving up hope of convincing regulators.

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On the Horns of the GMO Dilemma

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2-Sep-2014

Contact: Dr. Sibylle Kohlstdt s.kohlstaedt@dkfz.de German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ)

All human cells contain essentially the same DNA sequence their genetic information. How is it possible that shapes and functions of cells in the different parts of the body are so different? While every cell's DNA contains the same construction master plan, an additional regulatory layer exists that determines which of the many possible DNA programs are active. This mechanism involves modifications of genome-bound histone proteins or the DNA itself with small chemical groups (e.g. methylation). It acts on top of the genetic information and is thus called 'epi'-genetic from the corresponding Greek word that means 'above' or 'attached to'.

"Epigenetics has fundamentally changed our view on how the genetic information is used", says Dr. Karsten Rippe from the German Cancer Research Center, who is studying this process with his team. "Epigenetic modifications can be rapidly set or removed to reversibly change cell function. At the same time, epigenetic patterns can be stably inherited through cell division and possibly also to the next generation."

It turns out that deciphering the cell's 'epigenetic code' is a challenging task: Hundreds of proteins in the cell are linked in large networks to 'write', 'erase' or 'read' about 140 different chemical modifications of histone proteins and DNA that have been identified so far. Understanding how epigenetic regulation operates for a specific part of the genome thus requires an integrative approach that considers the connections between different factors. Accordingly, the researchers, together with their colleagues from the DKFZ and the LMU Munich, conducted a comprehensive analysis of a prototypic epigenetic network. They studied how certain DNA sequences were silenced by histone and DNA methylation that would make the genome instable if active and would thus favor cancer development.

Based on maps of epigenetic signals and interactions of proteins with the genome, they developed a mathematical model for epigenetic silencing. "The silencing mechanism we found works much like throwing a loop with a lasso to catch something", says Katharina Mller-Ott, the first author of the study: "Several factors bind the silencing enzyme stably to certain sites in the genome. Because the DNA randomly moves around and forms transient loops, the enzyme hits other regions in the genome nearby, which then become modified and are switched off."

By virtue of their quantitative description of this process, the researchers were able to predict how the silencing network would react in response to perturbations like changes of the abundance of proteins or the activity of the enzymes involved. The scientists in the groups of Karsten Rippe and Thomas Hfer at the DKFZ are now continuing to further develop and apply their model to deregulated epigenetic signaling in leukemia. By evaluating genome-wide maps of epigenetic signals with mathematical models they are identifying tumor-specific changes in cell samples from patients with blood cancer. Furthermore, they are dissecting how epigenetic signals can be used to predict therapy response and how drugs affect the epigenetic program.

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The project was supported by the German Federal Ministry of Education and Research (BMBF).

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Throwing a loop to silence gene expression

John Glass - Digitizing Life Using Synthetic Genomics
Watch on LabRoots at http://labroots.com/user/webinars/details/id/321 In 2010, our team of synthetic biologists announced the creation of a bacterial cell that had a chemically synthesized...

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9 hours ago by Catherine Hockmuth UC San Diego bioengineers have completed the genome sequencing of a particularly harmful strain of E. coli that has been tied to outbreaks of food poisoning. The circular map shows the completed sequence with lighter color regions representing gaps in a 2001 sequencing of the strain that have now been completed with current technology. Credit: The Systems Biology Research Group at UC San Diego.

(Phys.org) Researchers at the University of California, San Diego have produced the first complete genome sequencing of a strain of E. coli that is a common cause of outbreaks of food poisoning in the United States. Although the E. coli strain EDL933 was first isolated in the 1980s, it gained national attention in 1993 when it was linked to an outbreak of food poisoning from Jack-in-the-Box restaurants in the western United States.

Their paper published online Aug. 14 in the journal Genome Announcements reports the full, complete sequence with no gaps. Their analysis includes so-called jumping genes that can move around the same genome, sometimes causing damage to individual genes or enabling antibiotic resistance.

"With a complete genome sequence, we can now pinpoint the precise location of all such elements, which might help to track and treat future outbreaks," said Ramy Aziz, the senior author on the paper. Aziz led the research as a visiting scientist working in Bernhard Palsson's Systems Biology Research Group at UC San Diego Jacobs School of Engineering. Aziz is also a professor at Cairo University in Egypt.

The genome sequence for this historical strain was first published in 2001, but there were many gaps in the genome that could not be closed with the sequencing technology available to scientists in 2001. Given the importance of this strain as a major cause of food poisoning, Palsson's Systems Biology Research Group recently sequenced its genome using a combination of sequencing data from instruments made by Pacific Biosciences and Illumina.

"New sequencing and assembly methods are enabling a full expose of pesky pathogens; there is no place to hide genetic characteristics anymore. The full genetic delineation of multiple pathogenic strains is likely to not only improve our understanding of their characteristics, but to find and exploit their vulnerabilities, said Palsson, the Galletti Professor of Bioengineering at UC San Diego.

Explore further: New models predict where E. coli strains will thrive

More information: Paper: genomea.asm.org/content/2/4/e00821-14.full.pdf

Bioengineers at the University of California, San Diego have used the genomic sequences of 55 E. coli strains to reconstruct the metabolic repertoire for each strain. Surprisingly, these reconstructions do an excellent job of ...

(Phys.org) Bioengineers at the Jacobs School have created a better way to sequence genomes from individual cells. The breakthrough, which relies on microwells just 12 nanoliters in volume (see image), ...

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Scientists sequence complete genome of E. coli strain responsible for food poisoning

Cecile Janssens - Predictive and not understanding the mixed messages of our DNA
Watch on LabRoots at http://labroots.com/user/webinars/details/id/344 When whole genome and whole exome sequencing are introduced into health care, and offered directly to consumers in commercial...

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Matthew Lebo - Genome and exome sequencing in a clinical laboratory
Watch on LabRoots at http://labroots.com/user/webinars/details/id/335 With advances in next-generation sequencing, whole-exome and genome sequencing (WGES) i...

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Matthew Lebo - Genome and exome sequencing in a clinical laboratory - Video

Its a murderer on a killing spree, and now it has a new and remarkably complete genetic mug shot.

An international team of scientists has sequenced the RNA of 99 Ebola virus samples collected during the early weeks of the outbreak in Sierra Leone. The feat, described Thursday in the journal Science, gives researchers a powerful new tool in their effort to contain the deadly virus.

The genome sequence of a virus is the blueprint on which that virus is built, said Pardis Sabeti, the Harvard geneticist who helped oversee the study. Diagnostics are built on knowing that sequence; vaccines are also built using genome sequences. And if you want to build those as best you can, you want to know what the virus looks like today.

Scientists are already scouring that sequence for clues to help them design effective drugs and vaccines. It could take years to find them all, said Sabeti, who studies infectious diseases at Harvard and at the Broad Institute in Cambridge, Mass.

For now, evidence embedded in the RNA reveals that the Ebola virus responsible for killing at least 1,552 people so far originated with a single transmission from an animal to a human in Guinea. It also shows that this lineage, which first emerged in humans in 2013, diverged from other variants of Ebola in 2004.

Sabeti and her team began sequencing Ebola samples in June, just days after the virus was first detected in Sierra Leone on May 25. The results have been available to scientists on the National Center for Biotechnology Informations website since mid-June, almost as soon as the sequencing machines spit them out.We want to enable everyone in the scientific community to look at the genetic sequences at once and crowd-source a solution, she said.

The urgency for better treatments is real for Sabeti and her colleagues. Five of the study co-authors in Sierra Leone have died of Ebola since contributing to the research.

Among them were Dr. Sheik Humarr Khan, who had 10 years experience treating patients who contracted deadly viruses; Mbalu Fonnie, a senior matron of nursing and midwife; lab technician Mohamed Fullah; and nurses Alex Moigboi and Alice Kovoma.

It has been an emotional time for us, said study co-leader Stephen Gire, a research scientist at Harvard and the Broad Institute who studies the evolution of viruses. It makes us want to work harder to get this information out there.

The 99 sequences described in the study were collected from 78 patients seen at Kenema Government Hospital during the first three weeks of the outbreak. Samples were taken twice from some patients, so that researchers could see how the virus mutates in a single person.

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The most complete Ebola genome yet: What it can tell us