Daily Archives: September 2, 2014

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.

Read more from the original source:
On the Horns of the GMO Dilemma

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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

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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