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Synthesizing a Genome from Scratch

In a technical tour de force, scientists at the J. Craig Venter Institute, in Rockville, MD, have synthesized the genome of the bacterium Mycoplasma genitalium entirely from scratch. The feat is a stepping stone in creating precisely engineered microbial machines capable of generating biofuels and performing other useful functions.

"It really is groundbreaking that you can synthetically build a genome for a bacterium," says Chris Voigt, a synthetic biologist at the University of California, San Francisco, who was not involved in the project. "It's bigger by orders of magnitude than what's been done before."

Biologists creating genetically engineered organisms now routinely order pieces of DNA that are 10,000 to 20,000 base pairs long--big enough to incorporate the genes for a single metabolic pathway. That allows researchers to engineer microbes that can perform specific tasks, but the ability to synthesize entire genomes could grant a whole new level of control over biological design. (See "Tumor-KillingBacteria.")

In the new study, scientists ordered 101 DNA fragments, encompassing the entire Mycoplasma genome, from commercial DNA synthesis companies. These fragments were designed so that each overlapped its neighboring sequence by a small amount; these overlapping stretches stick together, thanks to the chemical properties of DNA. Researchers then bound the fragments piece by piece, eventually generating the full 582,970 base pair Mycoplasma sequence. The findings were published Thursday in the online edition of Science.

http://www.technologyreview.com/Biotech/20112/

Evolution of human genome's 'guardian' gives people unique protections from DNA damage

Human evolution has created enhancements in key genes connected to the p53 regulatory network - the so-called guardian of the genome - by creating additional safeguards in human genes to boost the network's ability to guard against DNA damage that could cause cancer or a variety of genetic diseases, an international team of scientists led by Cincinnati Children's Hospital Medical Center writes in the Jan. 22 Proceedings of the National Academy of Sciences. Because genetically engineered mouse models are increasingly powerful tools in understanding the risks and mechanisms of human diseases - and rodents do not have the same evolution-based safeguards in p53 function as humans - the study also underscores the need for additional considerations in the interpretation of research using rodent models.

"Our findings are especially important because rodents are often used as model organisms to investigate the genetic origins of diseases that affect humans, such as cancer investigators evaluating the impact of DNA-damaging agents," said Anil Jegga, DVM, a researcher in the Division of Biomedical Informatics at Cincinnati Children's. "Rodent models remain important to our understanding of disease processes, although our study suggests the need to address experimentally the differences in p53 regulatory pathways between humans and rodent models."

In the study, Jegga and his colleagues used comparative functional genomics to look systematically at small DNA sequences associated with the promoters, or enhancers, of specific genes that carry out orders from p53. These promoter elements act like antennae - responding to activated p53 by boosting target gene expression and function inside a cell's nucleus. By comparing these response elements across nearly 50 different binding sites of genes in the p53 network, and looking specifically at genes that repair DNA damage in 14 species (from zebra fish to humans), researchers were able to reveal critical evolutionary changes in their function. The 14 species represented an estimated 500 million years of evolutionary separation, helping investigators determine how the function of p53 response elements was conserved or changed as different species developed. Dr. Jegga said researchers were surprised to find the acquisition of functional response for certain genes involved in DNA metabolism or repair to be mostly unique in humans. While the functional ability of some genes is shared with chimpanzees and rhesus monkeys, researchers said DNA metabolism and repair function it is not shared at all with rodents.

In humans, when DNA damage is detected, the p53 network seems to have gained additional capabilities that allow it to slow cell growth, initiate repairs or, if needed, apoptotic cell death. Apoptotic, or programmed cell death capability in the p53 network, is thought to be evolutionarily conserved throughout the development of vertebrate species and was probably established after the divergence of vertebrates and non-vertebrates. DNA metabolism and repair capabilities controlled by p53 may have emerged more recently in evolutionary history to create primate-specific response characteristics, the researchers explained.

http://www.brightsurf.com/news/headlines/35373/Evolution_of_human_genomes_guardian_gives_people_unique_protections_from_DNA_damage.html

Pancreatic Stem Cells in Adult Mice Are Similar to Their Embryonic Counterpart

Researchers discovered that adult mice pancreas harbor stem cells with the capacity to generate new insulin-producing beta cells. “One of the most interesting characteristics of these adult progenitor cells is that they are almost indistinguishable from embryonic progenitors,” says Harry Heimberg, M.D., Ph.D., of the JDRF Center at Vrije Universiteit Brussel. “In terms of their structure and gene expression, there are no major differences. They look and behave just like embryonic beta cell progenitors.”

In the new study, Dr. Heimberg’s team tied off a duct that drains digestive enzymes from the pancreas. That injury led to a doubling of beta cells in the pancreas within two weeks. The animals’ pancreases also began producing more insulin, evidence that the new beta cells were fully functional, Dr. Heimberg explains. He suspects the regenerative process is sparked by an inflammatory response in the enzyme-flooded pancreas.

They further found that the production of new beta cells depends on a gene called Neurogenin 3 (Ngn3), which is known to play a role in the pancreas during embryonic development.

http://www.genengnews.com/news/bnitem.aspx?name=29390546