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Archive - Sep 21, 2015

Genes from Parasitic Wasps Are Present in Many Butterflies Following Integration of Wasp-Associated Bracoviruses into Butterfly Genomes During Parasitization Process

Research teams from the University of Valencia in Spain and the University of Tours in France have discovered that genes originating from parasitic wasps are present in the genomes of many butterflies. These genes were acquired through a wasp-associated virus that integrates into DNA. Wasp genes have now been domesticated and likely play a role in in protecting butterflies against other pathogenic viruses. These results, published online in the open-access journal PLOS Genetics on September 17, 2015, reveal that butterflies, including the Monarch, an iconic species for naturalists and well-known for its spectacular migrations, constitute naturally produced genetically modified organisms (GMOs) during the course of evolution. This finding “relativizes” the novelty of producing GM insects, because such insects already exist in nature, but also highlights that genes introduced in GM insects can be transferred between distant species. The PLOS Genetics article is titled “Recurrent Domestication by Lepidoptera of Genes from Their Parasites Mediated by Bracoviruses.” To reproduce, braconid wasps lay their eggs inside caterpillars and inject a “giant virus” named bracovirus to circumvent the caterpillars' immune response. Bracoviruses can integrate into the DNA of parasitized caterpillars and control caterpillar development, enabling wasp larvae to colonize their host. Bracovirus genes can be detected in the genomes of several species of butterfly and moth, including the famous Monarch (Danaus plexippus), the silkworm (Bombyx mori), and insect pests such as the Fall Armyworm (Spodoptera frugiperda) and the Beet Armyworm (Spodoptera exigua).

Modular System of Zinc Finger Proteins, Inteins, and Exteins Can Detect Any Particular DNA Sequence in Cells and Trigger a Specific Response Such As Cell Death

MIT biological engineers have developed a modular system of proteins that can detect a particular DNA sequence in a cell and then trigger a specific response, such as cell death. This system can be customized to detect any DNA sequence in a mammalian cell and then trigger a desired response, including killing cancer cells or cells infected with a virus, the researchers say. “There is a range of applications for which this could be important,” says Dr. James Collins, the Termeer Professor of Medical Engineering and Science in MIT’s Department of Biological Engineering and Institute of Medical Engineering and Science (IMES). “This allows you to readily design constructs that enable a programmed cell to both detect DNA and act on that detection, with a report system and/or a respond system.” Dr. Collins is the senior author of an article published online on September 21, 2015 in Nature Methods paper describing the technology, which is based on a type of DNA-binding proteins known as zinc fingers. The article is titled “DNA Sense-and-Respond Protein Modules for Mammalian Cells.” These zinc finger proteins can be designed to recognize any DNA sequence. “The technologies are out there to engineer proteins to bind to virtually any DNA sequence that you want,” says Dr. Shimyn Slomovic, an IMES postdoc and the paper’s lead author. “This is used in many ways, but not so much for detection. We felt that there was a lot of potential in harnessing this designable DNA-binding technology for detection.” To create their new system, the researchers needed to link zinc fingers’ DNA-binding capability with a consequence — either turning on a fluorescent protein to reveal that the target DNA is present or generating another type of action inside the cell.

Epicardial Protein FSTL1 Stimulates Heart Muscle Regeneration and Scarring Reduction Following Heart Attack; FSTL1 Patch Implanted in Heart Improves Cardiac Function and Survival Rates in Animal Models; Team Working Toward 2017 Human Clinical Trials

An international team of researchers has identified a protein that helps heart muscle cells regenerate after a heart attack. Researchers also showed that a patch loaded with the protein and placed inside the heart improved cardiac function and survival rates after a heart attack in mice and pigs. Animal hearts regained close to normal function within four to eight weeks after treatment with the protein patch. It might be possible to test the patch in human clinical trials as early as 2017. The team, led by Professor Pilar Ruiz-Lozano at Stanford University and including researchers from the University of California, San Diego (UC San Diego) and Sanford Burnham Prebys Medical Discovery Institute (SBP), published its findings online on September 16, 2015 in Nature. The article is titled “Epicardial FSTL1 Reconstitution Regenerates the Adult Mammalian Heart.” "We are really excited about the prospect of bringing this technology to the clinic," said Dr. Mark Mercola, Professor of Bioengineering at UC San Diego and Professor in the Development, Aging, and Regeneration Program at SBP. "It's commercially viable, clinically attractive, and you don't need immunosuppressive drugs." High-throughput technology in Dr. Mercola's lab was critical in identifying a natural human protein, called follistatin-like 1 (FSTL1), and showing that it can stimulate cultured heart muscle cells to divide. Researchers, led by Dr. Ruiz-Lozano, at Stanford embedded the protein in a patch and applied it to the surface of mouse and pig hearts that had undergone an experimental form of myocardial infarction or "heart attack." Remarkably, FSTL1 caused heart muscle cells already present within the heart to multiply and re-build the damaged heart and reduce scarring.