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Archive - Nov 26, 2012


Watermelon Genome Decoded

Are juicier, sweeter, more disease-resistant watermelons on the way? An international consortium of more than 60 scientists from the United States, China, and Europe has published the genome sequence of watermelon (Citrullus lanatus) — information that could dramatically accelerate watermelon breeding toward production of a more nutritious, tastier, and more disease-resistant fruit. The watermelon genome sequence was published in the November 25, 2012 online version of Nature Genetics. The researchers discovered that a large portion of disease-resistance genes were lost in the domestication of watermelon. With the high-quality watermelon sequence now complete, it is hoped that breeders can now use the information to recover some of these natural disease defenses. The authors reported that the genome of the domesticated watermelon contained 23,440 genes, roughly the same number of genes as in humans. The group compared the genomes of 20 different watermelons and developed a first-generation genetic variation map for watermelon. This information allowed them to identify genomic regions that have been under human selection, including those associated with fruit color, taste, and size. “Watermelons are an important cash crop and among the top five most consumed fresh fruits; however, cultivated watermelons have a very narrow genetic base, which presents a major bottleneck to its breeding. Decoding the complete genome of the watermelon and resequencing watermelons from different subspecies provided a wealth of information and toolkits to facilitate research and breeding,” said Dr. Zhangjun Fei, a scientist at the Boyce Thompson Institute (BTI) for Plant Research at Cornell University, and one of the leaders of this project. Dr. Fei worked with BTI scientists on different aspects of the research, including Dr.

Deciphering Bacterial Doomsday Decisions

As a homeowner prepping for a hurricane, the bacterium Bacillus subtilis uses a long checklist to prepare for survival in hard times. In a new study, scientists at Rice University and the University of Houston uncovered an elaborate mechanism that allows B. subtilis to begin preparing for survival, even as it delays the ultimate decision of whether to “hunker down” and withdraw into a hardened spore. The new study by computational biologists at Rice and experimental biologists at the University of Houston was published online on November 19, 2012 in PNAS. “The gene-expression program that B. subtilis uses to form spores involves hundreds of genes,” said Dr. Oleg Igoshin, lead scientist on the study and professor of bioengineering at Rice. “Many of these genes are known and have been studied for decades, but the exact mechanism that B. subtilis uses to make the decision to form a spore has remained a mystery.” B. subtilis is a common soil bacterium that forms a spore when food runs short. Spore formation involves dramatic changes. The cell first asymmetrically divides within its outer wall, forming one large chamber and one small one. As spore formation progresses, one chamber envelopes the other, which becomes a vault for the organism’s DNA and a small set of proteins that can “reboot” the organism when it senses that outside conditions have improved. B. subtilis is harmless to humans, but some dangerous bacteria like anthrax also form spores. Scientists are keen to better understand the process, both to protect public health and to explore the evolution of complex genetic processes. During spore formation, scientists know that a bacterium channels its energy into producing proteins that help prepare the cell to become a spore.

Possible New Treatment for Ewing Sarcoma

Discovery of a new drug with a high potential to treat Ewing sarcoma, an often deadly cancer of children and young adults, and the previously unknown mechanism behind it, come hand-in-hand in a new study by researchers from Huntsman Cancer Institute (HCI) at the University of Utah. The report appeared November 26, 2012 online in the journal Oncogene. “Ewing sarcoma is almost always caused by a cancer-causing protein called EWS/FLI," said Stephen Lessnick, M.D., Ph.D., director of HCI's Center for Children's Cancer Research, professor in the Department of Pediatrics at the University of Utah School of Medicine, and an HCI investigator. In the lab, Dr. Lessnick and his colleagues found that an enzyme, called lysine-specific demethylase (LSD-1), interacts with EWS/FLI to turn off gene expression in Ewing sarcoma. By turning off specific genes, the EWS/FLI-LSD1 complex causes Ewing sarcoma development. "This makes LSD-1 an important target for the development of new drugs to treat Ewing sarcoma," Dr. Lessnick said. "For a long time, we've known that EWS/FLI works by binding to DNA and turning on genes that activate cancer formation," said Dr. Lessnick. "It was a surprise to find out that it turns genes off as well. The beauty, if there's anything beautiful about a nasty disease like this, is that if we can inhibit EWS/FLI, we can inhibit this cancer, because EWS/FLI is the master regulator of Ewing sarcoma," Dr. Lessnick added. While Dr.