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Archive - Feb 19, 2018


Genome of Asexually Reproducing Amazon Molly Fish Sequenced

No species is immune from the suffering of unrequited love, but scientists expect to learn volumes about the biological basis of sex from the newly sequenced genome of an all-female, asexual Texas native - the Amazon molly - that has thrived over millennia. The fresh waters along the Texas-Mexico border serve as home to this evolutionary anomaly - a fish that has flourished by defying nature's odds to reproduce asexually through a natural form known as parthenogenesis in which growth and development of embryos occurs without fertilization, resulting only in daughters that are true clones of their mothers. Texas A&M University Hagler Institute for Advanced Study (HIAS) Faculty Fellow Dr. Manfred Schartl led the international team that recently sequenced the first Amazon molly genome and the genomes of the original parental species that created this unique fish in an effort to better understand how its reproduction deviates from the male-female sexual norm and why the Amazon molly as a species has fared so well in the process. The findings from their National Institutes of Health-funded research were published online on February 12, 2018 in Nature Ecology & Evolution. The open-access article is titled” Clonal Polymorphism and High Heterozygosity in the Celibate Genome of the Amazon Molly.” "The existence of two sexes, male and female, is one of the oldest and most widespread phenomena in biology," says Dr. Schartl, a world leader in cellular and molecular biology of Xiphophorus model systems, including platyfish and swordtails. "Studies on the exceptional case of asexuality helps us to better understand the biological meaning and evolution of sex." Animals that reproduce asexually are rare, compared to the overwhelming majority of species that exist as males and females and reproduce sexually.

Ancient Fused Gene Offers Insight into How Mosses Build Cell Walls

Researchers have identified a fused gene in moss that provides insight into how moss cells build their external walls. The same discovery raises questions about the one-of-a-kind gene that codes for two distinct proteins that participate in two distinct functions. The research team identified the novel gene, known as For1F, while studying exocytosis. Exocytosis is the process by which cells secrete packets of protein and carbohydrates outside their membranes to support extracellular processes like the construction of cell walls. The gene discovered in the research couples the exocytosis-regulating protein Sec10 with formin, a protein that regulates the remodeling of the actin cytoskeleton critical to forming cell shapes. The new study also shows that the gene fusion occurred early in moss evolution and has been retained for more than 170 million years. "We were surprised to find this fused gene in the moss genome," said Magdalena Bezanilla, PhD, the Ernest Everett Just 1907 Professor of Biology at Dartmouth College. "Through our research, we know that the analysis is correct; now it will be interesting to explore the advantage of this coupling of proteins." Dr. Bezanilla led a team at Dartmouth and the University of Massachusetts-Amherst to conduct the study. The research was published online on January 26, 2018 in the Journal of Cell Biology. The article is titled “An Ancient Sec10–Formin Fusion Provides Insights into Actin-Mediated Regulation of Exocytosis.” Once For1F was observed, Dr. Bezanilla and her team set out to determine how unique this particular conjoined arrangement is. By consulting the database of the 1000 Genomes Project, the researchers found that the fused gene was evident in many diverse species of mosses, but not in other plants.

Progress Reported in Using CRISPR/Cas9 Editing to Correct Sickle Cell Mutation

Scientists have successfully used gene editing to repair 20 to 40 percent of stem and progenitor cells taken from the peripheral blood of patients with sickle cell disease, according to Rice University bioengineer Gang Bao., PhD. Dr. Bao, in collaboration with colleagues at the Baylor College of Medicine, Texas Children's Hospital, and Stanford University, is working to find a cure for the hereditary disease. A single DNA mutation causes the body to make sticky, crescent-shaped red blood cells that contain abnormal hemoglobin and can block blood flow in limbs and organs. In his talk on February 16, 2018 at the annual American Association for the Advancement of Science (AAAS) meeting ( in Austin, Texas, Dr. Bao revealed results from a series of tests to see whether CRISPR/Cas9-based editing can fix the mutation. His presentation was part of a scientific session titled "Gene Editing and Human Identity: Promising Advances and Ethical Challenges." ( "Sickle cell disease is caused by a single mutation in the beta-globin gene (in the stem cell's DNA)," Dr. Bao said. "The idea is to correct that particular mutation, and then stem cells that have the correction would differentiate into normal blood cells, including red blood cells. Those will then be healthy blood cells." Dr. Bao's lab collaborated with Dr. Vivien Sheehan, an Assistant Professor of Pediatrics and Hematology at Baylor and a member of the Sickle Cell Program at Texas Children's, to collect stem and progenitor cells (CD34-positive cells) from patients with the disease. These cells were then edited in the Bao lab with CRISPR/Cas9 together with a custom template, a piece of DNA designed to correct the mutation.