From gene to function: Genome wide study into new gene functions in the formation of platelets
In a study into the genetics of blood cell formation, researchers have identified 68 regions of the genome that affect the size and number of platelets. Platelets are small cells that circulate in the blood and are key to the processes of blood clotting and wound healing. In this genome-wide study, the team used a multidisciplinary approach to successfully identify new genetic variants involved in the formation of platelets and more importantly, defined the function of genes near these variants using a series of biological analyses. Abnormally high or low platelet counts can lead to disease. An increase in the number of platelets, or an increase in their size can lead to an increased risk for thrombotic events, like heart attacks and strokes. In this collaborative study, the team first developed a prioritisation strategy that allowed them to identify and pinpoint the genes underlying the formation of platelets through biological annotations of these genes.
Mechanisms cells use to remove bits of RNA from DNA strands
When RNA component units called ribonucleotides become embedded in genomic DNA, which contains the complete genetic data for an organism, they can cause problems for cells. It is known that ribonucleotides in DNA can potentially distort the DNA double helix, resulting in genomic instability and altered DNA metabolism, but not much is known about the fate of these ribonucleotides. A new study provides a mechanistic explanation of how ribonucleotides embedded in genomic DNA are recognized and removed from cells. "We believe this is the first study to show that cells utilize independent repair pathways to remove mispaired ribonucleotides embedded in chromosomal DNA, which can be sources of genetic modification if not removed," said Francesca Storici, an assistant professor in the School of Biology at the Georgia Institute of Technology. The findings were reported Dec. 4, 2011 in the advance online publication of the journal Nature Structural & Molecular Biology.
Cell Cycle & Cytokinesis - BioChemWeb.org
Cell Cycle Regulation and the Control of Cell Proliferation (Cell Growth + Cell Division) Cell Cycle Research - General resource with links to relevant recent literature, news and job listings. (Ion Channel Media Group) Cell Division - Undergraduate-level lectures on cell division. (Cell Biology Lectures, Mark Hill, University of New South Wales, Australia) The Eukaryotic Cell Cycle and Cancer - Introduction to the eukaryotic cell cycle as it relates to the genetics of cancer. (Phillip McClean, North Dakota State University) (Just above Beginner's Level) ICRF FACS Laboratory Cell Cycle Analysis - Methods for cell cycle analysis using flow cytometry. See also the Apoptosis, Cell Senescence and Signal Transduction pages. Mitosis, Meiosis and the Mechanics of Cell Division See also the Cytoskeleton, Cell Motility and Motors page. Cancer Resources See also the Discussion Groups section of the General Resources and Tutorials page. Labs Studying Visits:
Long non-coding RNA prevents the death of maturing red blood cells
A long non-coding RNA (lncRNA) regulates programmed cell death during one of the final stages of red blood cell differentiation, according to Whitehead Institute researchers. This is the first time a lncRNA has been found to play a role in red blood cell development and the first time a lncRNA has been shown to affect programmed cell death. "Programmed cell death, or apoptosis, is very important, particularly in the hematopoietic (blood forming) system, where inhibition of cell death leads to leukemias," says Whitehead Institute Founding Member Harvey Lodish, who is also a professor of biology and a professor of bioengineering at MIT. "We know a lot about the genes and proteins that regulate apoptosis, but this is the first example of a non-coding RNA that plays a role in blood cells. And if an upregulated lncRNA is associated with cancer-cell survival, it may represent a new avenue of attack for therapeutics. LncRNAs were first identified in the 1980s.
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Cancer drug cisplatin found to bind like glue in cellular RNA
An anti-cancer drug used extensively in chemotherapy binds pervasively to RNA -- up to 20-fold more than it does to DNA, a surprise finding that suggests new targeting approaches might be useful, according to University of Oregon researchers. Medical researchers have long known that cisplatin, a platinum compound used to fight tumors in nearly 70 percent of all human cancers, attaches to DNA. Its attachment to RNA had been assumed to be a fleeting thing, says UO chemist Victoria J. DeRose, who decided to take a closer look due to recent discoveries of critical RNA-based cell processes. "We're looking at RNA as a new drug target," she said. The National Institutes of Health- and UO-funded research is detailed in a paper placed online ahead of regular publication in ACS Chemical Biology, a journal of the American Chemical Society. The researchers applied cisplatin to rapidly dividing and RNA-rich yeast cells (Saccharomyces cerevisiae, a much-used eukaryotic model organism in biology).
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Computer assisted design (CAD) for RNA
The computer assisted design (CAD) tools that made it possible to fabricate integrated circuits with millions of transistors may soon be coming to the biological sciences. Researchers at the U.S. Department of Energy (DOE)'s Joint BioEnergy Institute (JBEI) have developed CAD-type models and simulations for RNA molecules that make it possible to engineer biological components or "RNA devices" for controlling genetic expression in microbes. This holds enormous potential for microbial-based sustainable production of advanced biofuels, biodegradable plastics, therapeutic drugs and a host of other goods now derived from petrochemicals. "Because biological systems exhibit functional complexity at multiple scales, a big question has been whether effective design tools can be created to increase the sizes and complexities of the microbial systems we engineer to meet specific needs," says Jay Keasling, director of JBEI and a world authority on synthetic biology and metabolic engineering.
