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Acquired traits can be inherited via small RNAs

Acquired traits can be inherited via small RNAs
Columbia University Medical Center (CUMC) researchers have found the first direct evidence that an acquired trait can be inherited without any DNA involvement. The findings suggest that Lamarck, whose theory of evolution was eclipsed by Darwin's, may not have been entirely wrong. The study is slated to appear in the Dec. 9 issue of Cell. "In our study, roundworms that developed resistance to a virus were able to pass along that immunity to their progeny for many consecutive generations," reported lead author Oded Rechavi, PhD, associate research scientist in biochemistry and molecular biophysics at CUMC. In an early theory of evolution, Jean Baptiste Larmarck (1744-1829) proposed that species evolve when individuals adapt to their environment and transmit those acquired traits to their offspring. However, some evidence suggests that acquired traits can be inherited. Dr. RNAi is triggered by doubled-stranded RNA (dsRNA), which is not found in healthy cells. Related:  Genetics 1

The Illustrated Guide to Epigenetics Illustrations by Joe Kloc This month marks the ten-year anniversary of the sequencing of the human genome, that noble achievement underpinning the less noble sales of 23andMe's direct-to-consumer genetic tests. To commemorate the scientific occasion, we've created an illustrated introduction to one subfield of genetics likely to produce even more dubious novelty science projects someday: epigenetics. What is epigenetics? Human life begins as a single cell equipped with all of the genetic information—known as the genome—it will need to develop into a full-grown adult. FIGURE 1: Through a process called mitosis, a single cell (A) splits into two cells (B) with identical genetic information. FIGURE 2: DNA coils around proteins called histones, forming a nucleosome. How does the epigenome work? Molecular "caps" called methyl groups can be attached to genes in order to effectively block them from giving instructions to the cell (FIGURE 3). Where do the different epigenomes come from?

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.

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.

The Ductile Helix: "Jumping Genes" May Influence Brain Activity Mobile DNA molecules that jump from one location in the genome to another may contribute to neurological diseases and could have subtle influences on normal brain function and behavior, according to a study published October 30 in Nature. (Scientific American is part of Nature Publishing Group.) Retrotransposons are mobile genetic elements that use a copy-and-paste mechanism to insert extra copies of themselves throughout the genome. Researchers from the Roslin Institute in Edinburgh, Scotland, have now comprehensively mapped retrotransposon insertion sites in the genomes of normal human brain cells for the first time. They used state-of-the-art DNA sequencing technology to screen for retrotransposons in tissue samples taken postmortem from three individuals who were healthy when alive and had no neurological disease or signs of abnormality in their brain tissue. "Each sample had its own set of unique retrotransposition events," senior author Geoffrey Faulkner says.

Cell Cycle & Cytokinesis - 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:

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).

Synthetic RNA lessens severity of fatal disease A team of University of Missouri researchers have found that targeting a synthetic molecule to a specific gene could help the severity of the disease Spinal Muscular Atrophy (SMA) -- the leading genetic cause of infantile death in the world. "When we introduced synthetic RNA into mice that carry the genes responsible for SMA, the disease's severity was significantly lowered," said Chris Lorson, researcher at the Bond Life Sciences Center and professor in the Department of Veterinary Pathobiology and the Department of Molecular Microbiology and Immunology. "The mice that receive synthetic RNA gain more weight, live longer, and had improvements in motor skills. These results are very exciting." SMA is a rare genetic disease that is inherited by one in 6,000 children, who often die young because there is no cure. While the results are promising, Lorson notes additional research is needed before synthetic RNA could be used on humans for SMA.