Researchers are clarifying epigenetic intricacies such as missing heritability, disease markers, methylated proteins, and imprinted genes. Learn about the history of epigenetics in this timeline spanning 130 years.
The striking differences between humans and chimps aren’t so much in the genes we have, which are 99 percent the same, but in the way those genes are used, according to new research from a Duke University team.
It’s rather like the same set of notes being played in very different ways.
In two major traits that set humans apart from chimps and other primates – those involving brains and diet – gene regulation, the complex cross-talk that governs when genes are turned on and off, appears to be significantly different.
Three Boston University biomedical engineers have created a genetic dimmer switch that can be used to turn on, shut off, or partially activate a gene’s function. Professor James Collins, Professor Charles Cantor and doctoral candidate Tara Deans invented the switch, which can be tuned to produce large or small quantities of protein, or none at all
This switch helps advance the field of synthetic biology, which rests on the premise that complex biological systems can be built by arranging components or standard parts, as an electrician would to build an electric light switch. Much work in the field to date uses bacteria or yeast, but the Boston University team used more complex mammalian cells, from hamsters and mice. The switch has several new design features that extend possible applications into areas from basic research to gene therapy.
Over 30% of our genes are under the control of small molecules called microRNAs. They prevent specific genes from being turned into protein and regulate many crucial processes like cell division and development, but how they do so has remained unclear. Now researchers from the European Molecular Biology Laboratory (EMBL) have developed a new method that uncovered the mode of action of microRNAs in a test tube. The study, which is published in the current online issue of Nature, reveals that microRNAs block the initiation of translation, the earliest step in the process that turns genetic information stored on messenger RNAs into proteins.
Continue reading “Mechanism of microRNAs deciphered”
The last few years have been very good to ribonucleic acid (RNA). Decades after DNA took biology by storm, RNA was considered little more than a link in a chain–no doubt a necessary link, but one that, by itself, had little to offer. But with the discoveries of RNA interference and microRNAs, this meager molecule has been catapulted to stardom as a major player in genomic activity.
Now, a team of scientists led by David Bartel, a professor in MIT’s Department of Biology, has discovered an entirely new class of RNA molecules.
Dana-Farber Cancer Institute researchers have developed a powerful method for charting the positions of key gene-regulating molecules called nucleosomes throughout the human genome. The mapping tool could help uncover important clues for understanding and diagnosing cancer and other diseases, the scientists say. Moreover, it may shed light on the role of nucleosomes in the process of “reprogramming” an adult cell to its original embryonic state, which is a critical operation in cloning.
Continue reading “Scientists map key landmarks in human genome”
A two-step process appears to regulate cell fate decisions for many types of developing cells, according to researchers from the University of Chicago.
This finding sheds light on a puzzling behavior. For some differentiating stem cells, the first step leads not to a final decision but to a new choice. In response to the initial chemical signal, these cells take on the genetic signatures of two different cell types. It often requires a second signal for them to commit to a single cellular identity.
In the Aug. 25 2006 issue of Cell, the researchers, working with hematopoietic stem cells, which give rise to the many types of blood cells, show how “pioneer transcription factors” trigger the first step, pushing these stem cells towards this mixed lineage, midway between two related cell types — in this case between a macrophage and a neutrophil.
Continue reading “Researchers map out networks that determine cell fate”
An organelle called the nucleolus resides deep within the cell nucleus and performs one of the cell’s most critical functions: it manufactures ribosomes, the molecular machines that convert the genetic information carried by messenger RNA into proteins that do the work of life.
Gary Karpen and Jamy Peng, researchers in the Life Sciences Division of the Department of Energy’s Lawrence Berkeley National Laboratory, have now discovered two pathways that regulate the organization of the nucleolus and other features of nuclear architecture, maintaining genome stability in the fruit fly Drosophila melanogaster.
Continue reading “Regulating the nuclear architecture of the cell”
The gene, called GATA-3, is in a family of genes that guides development of stem cells into mature cells. University of California, San Francisco researchers have now found that GATA-3 is also required for mature mammary cells to remain mature in the adult. In research focusing on mice mammary glands, they found that without GATA-3, mature cells revert to a less specialized, “undifferentiated” state characteristic of aggressive cancer.
The new finding suggests that this gene may play a key role in the development of breast cancer, the scientists report in the December 1 issue of the journal CELL.
Continue reading “‘Cancer prognosis gene’ found to control the fate of breast cells”
A jumping gene first identified in a cabbage-eating moth may one day provide a safer, target-specific alternative to viruses for gene therapy, researchers say.
They compared the ability of the four best-characterized jumping genes, or transposons, to insert themselves into a cell’s DNA and produce a desired change, such as making the cell resistant to damage from radiation therapy.
They found the piggyBac transposon was five to 10 times better than the other circular pieces of DNA at making a home and a difference in several mammalian cell lines, including three human ones.
Continue reading “Jumping gene could provide non-viral alternative for gene therapy”
Scientists have completed the first draft of the genetic code for breast and colon cancers. Their report, published online in the September 7 issue of Science Express, identifies close to 200 mutated genes, now linked to these cancers, most of which were not previously recognized as associated with tumor initiation, growth, spread or control.
Osteoporosis, a disease characterized by a decrease in bone mass and density and which makes people more susceptible to bone fractures and deformities, afflicts some 10 million Americans over the age of 50. Researchers at the Harvard School of Public Health (HSPH) have discovered that eliminating a protein, Schnurri-3 (Shn3), in mice led to profound increases in bone mass throughout their skeletal system. The results may have implications for the treatment of osteoporosis. The study was published in the May 26 edition of Science.
Researchers at Dana-Farber Cancer Institute report that a common "oncogene engine" – a small family of malfunctioning cell growth switches – drives several seemingly unrelated, lethal forms of cancer, including malignant melanoma. The finding suggests that it may be possible to attack these different cancers with the same therapy.
Scientists eager to help develop a new generation of pharmaceuticals are studying cellular proteins called transcription factors, which bind to upstream sequences of genes to turn the expression of those genes on or off. Some pharmaceutical companies are also hoping to develop drugs that selectively block the binding of transcription factors as a way to short-circuit the harmful effects of diseases.
Bioengineering researchers at UCSD and two research institutes in Germany report in the June 16 issue of PLoS Computational Biology that transcription factors act not only in isolation, but also in pairs, trios, and combinations of up to 13 to regulate distinct sets of genes.