For decades, biology textbooks have been clear – our traits are the product of our genes. But a new study by Yale University researchers published Dec. 26 in Nature Genetics suggests another mechanism can regulate variations of traits even in genetically identical individuals.
A particular type of RNA works in concert with a common protein to protect organisms from harmful genetic variations without the help of genes, reports Haifan Lin, director of the Yale Stem Cell Center, professor of cell biology and genetics and senior author of the paper.
“This mechanism may help explain how ordinary
UC San Diego scientists have dramatically improved the success rate of genetically modifying human embryonic stem cells. This advance brings the promise of better treatment of genetic diseases.
The new approach works in 20 percent of embryonic stem cells, compared to less than 1 percent treated with standard methods, said Yang Xu, a UCSD professor of biology, who led the study, assisted by Hoseok Song and Sun-Ku Chung, postdoctoral fellows in his lab.
The study was published Thursday in the journal Cell Stem Cell.
Some genetic diseases can’t be studied adequately in animals, Xu said, so the ability to produce human cells
Researchers have created mammalian cells containing a single set of chromosomes in research funded by the Wellcome Trust and EMBO. The technique should allow scientists to better establish the relationships between genes and their function.
Mammal cells usually contain two sets of chromosomes – one set inherited from the mother and one from the father. The genetic information contained in these chromosome sets helps determine how our bodies develop. Changes in this genetic code can lead to or increase the risk of developing disease.
To understand how our genes function, scientists manipulate the genes in animal models – such as the
Mental retardation, altered facial characteristics, and heart problems are all problems suffered by children affected by Costello syndrome, a genetic disease that is being studied by researchers in Milan at the Italian Foundation for Cancer Research (FIRC) Institute of molecular oncology (IFOM) using the zebrafish as a model.
The cause of the disease – explained the scientists in the January issue of ‘Disease Models & Mechanisms’ monthly magazine – is a mutation of the Ras gene, the same alteration observed in 20pct of tumors. One out of every five cases of cancer and the rare genetic disease have a common