SAN FRANCISCO, Aug. 28 -- Researchers at the University of California, Berkeley, have found a way to boost the efficiency of a gene-editing tool, known as clustered regularly interspaced short palindromic repeats associated protein 9 (CRISPR-Cas9), so that it cuts and disables genes up to fivefold in most types of human cells. While the key to figuring out the role of genes or the proteins they code for in the human body or in disease is disabling the gene to see what happens when it is removed, CRISPR-Cas9 is the go-to technique for knocking out genes in human cell lines to discover what the genes do and holds the promise of accelerating the process of making knockout cell lines. However, researchers must sometimes make and screen many variations of the genetic scissors to find one that works well. In the new study, published in a the journal Nature Communications, the UC Berkeley researchers found that this process can be made more efficient by introducing into the cell, along with the CRISPR-Cas9 protein, short pieces of deoxyribonucleic acid (DNA) that do not match any DNA sequences in the human genome. The short pieces of DNA, called oligonucleotides, seem to interfere with the DNA repair mechanisms in the cell to boost the editing performance of even mediocre CRISPR-Cas9s between 2½ and 5 times. "It turns out that if you do something really simple - just feed cells inexpensive synthetic oligonucleotides that have no homology anywhere in the human genome - the rates of editing go up as much as five times," said lead researcher Jacob Corn, the scientific director of UC Bekeley's Innovative Genomics Initiative and an assistant adjunct professor of molecular and cell biology. The technique boosts the efficiency of all CRISPR-Cas9s, even those that initially failed to work at all. Corn portrays CRISPR-Cas9 gene editing as a competition between cutting and DNA repair: once Cas9 cuts, the cell exactly replaces the cut DNA, which Cas9 cuts again, in an endless cycle of cut and repair until the repair enzymes make a mistake and the gene ends up disfunctional. Perhaps, he said, the oligonucleotides decrease the fidelity of the repair process, or make the cell switch to a more error-prone repair that allows Cas9 to more readily break the gene. The next frontier, he was quoted as saying in a UC Berkeley news release, is trying to take advantage of the peculiarities of DNA repair to improve sequence insertion, in order to replace a defective gene with a normal gene and possibly cure a genetic disease.

LONDON, Aug. 26 -- An international team of researchers has discovered a gene that is linked to the regulations of our coffee consumption, a study says.Previous studies have investigated the biological mechanisms of caffeine metabolism. The new findings suggest that the gene reduces the ability of cells to breakdown caffeine, causing it to stay in the body for longer.

According to the study published Friday by the University of Edinburgh, the team analyzed genetic information from 370 people living in a small village in south Italy and 843 people from six villages in northeast Italy.

They found that people with a DNA variation in a gene called PDSS2 tended to consume fewer cups of coffee than people without the variation. The effect was equivalent to around one fewer cup of coffee per day on average, according to the study.

The researchers carried out the same study in a group of 1,731 people from the Netherlands. The result was similar but the effect of the gene on the number of cups of coffee consumed was slightly lower.

One explanation is that the different styles of coffee that are drunk in the two countries lead to the difference, says the researchers.

In Italy, people tend to drink smaller cups such as espresso while people in the Netherlands prefer larger cups that contain more caffeine overall.

The results of this study add to existing research suggesting that our drive to drink coffee may be embedded in our genes, said Dr Nicola Pirastu, Chancellor's Fellow at the University of Edinburgh's Usher Institute.

Pirastu is one of the authors of the study.

However, larger studies are needed to confirm the discovery and also to clarify the biological link between PDSS2 and coffee consumption, says Pirastu.

The study has been published in the journal Scientific Reports.