legal alien. own body's mitochondria can trigger an immune response.
Louisa Howard
Your mother may have given you his eyes, but it could also give you the mitochondrial DNA that carries disease-causing mutations. A study in mice shows that two techniques can significantly reduce the amount of this potentially dangerous DNA in eggs and embryos, thus potentially sparing children from disease. The methods could provide alternatives to a controversial mitochondrial replacement procedure that would result in so-called embryos of three parents.
Although researchers have not yet tested the method in human embryos, work "is unprecedented," says molecular biologist Mikhail Alexeyev of South Alabama in Mobile University, which has not was connected to the study. "It is the first time that this was done in an embryo."
Mitochondria produce energy that powers cells. Organelles carry their own DNA, separate from nuclear DNA which contains the bulk of the cell genes. This is not their only quirk. You inherit your mitochondrial DNA from your mother, because the embryo retains only the mitochondria came from the egg, not sperm. However, about a 0 women carry the defective mitochondrial DNA, and their children may develop serious or fatal diseases such as cyclic vomiting syndrome, which results in nausea and fatigue, and Leigh's syndrome, in which babies gradually lose strength and muscle control.
Mitochondrial diseases are rare, but they are incurable today. Researchers are therefore developing several ways to drop the defective mitochondrial DNA or prevent its transmission to offspring if doctors know that the mother carries defects in these organelles. Technical, replacing mitochondrial DNA therapy, involves transferring nuclear DNA from the mother of one of his eggs in the egg of a woman with normal mitochondrial DNA. The egg tray is then fertilized and implanted in the mother. However, stirred controversy technique. Some scientists question its safety, and ethicists are opposites because all baby products contain three persons DNA. Earlier this year, the UK approved the procedure for patients, and the Food and Drug Administration is planning to leave the United States.
Instead of exchanging bad mitochondria to the right, a team led by biologist Juan Carlos Izpisúa development Belmonte of the Salk Institute for Biological Studies in San Diego, California, decided to change the transmission of organelle DNA. Researchers first tested an RNA strand that carries the instructions for making an enzyme-DNA snipping and an address segment which directs it to the mitochondria. Inserting the strand in their mitochondria spurs cells to produce the enzyme, known as a restriction endonuclease that cuts the defective mitochondrial DNA and leads to its destruction.
Izpisúa Belmonte and his colleagues injected RNA in eggs and early embryos of mice that harbor two varieties of mitochondrial DNA, which makes them a suitable model to test the reduction of a mutation disease. The enzyme slices of a variety, but leave the other intact. The technique has reduced the abundance of variety of targeted mitochondrial DNA in eggs and embryos, the researchers report today in Cell . To determine whether the injured embryos method, researchers have implanted some of them into female mice. The animals have given birth to healthy pups, who also produced normal young.
In this experiment, both types of mitochondrial DNA were normal. But the results show that it is possible to reduce the transmission of a variety of mitochondrial DNA to the next generation.
The restriction endonuclease technology have limited use, the researchers note, because it would work against only a mutation that occurs in two mitochondrial diseases. So they turned to a second targeting technique of DNA, known as TALENs, which involves inducing cells to produce enzymes that work together like a pair of scissors to cut DNA. Researchers can customize these molecular scissors to determine all mitochondrial DNA sequences they want.
When the team injected RNA for TALENs enzymes in mouse eggs that contained two varieties of mitochondrial DNA, it similarly reduces the levels of a type. To measure whether the technique could reduce pathogenic mitochondrial mutations, the researchers created hybrid cells by fusion of mouse eggs to human cells that harbor one of two flaws that cause disease. The team showed that the technical TALENs significantly reduces the amounts of DNA in defective hybrid cells.
fertility clinics have the expertise to perform both RNA-injection procedures, Izpisúa said Belmonte. Though neither technical eliminated the targeted DNA eggs or embryos, which is probably not necessary, he said. Most people usually have a mixture of varieties of mitochondrial DNA, and disease results when the proportion of "bad" Mitochondrial DNA is between 60% and 95%. "We want to decrease below the level for diseases to appear," says Alejandro Ocampo, a postdoc in the lab and co-author of Izpisúa Belmonte on paper.
cell and molecular biologist Giovanni Manfredi of Weill Cornell Medical College in New York gives high marks to study. "They can drop the amount of mutant DNA significantly to levels that ... the probability of having a disease is virtually zero." He predicted that technical will not draw the ethical objections of replacement therapy for mitochondrial DNA because "mitochondrial DNA remains that of the mother."
Izpisúa Belmonte and his colleagues are already testing whether techniques do work and are safe in eggs and human embryos discarded by fertility clinics.
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