Pretty Finches
Check out Ed Yong’s story about the mating habits of these beautiful birds at Not Exactly Rocket Science.
Month: October 2012 (page 9 of 10)
Coming soon? Probably not, but this is still interesting. Scientists have used RNA interference to knock down expression of the protein beta-lactoglobulin (also known as BLG), which is one milk protein that causes allergic reactions in animals. The study is published in PNAS. Read on from Popular Science:
The team used RNA interference to inhibit the expression of certain genes that code for the production of BLG, which causes allergic reactions in people and isn’t found in human milk. They tested it on mice first, and then engineered a cow egg cell’s nucleus to express the same micro RNAs that shut down BLG. This engineered ovum was fertilized and implanted into a surrogate mother.
The team started with 57 embryos and ultimately got one healthy calf, but unexpectedly, it was born with no tail. The researchers believe this mutation is unrelated to the transgenic change, but they still need to figure out exactly what caused it.
Insulin is produced by beta cells in the pancreas and is the hormone responsible for regulating and moving glucose in our bodies. Over time, some people become resistant to insulin, which causes their beta cells to have to work harder to regulate their blood sugar . Researchers had previously thought that diabetes stemmed from the death of these beta cells as they got tired trying to keep up with the body’s growing insulin needs. Now a group of researchers believes that the cells don’t die, but they revert back to an earlier developmental state:
In earlier work, Dr. Accili sought to understand what happened to beta cells at the molecular level as diabetes progressed. He investigated the role played by a protein called FOXO1, which seems to disappear as beta cells stop producing insulin.
In the new work, published in September in the journal Cell, Dr. Accili, Chutima Talchai, then a postdoctoral fellow in his laboratory, and their colleagues genetically engineered mice that lacked FOXO1 in beta cells. At first the animals appeared normal. But as they were subjected to stress —pregnancy for the females, aging for the males — the mice developed high blood sugar, decreased insulin secretion and other signs of Type 2 diabetes.
The mice also began to produce proteins normally found only during fetal development. Some of their beta cells, Dr. Accili found, had come to resemble progenitor cells. Similar to stem cells, these are destined to become, or “differentiate” into, hormone-producing cells as the animal matures. Their appearance in adult mice was a surprise. Dr. Accili also showed that this process — in which beta cells lost their identities, or de-differentiated — accounted for virtually all of the animals’ decrease in insulin-producing capacity. It wasn’t happening just on the margins.
Stresses that can lead to this development include pregnancy and obesity. Other scientists are looking into this result to determine if there could be any way to reverse this process and make the cells re-mature into full beta cells. For more check out the New York Times.