:: Posted by American Biotechnologist on 11-21-2013
Obesity may alter the way we taste at the most fundamental level: by changing how our tongues react to different foods.
In a Nov. 13 study in the journal PLOS ONE, University at Buffalo biologists report that being severely overweight impaired the ability of mice to detect sweets.
Compared with slimmer counterparts, the plump mice had fewer taste cells that responded to sweet stimuli. What’s more, the cells that did respond to sweetness reacted relatively weakly.
The findings peel back a new layer of the mystery of how obesity alters our relationship to food.
“Studies have shown that obesity can lead to alterations in the brain, as well as the nerves that control the peripheral taste system, but no one had ever looked at the cells on the tongue that make contact with food,” said lead scientist Kathryn Medler, PhD, UB associate professor of biological sciences.
:: Posted by American Biotechnologist on 11-08-2013
One of biology’s most fundamental processes is something called transcription. It is just one step of many required to build proteins—and without it life would not exist. However, many aspects of transcription remain shrouded in mystery. But now, scientists at the Gladstone Institutes are shedding light on key aspects of transcription, and in so doing are coming even closer to understanding the importance of this process in the growth and development of cells—as well as what happens when this process goes awry.
In the latest issue of Molecular Cell, researchers in the laboratory of Gladstone Investigator Melanie Ott, MD, PhD, describe the intriguing behavior of a protein called RNA polymerase II (RNAPII). The RNAPII protein is an enzyme, a catalyst that guides the transcription process by copying DNA into RNA, which forms a disposable blueprint for making proteins. Scientists have long known that RNAPII appears to stall or “pause” at specific genes early in transcription. But they were not sure as why.
Read more …
:: Posted by American Biotechnologist on 10-24-2013
Just 13 days in space may be enough to cause profound changes in eye structure and gene expression, report researchers from Houston Methodist, NASA Johnson Space Center, and two other institutions in the October 2013 issue of Gravitational and Space Research.
The study, which looked at how low gravity and radiation and oxidative damage impacts mice, is the first to examine eye-related gene expression and cell behavior after spaceflight.
“We found many changes in the expression of genes that help cells cope with oxidative stress in the retina, possibly caused by radiation exposure,” said Houston Methodist pathologist Patricia Chévez-Barrios, M.D., the study’s principal investigator. “These changes were partially reversible upon return to Earth. We also saw optic nerve changes consistent with mechanical injury, but these changes did not resolve. And we saw changes in the expression of DNA damage repair genes and in apoptotic pathways, which help the body destroy cells that are irreparably damaged.”
Since 2001, studies have shown astronauts are at increased risk of developing eye problems, like premature age-related macular degeneration. Experts suspect the cause is low gravity, heightened exposure to solar radiation, or a combination of the two.
:: Posted by American Biotechnologist on 10-17-2013
Duke researchers have connected very rare and precise duplications and deletions in the human genome to their complex disease consequences by duplicating them in zebrafish.
The findings are based on detailed studies of five people missing a small fragment of their genome and suffering from a mysterious syndrome of craniofacial features, visual anomalies and developmental delays.
When those patient observations were coupled to analyses of the anatomical defects in genetically altered zebrafish embryos, the researchers were able to identify the contribution specific genes made to the pathology, demonstrating a powerful tool that can now be applied to unraveling many other complex and rare human genetic conditions.
The findings are broadly important for human genetic disorders because copy-number variants (CNVs) — fragments of the genome that are either missing or existing in extra copies — are quite common in the genome. But their precise contribution to diseases has been difficult to determine because CNVs can affect the function of many genes simultaneously.