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Monday, 2 March 2009

Micro-fun and new antibiotics, 2009

Today:

  1. Researchers discover a protein that amplifies cell death
  2. New family of antibacterial agents uncovered
  3. Evolutionary process more detailed than previously believed, study shows
  4. Rethinking the Genetic Theory of Inheritance
  5. Scientists discover gene responsible for brain's aging
Ok, don't freak out, most of the articles are just 2 or 3 paragraphs. They are short. But very important. Especially article number 3 which gives new insight on evolution.

Researchers discover a protein that amplifies cell death

Scientists at Albert Einstein College of Medicine of Yeshiva University have identified a small intracellular protein that helps cells commit suicide. The finding could lead to drugs for combating cancer and other diseases characterized by overproduction of cells.

In response to stress or as a natural part of aging, many cells undergo programmed suicide, also known as apoptosis. Cancer cells often become immortal and dangerous by developing the ability to suppress apoptosis.

Dr. Shields' laboratory was the first to show that beside the nucleus and mitochondria of the cell, a cellular organelle known as the Golgi apparatus also plays a role in apoptosis.

The Golgi package proteins and other substances made by cells and direct them to their destination within the cell. The team showed that a protein called p115 which is vital for maintaining the structure of the Golgi splits into two pieces early in apoptosis and that the smaller of these protein fragments helps to maintain the cell-suicide process. source

My comment: Not too much to comment. But knowing how to control cell-suicides is obviously very important step in the fight with cancer.

New family of antibacterial agents uncovered

The protein identified by Joachim Grötzinger, Thomas Bosch and colleagues at the University of Kiel, hydramacin-1, is unusual (and also clinically valuable) as it shares virtually no similarity with any other known antibacterial proteins except for two antimicrobials found in another ancient animal, the leech.

Hydramacin proved to be extremely effective though; in a series of laboratory experiments, this protein could kill a wide range of both Gram-positive and Gram-negative bacteria, including clinically-isolated drug-resistant strains like Klebsiella oxytoca (a common cause of nosocomial infections). Hydramacin works by sticking to the bacterial surface, promoting the clumping of nearby bacteria, then disrupting the bacterial membrane. source

My comment: Isn't it amazing that Nature already has everything we need? I hope this new antibiotics get on market really soon, though without proper understanding what causes bacterial mutation and resistance, it won't be very useful.

Evolutionary process more detailed than previously believed, study shows

Working with populations of yeast cells, which were color-coded by fluorescent markers, Katy Kao, assistant professor in the Artie McFerrin Department of Chemical Engineering, and Stanford University colleague Gavin Sherlock were able to evolve the cells while maintaining a visual analysis of the entire process.

Their research, which appears in the December edition of Nature Genetics, shows the evolutionary process to be much more dynamic than initially thought, with multiple beneficial adaptations arising within a population. These adaptations, Kao explained, triggered a competition between these segments, known as "clonal interference."

It's the first direct experimental evidence of this phenomenon in eukaryotic cells, or cells with nuclei, and it contrasts the widely accepted classical model of evolution, which doesn't account for simultaneously developing beneficial adaptations, she said.

Observing the color-coded yeast populations as they evolved to respond to their environment, Kao saw some colors expand while others contracted - a sign that adaptations were occurring. But rather than one segment of the population continuing to shrink until it was completely replaced, some segments were able to compete long enough to acquire further adaptations. When this happened, Kao explained, these populations of cells - once apparently less-fit - began to swell while once-dominant populations started to shrink. This constant reduction and burgeoning of populations signaled the development of multiple beneficial adaptations and a subsequent competition by the cells that acquired them, Kao said.

"Essentially, we were watching evolution in action," Kao said.

In addition to determining if and when a population acquired an adaptation, Kao also identified the specific adaptations that were acquired. She accomplished this using a DNA-based technology that enabled her to determine the specific locations on the genes of the yeast cells that expressed beneficial adaptations.

What she found was that as populations rise and fall, some of these beneficial adaptations factor into the continued evolution of the organism; others don't. source

My comment: This is one of the most important recent experiments for me. It not only proves evolution, but also shows that it's much more complicated than what Darwin thought and what stupid creationist love to point to us. It's perfectly logical, but it's great to see it in Reality.

Rethinking the Genetic Theory of Inheritance

Scientists at the Centre for Addiction and Mental Health (CAMH) have detected evidence that DNA may not be the only carrier of heritable information; a secondary molecular mechanism called epigenetics may also account for some inherited traits and diseases. These findings challenge the fundamental principles of genetics and inheritance, and potentially provide a new insight into the primary causes of human diseases.

The CAMH study showed that epigenetic factors - acting independently from DNA - were more similar in monozygotic twins than dizygotic twins. This finding suggests that there is a secondary molecular mechanism of heredity. The epigenetic heritability may help explain currently unclear issues in human disease, such as the presence of a disease in only one monozygotic twin, the different susceptibility of males (e.g. to autism) and females (e.g. to lupus), among numerous others. source

My comment: Yes, like I said, there is much more to heredity than we currently know. But we're working on it. I'm sure that in the end, it will turn out that DNA serves for much more than we think and that the whole cell can inherit memories and diseases.

Scientists discover gene responsible for brain's aging

According to a new study published in The Journal of Neuroscience, a research team from the Université de Montréal, Maisonneuve-Rosemont Hospital and Lawrence Berkeley National Laboratory have identified a gene that controls the normal and pathological aging of neurons in the central nervous system: Bmi1.

Dr. Gilbert Bernier, of the Université de Montréal and Maisonneuve-Rosemont Hospital, led a team that identified a mutation in mice that dramatically accelerates the process of aging in the brain and the eye. The new study reveals that neurons in the retina and cerebral cortex require a gene called Bmi1 to prevent activation of the p53 pathway and the accumulation of free radicals. source

My comment: Wonderful, when we would see a supplements blocking that gene?

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