Lifeboat Foundation

Various diseases of the digestive tract, for example severe intestinal inflammation in humans, are closely linked to disturbances in the natural mobility of the intestine. What role the microbiome—i.e. the natural microbial community colonizing the digestive tract—plays in these rhythmic contractions of the intestine, also known as peristalsis, is currently the subject of intensive research. It is particularly unclear how the contractions are controlled and how the cells of the nervous system, that act as pacemakers, function together with the microorganisms.

A research team from the Cell and Developmental Biology group at Kiel University has now succeeded in demonstrating for the first time, using the freshwater polyp Hydra as an example, that phylogenetically old neurons and bacteria actually communicate directly with each other. Surprisingly, they discovered that the nerve cells are able to cross-talk with the microorganisms via immune receptors, i.e., to some extent with the mechanisms of the immune system.

On this basis, the scientists of the Collaborative Research Center (CRC) 1182 “Origin and Function of Metaorganisms” formulated the hypothesis that the nervous system has not only taken over sensory and motor functions from the onset of evolution, but is also responsible for communication with the microbes. The Kiel researchers around Professor Thomas Bosch published their results together with international colleagues today in the journal Proceedings of the National Academy of Sciences (PNAS).

Canada’s highest court has issued a ruling today upholding a federal law preventing third parties, such as employers and insurance companies, from demanding genetic information from individuals.

In a 5–4 decision, the Supreme Court of Canada has decided the Genetic Non-Discrimination Act is a constitutional exercise of federal powers.

Most cells in your body come with two genetic libraries; one in the nucleus, and the other inside structures called mitochondria — also known as the ‘powerhouses of the cell’.

Until now, we’ve only had a way to make changes to one.

A combined effort by several research teams in the US has led to a process that could one day allow us to modify the instructions making up the cell’s ‘other’ genome, and potentially treat a range of conditions that affect how we power our bodies.

A bacterial toxin cracks open door to new precision-editing tool for DNA in mitochondria.

Look deep inside our cells, and you’ll find that each has an identical genome –a complete set of genes that provides the instructions for our cells’ form and function.

But if each blueprint is identical, why does an eye cell look and act differently than a skin cell or brain cell? How does a stem cell—the raw material with which our organ and tissue cells are made—know what to become?

In a study published July 8, University of Colorado Boulder researchers come one step closer to answering that fundamental question, concluding that the molecular messenger RNA (ribonucleic acid) plays an indispensable role in cell differentiation, serving as a bridge between our genes and the so-called “epigenetic” machinery that turns them on and off.

Tessera Therapeutics is developing a new class of gene editors capable of precisely plugging in long stretches of DNA—something that Crispr can’t do.

The Genome Aggregation Database has collected 15,708 genomes and 125,748 exomes (the protein-coding part of the genome) to help shed light on how genetic mutations can lead to disease. Dr Daniel MacArthur, scientific lead of the gnomAD Project, explains how the project started, how they collect the data and what they hope to achieve.

By genetically engineering thale cress, scientists have made it grow like a succulent, more than doubling the plant’s water-use efficiency.

There is no really useful treatments for Pancreatic Cancer, also it’s really deadly. So this sounds like awesome science news! “Cancer cells in the pancreas seem to thrive off this hyperactive cholesterol synthesis. The team thinks this is probably because they are taking advantage of other molecules generated by the same pathway. They’re able to keep the pathway running and maintain their supply thanks to an enzyme called sterol O-acyltransferase 1 (SOAT1), which converts free cholesterol to its stored form and which pancreatic cancer cells have in abundance.” “When the researchers eliminated the SOAT1 enzyme through genetic manipulation, preventing cells from converting and storing their cholesterol, cancer cells stopped proliferating. In animal experiments, eliminating the enzyme stalled tumor growth.”

Scientists at Cold Spring Harbor Laboratory (CSHL) have found that they can stop the growth of pancreatic cancer cells by interfering with the way the cells store cholesterol. Their findings in mice and lab-grown pancreas models point toward a new strategy for treating the deadly disease.

The study, reported in the Journal of Experimental Medicine, was led by CSHL Professor David Tuveson’s team wanted to know why pancreatic cancer cells, like many cancer cells, manufacture abundant amounts of cholesterol. Cholesterol is an essential component of cell membranes, but the research team determined that pancreatic cancer cells make far more of it than they need to support their own growth. “This is unusual, because the cholesterol pathway is one of the most regulated pathways in metabolism,” says Tobiloba Oni, a graduate student in Tuveson’s lab.

Continue reading “Blocking cholesterol storage could stop growth of pancreatic tumors” »