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More developments in senescent cell signalling published this month.


Differentiated cells in a culture dish can assume a new identity when manipulated to express four transcription factors. This “reprogramming” process has sparked interest because conceivably it could be harnessed as a therapeutic strategy for tissue regeneration. Mosteiro et al. used a mouse model to study the signals that promote cell reprogramming in vivo. They found that the factors that trigger reprogramming in vitro do the same in vivo; however, they also inflict cell damage. The damaged cells enter a state of senescence and begin secreting certain factors that promote reprogramming, including an inflammatory cytokine called interleukin-6. Thus, in the physiological setting, cell senescence may create a tissue context that favors reprogramming of neighboring cells.

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For many years, scientists believed that our brains were unable to produce new neurons once we had been born, and that we all had to make do with the brain cells we started life with. Later, it became clear that new brain cells are in fact created in some key brain regions, replacing those that become damaged and protecting us from dementia. Now, researchers have discovered that the stem cells giving rise to these neurons originate in the membranes encasing the brain, known as the meninges.

Publishing their findings in the journal Cell Stem Cell, the authors claim that their discovery of this source of stem cells could one day lead to new treatments for brain damage or neurodegenerative disorders.

Most neurogenesis in the adult brain occurs in a region called the hippocampus, where the creation of new brain cells ensures our memories remain in working order as we age. The meninges penetrate the brain at every level, encapsulating a number of different regions, including the hippocampus.

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I have been evangelizing this for a while and glad to see others chiming in.


London, Nov 26 (IANS) Researchers have engineered cells with a “built-in genetic circuit” that produces a molecule that impairs the ability of cancer cells to survive and grow in their low oxygen environment.

The genetic circuit produces the machinery necessary for the production of a compound that inhibits a protein which has a significant and critical role in the growth and survival of tumours.

This results in the cancer cells being unable to survive in the low oxygen, low nutrient tumour micro-environment.

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Led by Nikolay Kandul, senior postdoctoral scholar in biology and biological engineering in the laboratory of Professor of Biology Bruce Hay, the team developed a technique to remove mutated DNA from mitochondria, the small organelles that produce most of the chemical energy within a cell. A paper describing the research appears in the November 14 issue of Nature Communications. There are hundreds to thousands of mitochondria per cell, each of which carries its own small circular DNA genome, called mtDNA, the products of which are required for energy production. Because mtDNA has limited repair abilities, normal and mutant versions of mtDNA are often found in the same cell, a condition known as heteroplasmy.

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Hitting the pause button on development in embryos has implications for understanding aging.


UC San Francisco researchers have found a way to pause the development of early mouse embryos for up to a month in the lab, a finding with potential implications for assisted reproduction, regenerative medicine, aging, and even cancer, the authors say.

The new study—published online November 23, 2016 in Nature —involved experiments with pre-implantation mouse embryos, called blastocysts. The researchers found that drugs that inhibit the activity a master regulator of called mTOR can put these early embryos into a stable and reversible state of suspended animation.

“Normally, blastocysts only last a day or two, max, in the lab. But blastocysts treated with mTOR inhibitors could survive up to 4 weeks,” said the study’s lead author, Aydan Bulut-Karslioglu, PhD, a post-doctoral researcher in the lab of senior author Miguel Ramalho-Santos, PhD, who is an associate professor of obstetrics/gynecology and reproductive sciences at UCSF.

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Progress towards making a blood scrubber to calibrate the pro aging factors in blood. Irina Conboy has spent the last 20 years working on parabiosis and signalling factors in blood and this is yet another step forward for their research.

Whilst many are seeking the secret sauce in young blood the data suggests it is much more likely the case that old blood contains too many pro-aging factors eg, TGF-beta, TNF-a, IL-6, CD38 etc… The aim is now to filter old blood and calibrate such factors in order to promote a pro-youthful signalling environment. If only this device was small enough to wear or implant.


In what could be a fresh chapter in the never-ending story of the search for eternal youth, scientists are to tinker with people’s blood in the hope of slowing down the ageing process and preventing age-related diseases.

Researchers in California plan to launch a clinical trial of the radical – and highly experimental – approach in the next six months, after a small study in mice found the treatment had promise.

People who take part in the trial will have their blood passed through a machine that resets abnormal levels of proteins seen in older blood. The scientists believe these high levels of certain proteins can hamper the growth and maintenance of healthy body tissues, and so contribute to their deterioration in old age.

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The ONUSblue alcohol detection patch tells you when you’ve reached the legal threshold and has the potential to save millions of lives. The company’s product roadmap is even more interesting with the detection of marijuana, methamphetime and a range of illegal recreational substances to follow.

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We’re only starting in this space.


Synthetic Biology (SynBio) includes a large field of applications. Within this area biochemists combine engineering concepts and techniques with biology to design new genes that produce a specific protein. When this protein is an enzyme, bacteria and yeast in which such a gene is implanted can produce specific chemicals through a fermentation process. A large and growing number of businesses is active in this field. This became apparent once again at the EFIB-conference in Glasgow, last October. The workshop was chaired by John Cumbers, founder of the American SynBioBeta, an internet-site dedicated to sharing information and news on synthetic biology.

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JBEI researchers develop efficient and affordable method for plant DNA assembly.

Researchers at the U.S. Department of Energy (DOE)’s Joint BioEnergy Institute (JBEI) in collaboration with Berkeley Lab’s Environmental Genomics & Systems Biology Division and the DOE Joint Genome Institute developed a versatile system (named jStack) which utilizes yeast homologous recombination to efficiently assemble DNA into plant transformation vectors. The new approach will impact plant engineering for the bioenergy, agricultural and pharmaceutical industries.

Although synthetic biology has provided solutions to many societal challenges, little research has been devoted to advancing synthetic biology in plants. Microbes, such as yeast and Escherichia coli (E. coli), have received much of the attention in developing synthetic biology tools due to their fast generation time and the ease of working with these organisms in laboratories. A shortage of characterized DNA parts, along with the difficulty of efficiently assembling multiple and large fragments of DNA into plant transformation vectors, has limited progress in studying and engineering plants to the same degree as their microbial counterparts.

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You get out what you put in.


You are what you eat, the old saying goes, but why is that so? Researchers have known for some time that diet affects the balance of microbes in our bodies, but how that translates into an effect on the host has not been understood. Now, research in mice is showing that microbes communicate with their hosts by sending out metabolites that act on histones—thus influencing gene transcription not only in the colon but also in tissues in other parts of the body. The findings publish November 23 in Molecular Cell.

“This is the first of what we hope is a long, fruitful set of studies to understand the connection between the microbiome in the gut and its influence on host health,” says John Denu, a professor of biomolecular chemistry at the University of Wisconsin, Madison, and one of the study’s senior authors. “We wanted to look at whether the gut microbiota affect epigenetic programming in a variety of different tissues in the host.” These tissues were in the proximal colon, the liver, and fat .

In the study, the researchers first compared germ-free mice with those that have active gut microbes and discovered that gut microbiota alter the host’s epigenome in several tissues. Next, they compared mice that were fed a normal chow diet to mice fed a Western-type diet—one that was low in complex carbohydrates and fiber and high in fat and simple sugars. Consistent with previous studies from other researchers, they found that the of mice fed the normal chow diet differed from those fed the Western-type diet.

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