Lifeboat Foundation

PerkinElmer has moved to expand its life sciences portfolio with CRISPR and gene editing offerings by snapping up the cell engineering specialist Horizon Discovery.

The $383 million, all-cash deal will add gene modulation tools that—in combination with its own work in applied genomics solutions—aims to provide next-generation research tools and the customized cell lines necessary for developers of new targeted therapies, and broaden PerkinElmer’s partnership work with academic researchers and the biopharma industry.

The Cambridge, U.K.-based Horizon, with about 400 employees worldwide with offices in the U.S. and Japan, provides genetic base editing technologies for living cell models using CRISPR reagents, as well as gene modulation products using RNA interference methods.

Researchers see structural changes in genetic material that allow memories to strengthen when remembered.

In a review published in the journal *Science*, Jain and Steele Laboratories colleagues Hadi T. Nia, PhD, and Lance L. Munn, PhD, describe four distinct physical hallmarks of cancer that affect both cancer cells and the tumor microenvironment, contributing to both tumor growth and the development of resistance to powerful cancer drugs.

One widely accepted model of cancer holds that a normal cell goes rogue because of genetic mutations or an environmental insult. In this model, the altered cell starts replicating out of control and takes over normal tissues, displaying eight hallmarks that include the ability to promote and sustain the growth of tumors, evade immune system attempts to suppress growth, stimulate blood flow to tumors and both invade local tissues and metastasize (spread) elsewhere in the body.

But this model fails to take into account how physical processes affect tumor progression and treatment, say the authors. In addition to the aforementioned eight biological hallmarks of cancer proposed by Robert Weinberg, PhD, from MIT, and Douglas Hanahan, PhD, from the Swiss Federal Institute of Technology in Lausanne, Jain and colleagues propose adding four distinct physical hallmarks that capture the biomechanical abnormalities in tumors: elevated solid stress; elevated interstitial fluid pressure; increased stiffness and altered material properties; and altered tissue micro-architecture.

Continue reading “Melding biology and physical sciences yields deeper understanding of cancer” »

Li’l Kurt is a genetic marvel.

In an effort to increase genetic diversity among horses, scientists have gone sci-fi and used frozen 40-year-old cells to create Kurt, the very first clone of a Przewalski’s horse.

Continue reading “Scientists Cloned the Most Endangered Horse in the World—From 40-Year-Old DNA” »

Mice who ate a diet high in fat and cholesterol were more likely to see their hair turn from black to white and experience hair loss. The diet also appeared to cause inflammation of the skin.

In the first stage of the study, the researchers genetically modified mice to develop atherosclerosis, a condition in which fat deposits form in the arteries.

They then fed mice either a Western diet high in fat and cholesterol or untreated rat chow from the age of 12 to 20 weeks. As expected, the mice who consumed the Western diet saw their hair turn white and fall out, and develop skin lesions. And the longer the mice ate the diet, the worse their symptoms became. By week 36, three quarters of the animals had skin lesions.

The great powerful guppy can essentially evolve 10 million times faster than usual. Which could lead to humans evolving faster too leading to a biological singularity.

Although natural selection is often viewed as a slow pruning process, a dramatic new field study suggests it can sometimes shape a population as fast as a chain saw can rip through a sapling. Scientists have found that guppies moved to a predator-free environment adapted to it in a mere 4 years—a rate of change some 10,000 to 10 million times faster than the average rates gleaned from the fossil record. Some experts argue that the 11-year study, described in today’s issue of Science,* may even shed light on evolutionary patterns that occur over eons.

A team led by evolutionary biologist David Reznick of the University of California, Riverside, scooped guppies from a waterfall pool brimming with predators in Trinidad’s Aripo River, then released them in a tributary where only one enemy species lurked. In as little as 4 years, male guppies in the predator-free tributary were already detectably larger and older at maturity when compared with the control population; 7 years later females were too. Guppies in the safer waters also lived longer and had fewer and bigger offspring.

Continue reading “Guppy Evolution Fast Forwards” »

Many of the fundamental principles in biology and essentially all pathways regulating development were identified in so-called genetics screens. Originally pioneered in the fruit fly Drosophila and the nematode C. elegans, genetic screens involve inactivation of many genes one by one. By analyzing the consequences of gene loss, scientists can draw conclusions about its function. This way, for example, all genes required for formation of a brain can be identified.

Genetic screens can routinely be carried out in flies and worms. In humans, a wealth of knowledge exists about genetic disorders and the consequences of disease-relevant mutations, but their systematic analysis was impossible. Now, the Knoblich lab at IMBA has developed a groundbreaking technique allowing hundreds of genes to be analyzed in parallel in human tissue. They named the new technology CRISPR-LICHT and published their findings in the journal Science.

By using cerebral organoids, a 3D cell culture model for the human brain developed in Jürgen Knoblich’s group at IMBA, hundreds of mutations can now be analyzed for their role in the human brain using CRISPR-LICHT.

While our circadian body clock dictates our preferred rhythm of sleep or wakefulness, a relatively new concept—the epigenetic clock—could inform us about how swiftly we age, and how prone we are to diseases of old age.

People age at different rates, with some individuals developing both characteristics and diseases related to aging earlier in life than others. Understanding more about this so-called ‘biological age’ could help us learn more about how we can prevent diseases associated with age, such as dementia. Epigenetic markers control the extent to which genes are switched on and off across the different cell-types and tissues that make up a human body. Unlike our genetic code, these epigenetic marks change over time, and these changes can be used to accurately predict biological age from a DNA sample.

Now, scientists at the University of Exeter have developed a new epigenetic clock specifically for the human brain. As a result of using human brain tissue samples, the new clock is far more accurate than previous versions, that were based on blood samples or other tissues. The researchers hope that their new clock, published in Brain and funded by Alzheimer’s Society, will provide insight into how accelerated aging in the brain might be associated with brain diseases such as Alzheimer’s disease and other forms of dementia.

The coronavirus disease 2019 (COVID-19) pandemic does not affect everyone equally. While anyone can contract COVID-19, accumulating data suggest that older people or those with pre-existing comorbidities are far more likely to have severe complications or die from the disease. While researchers scramble to unravel the mechanisms of action underlying the disease’s wide-ranging effects, news that the disease hits older people hardest has been received without demur: it is widely accepted that to be old is to be fragile. Indeed, even in so-called normal times, everyone expects more things break as people age: bones, hearts, brains. In the context of the pandemic, being old is seen as just one more comorbidity.

It should not be.

We accept growing old and losing our vitality as an inevitability of life. To do so is to overlook the fact that ageing is, fundamentally, a plastic trait—influenced both by our genetic predispositions and many (controllable) environmental factors. Anecdotally we know this to be true: for some, being in their eighties means being confined to a wheelchair whereas for others, like Eileen Noble, who at 84 years old was the oldest runner in 2019’s London Marathon, it decidedly does not. The burgeoning field of biogerontology is now beginning to amass data in support of such observations. Single genetic mutations in evolutionarily conserved pathways across model organisms—ranging from fruit flies to mice—increase lifespan by up to 80%. Crucially, not only do these animals live longer, they also have a longer youthspan—the proportion of their lives in which they retain the trappings of youth such as peak mobility, immunity, and stress resilience.