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Dr David Sinclair talks about what epigenetic reprogramming can achieve in animal and human in this short. Please note that the links below are affiliate link…
Research from the Babraham Institute has developed a method to ‘time jump’ human skin cells by 30 years, turning back the ageing clock for cells without losing their specialised function. Work by researchers in the Institute’s Epigenetics research programme has been able to partly restore the function of older cells, as well as rejuvenating the molecular measures of biological age. The research is published today in the journal eLife and whilst at an early stage of exploration, it could revolutionise regenerative medicine.
What is regenerative medicine?
As we age, our cells’ ability to function declines and the genome accumulates marks of ageing. Regenerative biology aims to repair or replace cells including old ones. One of the most important tools in regenerative biology is our ability to create ‘induced’ stem cells. The process is a result of several steps, each erasing some of the marks that make cells specialised. In theory, these stem cells have the potential to become any cell type, but scientists aren’t yet able to reliably recreate the conditions to re-differentiate stem cells into all cell types.
Researchers have created synthetic human embryos using stem cells, according to media reports. Remarkably, these embryos have reportedly been created from embryonic stem cells, meaning they do not require sperm and ova.
This development, widely described as a breakthrough that could help scientists learn more about human development and genetic disorders, was revealed this week in Boston at the annual meeting of the International Society for Stem Cell Research.
The research, announced by Professor Magdalena Żernicka-Goetz of the University of Cambridge and the California Institute of Technology, has not yet been published in a peer-reviewed journal. But Żernicka-Goetz told the meeting these human-like embryos had been made by reprogramming human embryonic stem cells.
Researchers have discovered that senescent pigment cells in skin moles can stimulate robust hair growth, challenging the belief that these cells impede regeneration. The study showed that molecules osteopontin and CD44 play a key role in this process, potentially opening new avenues for therapies for common hair loss conditions.
The process by which aged, or senescent, pigment-making cells in the skin cause significant growth of hair inside skin moles, called nevi, has been identified by a research team led by the University of California, Irvine. The discovery may offer a road map for an entirely new generation of molecular therapies for androgenetic alopecia, a common form of hair loss in both women and men.
The study, published on June 21 in the journal Nature, describes the essential role that the osteopontin and CD44 molecules play in activating hair growth inside hairy skin nevi. These skin nevi accumulate particularly large numbers of senescent pigment cells and yet display very robust hair growth.
Cells in the human body, the building blocks of life, are arranged in a precise way. That’s necessary because pathways and spaces provide a means for cells to communicate, collaborate and function within the specific tissue or organ. Changes in cell arrangement can lead to uncontrolled cell growth, cell death and diseases, including cancer.
Scientists at the Mayo Clinic Center for Individualized Medicine and Mayo Clinic Comprehensive Cancer Center have developed an artificial intelligence method, called Spatially Informed Artificial Intelligence (SPIN-AI). This new deep-learning technique can analyze the genetic information of individual cells to reconstruct the precise layout of the cells in a tissue, without preexisting knowledge of how the cells are organized.
The new study detailing SPIN-AI is published in Biomolecules.
The chemical origin of life on Earth is a puzzle that scientists have been trying to piece together for decades. Many hypotheses have been proposed to explain how life came to be and what chemical and environmental factors on early Earth could have led to it. A step required in a number of these hypotheses involves the abiotic synthesis of genetic polymers—materials made up of a sequence of repeating chemical units with the ability to store and pass down information through base-pairing interactions.
One such hypothesis is the RNA (ribonucleic acid) world hypothesis, which draws from this concept and suggests that RNA could have been the original biopolymer of life both for genetic information storage and transmission, and for catalysis. However, in the absence of chemical activation of RNA monomers, studies have found that RNA polymerization would have been inefficient under primitive dry-down conditions without specialized circumstances such as lipid or salt-assisted synthesis or mineral templating.
While this does not necessarily make the RNA world hypothesis less plausible, primitive chemical systems were quite diverse and could not have possibly been as clean to just contain RNA and lipids, suggesting that other forms of primitive nucleic acid polymerization may have also taken place.
A new family of DNA elements which control the activation of certain genes known to cause a rare disease known as MSL3 syndrome in children has been identified.
The study led by researchers at the Queen Mary University of London and published in Nature Structural & Molecular Biology shines a new light on the mechanism behind this poorly understood disease, hoping that it can lead to better treatments for this and similar diseases in the future.
Mutations in the MSL3 gene are known to cause a rare disease in children called MSL3 syndrome—a newly discovered disease with only around 50 registered diagnoses worldwide, although scientists predict that more cases are currently undiagnosed.
The Y chromosome is the smallest chromosome, and holds the least amount of genes, but scientists are still learning about all of its biological functions. Research has shown that many men start to lose Y chromosomes in blood cells as they get older, and this phenomenon has been linked to some disorders including heart disease and now, cancer. Some studies have suggested that the loss of the Y chromosome may help explain why men tend to die at slightly younger ages compared to women, or why there are sex differences in some types of cancer… Two new studies reported in Nature have explored the link between cancer and the loss of the Y chromosome.
One study used a mouse model to show that a specific gene on the Y chromosome known as KDM5D increases the chance that some types of colorectal cancer will metastasize. The other research report showed that when some cells lose the Y chromosome, bladder tumors are better at evading the immune system, and the risk of aggressive bladder cancer increases.
People who owned black-and-white television sets until the 1980s didn’t know what they were missing until they got a color TV. A similar switch could happen in the world of genomics as researchers at the Berlin Institute of Medical Systems Biology of the Max Delbrück Center (MDC-BIMSB) have developed a technique called Genome Architecture Mapping (“GAM”) to peer into the genome and see it in glorious technicolor. GAM reveals information about the genome’s spatial architecture that is invisible to scientists using solely Hi-C, a workhorse tool developed in 2009 to study DNA interactions, reports a new study in Nature Methods by the Pombo lab.
“With a black-and-white TV, you can see the shapes but everything looks gray,” says Professor Ana Pombo, a molecular biologist and head of the Epigenetic Regulation and Chromatin Architecture lab. “But if you have a color TV and look at flowers, you realize that they are red, yellow and white and we were unaware of it. Similarly, there’s also information in the way the genome is folded in three-dimensions that we have not been aware of.”
Understanding DNA organization can reveal the basis of health and disease. Our cells pack a 2-meter-long genome into a roughly 10 micrometer-diameter nucleus. The packaging is done precisely so that regulatory DNA comes in contact with the right genes at the right times and turns them on and off. Changes to the three-dimensional configuration can disrupt this process and cause disease.
