Lifeboat Foundation

Tigers seem pretty straightforward: stripes, sharp claws, awe-inspiring grace wielded by hundreds of pounds of rippling muscle, fondness of sugary cereal, etc. But new research on the big cats’ DNA is the latest indication that underneath that striking orange and black pelage, not all tigers are the same. Scientists are now reporting that tigers are broken up into six distinct subspecies spread out across Asia.

In endangered species like tigers, pegging down the exact number of subspecies can be pretty important for conservation purposes. Being mindful of how the species is naturally divided up in the wild—and how populations may be evolving independently of one another—can allow conservationists to more effectively manage populations as cohesive units. Global tiger conservation has struggled with this since there’s been plenty of disagreement on how many subspecies even exist.

Proteins are the building blocks of the cell. They do most of the work and are essential for the structure, function and dynamic regulation of the cell and body’s tissues and organs. Proteins rarely work alone, they interact, form protein complexes or bind DNA and RNA to control what a cell does. These complexes are key pieces of many important reactions within the cell, such as energy metabolism or gene regulation. Any change in those interactions, which can for example be caused by a mutation, can make the difference between health and disease. Hence, for understanding how cells operate, or what might go wrong in ill cells, it is essential to know how their building blocks interact.

New technologies allowed scientists during the last decades to understand the genetic information an organism possess, which of this information is actively used and which proteins are made by the cell in different circumstances. Now it is a big challenge to understand how biomolecules such as proteins and RNA messenger molecules combine to form the complexes required for a functional cell. In other words, we know the ten thousands of parts a cell is build off, but we don’t know how they belong together.

In a paper published in Nature Communications, scientists at the Centre for Genomic Regulation (CRG) describe the development of a new method, named “rec-YnH”, which was designed to understand the complexes formed between hundreds of proteins and RNAs at the same time.

Continue reading “You are the company you keep—A new screening method detects direct biomolecule interactions” »

“Previous work mostly focused on what was going on at the microscale of DNA,” says study co-author Michael Shelley, group leader for biophysical modeling at the Flatiron Institute’s Center for Computational Biology in New York City and co-director of the Courant Institute’s Applied Mathematics Laboratory at New York University. “People didn’t really think about what was going on at the larger scale.”

Shelley and colleagues simulated the motions of chromatin, the functional form of DNA inside the nucleus. Chromatin looks like beads on a string, with ball-like clusters of genetic material linked by strands of DNA. The researchers propose that molecular machines along the DNA cause segments of the chromatin to straighten and pull taut. This activity aligns neighboring strands to face the same direction. That alignment, in turn, results in a cascading waltz of genetic material shimmying across the nucleus.

The dancing DNA may play a role in gene expression, replication and remodeling, though the exact effects remain unclear, the researchers reported online October 22 in Proceedings of the National Academy of Sciences.

Wonderful to see the continuing progress of Mr. Omar Flores, with the support of his lovely wife, actress Mayra Sierra, today on the Venga la Alegria (VLA) show on TV Azteca (http://www.aztecauno.com/vengalaalegria) — The importance of an integrated approach to curing spinal cord injury including family, physical therapists, and the medical team at Regenerage (https://regenerage.clinic/)

https://www.youtube.com/watch?v=RRLo45i8q_A&t=4s

On the 23rd of this month, Dr. David Sinclair did an Ask Me Anything over at the Futurology subreddit in support of the NAD+ Mouse Project on Lifespan.io. There were a range of interesting questions from the community about his work in aging research, particularly the role of NAD+ in aging.

Dr. David A. Sinclair is a Professor in the Department of Genetics at Harvard Medical School and a co-joint Professor in the Department of Physiology and Pharmacology at the University of New South Wales. He is the co-Director of the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging and a Senior Scholar of the Ellison Medical Foundation. He obtained his Ph.D. in Molecular Genetics at the University of New South Wales, Sydney in 1995. He worked as a postdoctoral researcher at M.I.T. with Dr. Leonard Guarente; there, he co-discovered a cause of aging for yeast as well as the role of Sir2 in epigenetic changes driven by genome instability.

More recently, he has been in the spotlight for his work with NAD+ precursors and their role in aging and has been helping to develop therapies that replace NAD+, which is lost with aging, in order to delay the diseases of old age. Below are a selection of questions and answers from the AMA, and we urge you to head over to Reddit Futurology to check out the other questions that people asked.

Many mutations accumulate in the esophagus as we age.

Scientists at the MRC Cancer Unit of the Wellcome Sanger Institute and other departments of the University of Cambridge discovered that healthy esophageal tissue accumulates very high numbers of mutations with age, to the point that, by the time middle age is reached, it is likely to contain more cells with a particular mutation than cells without it [1].

Abstract

Continue reading “Mutations Accumulate in Healthy Esophageal Tissue With Age” »

Protein Chrdl1 appears to regulate brain plasticity.

Researchers from the Salk Institute have discovered that a protein called Chrdl1, secreted by astrocytes, is responsible for driving synapse maturation and limiting brain plasticity later in life [1].

Abstract

Continue reading “Protein Produced by Astrocytes Involved in Brain Plasticity” »

Cancer is the poster child of age-related diseases, and a recent study sheds light on why the risk of cancer rises dramatically as we age.

Abstract

For many cancer types, incidence rises rapidly with age as an apparent power law, supporting the idea that cancer is caused by a gradual accumulation of genetic mutations. Similarly, the incidence of many infectious diseases strongly increases with age. Here, combining data from immunology and epidemiology, we show that many of these dramatic age-related increases in incidence can be modeled based on immune system decline, rather than mutation accumulation. In humans, the thymus atrophies from infancy, resulting in an exponential decline in T cell production with a half-life of ∼16 years, which we use as the basis for a minimal mathematical model of disease incidence. Our model outperforms the power law model with the same number of fitting parameters in describing cancer incidence data across a wide spectrum of different cancers, and provides excellent fits to infectious disease data.

Continue reading “Dr. Sam Palmer – Thymic Involution and Cancer Risk” »