Lifeboat Foundation

Aging/longevity link!

Molecular biologists and bioengineers at the University of California San Diego have unraveled key mechanisms behind the mysteries of aging. They isolated two distinct paths that cells travel during aging and engineered a new way to genetically program these processes to extend lifespan.

The research is described July 17 in the journal Science.

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New insights into an elusive process that protects developing sperm cells from damage in growing embryos, sheds light on how genetic information passes down, uninterrupted, through generations.

The study identified a protein, known as SPOCD1, which plays a key role in protecting the early-stage precursors to sperm, known as germ cells, from damage in a developing embryo.

During their development, germ cells undergo a reprogramming process that leaves them vulnerable to rogue genes, known as jumping genes, which can damage their DNA and lead to infertility.

It might seem as though humans have little in common with the lowly yeast cell. Humans have hair, skin, muscles, and bones, among other attributes. Yeast have, well, none of those things.

But besides their obvious differences, yeast and humans, and much of life for that matter, have a great deal in common, especially at the cellular level. One of these commonalities is the enzyme our cells use to make RNA copies of sections of our DNA. The enzyme slides along a strand of DNA that has been unpacked from the chromosome in which it resides, to “read” the genetic code, and then assembles an RNA strand that contains the same code. This copying process, known as transcription, is what happens at a molecular level when a gene is activated in an organism. The enzyme responsible for it, RNA polymerase, is found in all eukaryotic cells (cells with a nucleus) and it is essentially the same in all of them, whether the cells are from a redwood, an earthworm, a caribou, or a mushroom.

That fact has presented a mystery for scientists, though: Although the DNA in a yeast cell is different in many ways from the DNA in a human cell, the same enzyme is able to work with both. Now, a team of Caltech researchers has discovered one way this happens.

Glioblastoma is the most aggressive type of cancer that begins with the brain and develops from astrocytes, star-shaped brain cells that help protect the brain from diseases in the blood and provide the brain’s neurons with nutrients, with around 12,000 cases diagnosed in the United States each year. Glioblastoma cells have more genetic abnormalities than the cells of other types of astrocytoma brain cancer. Now researchers from the University of Virginia (UVA) School of Medicine report they have identified an oncogene responsible for this deadly cancer.

Their study, “A cytoskeleton regulator AVIL drives tumorigenesis in glioblastoma,” is published in Nature Communications and led by Hui Li, PhD, associate professor, pathology, at the University of Virginia School of Medicine and the UVA Cancer Center.

“Glioblastoma is a deadly cancer, with no effective therapies. Better understanding and identification of selective targets are urgently needed. We found that advillin (AVIL) is overexpressed in all the glioblastomas we tested including glioblastoma stem/initiating cells, but hardly detectable in non-neoplastic astrocytes, neural stem cells or normal brain,” the researchers wrote.

Scientists successfully edited RNA in a living animal in such a way that the repaired RNA then corrected a mutation in a protein that gives rise to a debilitating neurological disorder in people known as Rett syndrome.

The advance by researchers at Oregon Health & Science University publishes in the journal Cell Reports.

“This is the first example of using programmable RNA editing to repair a gene in mouse models of a neurological disease,” said senior author Gail Mandel, Ph.D., senior scientist in the OHSU Vollum Institute. “This gives us an approach that has some traction.”

For the first time, scientists have determined the complete sequence of a human chromosome, namely the X chromosome, from ‘telomere to telomere’. This is truly a complete sequencing of a human chromosome, with no gaps in the base pair read and at an unprecedented level of accuracy.

A step closer towards the complete blueprint of a human being

The Human Genome Project was a 13-year-long, publicly funded project initiated in 1990 with the objective of determining the DNA sequence of the entire human genome.

In 2003, history was made. For the first time, the human genome was sequenced. Since then, technological improvements have enabled tweaks, adjustments, and additions, making the human genome the most accurate and complete vertebrate genome ever sequenced.

Nevertheless, some gaps remain — including human chromosomes. We have a pretty good grasp of them in general, but there are still some gaps in the sequences. Now, for the first time, geneticists have closed some of those gaps, giving us the first complete, gap-free, end-to-end (or telomere-to-telomere) sequence of a human X chromosome.

The accomplishment was enabled by a new technique called nanopore sequencing, which enables ultra-long-reads of DNA strands, providing a more complete and sequential assembly.

In this premier episode of Lifespan News, Brent Nally discusses Unity Biotechnology’s human trials of novel senolytic drugs, including a Phase 2 human trial of a senolytic drug for knee osteoarthritis; two proteins that allow LDL cholesterol to enter our cells; Ponce de Leon Health and epigenetic age reversal; the reason why naked mole rats are so resistant to cancer; XPrize adding longevity to its impact roadmaps; and a promo code for Ending Age-Related Diseases 2020, our upcoming online conference.

You can get your ticket to EARD2020 at https://www.eventbrite.com/e/ending-age-related-diseases-202…4918805703

Continue reading “Lifespan.io Launches Lifespan News” »

Gene drive guarantees that a trait will be passed to the next generation. But should society use this tool to control insect populations?