Lifeboat Foundation

To better understand the role of bacteria in health and disease, National Institutes of Health researchers fed fruit flies antibiotics and monitored the lifetime activity of hundreds of genes that scientists have traditionally thought control aging. To their surprise, the antibiotics not only extended the lives of the flies but also dramatically changed the activity of many of these genes. Their results suggested that only about 30% of the genes traditionally associated with aging set an animal’s internal clock while the rest reflect the body’s response to bacteria.

“For decades scientists have been developing a hit list of common aging genes. These genes are thought to control the aging process throughout the animal kingdom, from worms to mice to humans,” said Edward Giniger, Ph.D., senior investigator, at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study published in iScience. “We were shocked to find that only about 30% of these genes may be directly involved in the aging process. We hope that these results will help medical researchers better understand the forces that underlie several age-related disorders.”

The results happened by accident. Dr. Giniger’s team studies the genetics of aging in a type of fruit fly called Drosophila. Previously, the team showed how a hyperactive immune system may play a critical role in the neural damage that underlies several aging brain disorders. However, that study did not examine the role that bacteria may have in this process.

The scientists found “biotin paint” on a protein named RSK1, which is part of a complex that keeps a nearby group of proteins, called RAS proteins, dormant. The scientists were surprised to discover that when they inactivated mutant KRAS, the nearby RSK1 complex stopped working as well. This allowed the RAS proteins to activate and take over the work of the missing mutant KRAS.

Cancer cells can become resistant to treatments through adaptation, making them notoriously tricky to defeat and highly lethal. Cold Spring Harbor Laboratory (CSHL) Cancer Center Director David Tuveson and his team investigated the basis of “adaptive resistance” common to pancreatic cancer. They discovered one of the backups to which these cells switch when confronted with cancer-killing drugs.

KRAS is a gene that drives cell division. Most pancreatic cancers have a mutation in the KRAS protein, causing uncontrolled growth. But, drugs that shut off mutant KRAS do not stop the proliferation. The cancer cells find a way to bypass the blockage and keep on dividing. Derek Cheng, the lead author of the study and a former Medical Scientist Training Program student in the Tuveson lab, compares this process to backup engines on a ship. He says, “You take away your main engine, you’re kind of on some backup engines. But it’s getting by on those. The ship isn’t sinking yet. It’s still moving at a slower pace. Ultimately what we want to do is sink the ship.”

Continue reading “How pancreatic cancer cells dodge drug treatments” »

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Cellular senescence, a state of permanent growth arrest, has emerged as a hallmark and fundamental driver of organismal aging. It is regulated by both genetic and epigenetic factors. Despite a few previously reported aging-associated genes, the identity and roles of additional genes involved in the regulation of human cellular aging remain to be elucidated. Yet, there is a lack of systematic investigation on the intervention of these genes to treat aging and aging-related diseases.

How many aging-promoting genes are there in the human genome? What are the molecular mechanisms by which these genes regulate aging? Can gene therapy alleviate individual aging? Recently, researchers from the Chinese Academy of Sciences have shed new light on the regulation of aging.

Continue reading “Scientists Develop New Gene Therapy Strategy to Delay Aging and Extend Lifespan” »

Circa 2017 using this can lead to near Ironman or foglet bodies with the ability to self heal the human body. It could be used on smartphones to heal people not needing a doctor in the future. This also would allow for the biological singularity to happen.

This device shoots new genetic code into cells to make them change their purpose. Researchers say the chip could someday be used to treat injuries in humans. But they’ve got a long, long way to go.

A once forgotten technology, RNA editing has been gaining traction as a treatment for genetic conditions given its key advantages over CRISPR gene editing.

Since CRISPR-Cas9 gene editing was first reported in 2012, its promise of making gene editing faster, cheaper, and easier than ever before led to an explosion in the number of publications referring to this gene editing technology.

An increasing number of research labs and companies are aiming to translate CRISPR gene editing into therapies for genetic diseases. However, further research has unveiled that there are more limitations to using CRISPR-Cas9 to cure diseases than initially expected. For example, the technology has been reported to introduce off-target changes to the DNA, raising concerns about its safety.

Novel study designed to correct genetic abnormalities of red blood cells.

Cleveland Clinic researchers are enrolling patients in a clinical trial that aims to work toward a cure for sickle cell disease, by changing the patient’s genetics. Sickle cell disease, a genetic blood disorder, is a painful and debilitating condition for which there are few approved therapies.

The multicenter study will evaluate the safety and effectiveness of a single dose of EDIT-301, an experimental one-time gene editing cell therapy that modifies a patient’s own blood-forming stem cells to correct the mutation responsible for sickle cell disease.

Continue reading “Cleveland Clinic Trial to Test Gene Therapy as Treatment of Sickle Cell Disease” »

This video explains the mendel’s law of segregation.

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Biologists in the UK and Austria have discovered 71 new imprinted genes in the mouse genome.

Biologists at the Universities of Bath and Vienna have discovered 71 new ‘imprinted’ genes in the mouse genome, a finding that takes them a step closer to unraveling some of the mysteries of epigenetics – an area of science that describes how genes are switched on (and off) in different cells at different stages in development and adulthood.

To understand the importance of imprinted genes to inheritance, we need to step back and ask how inheritance works in general. Most of the thirty trillion cells in a person’s body contain genes that come from both their mother and father, with each parent contributing one version of each gene. The unique combination of genes goes part of the way to making an individual unique. Usually, each gene in a pair is equally active or inactive in a given cell. This is not the case for imprinted genes. These genes – which make up less than one percent of the total of 20000+ genes – tend to be more active (sometimes much more active) in one parental version than the other.

The metazoan mitochondrial genome (mitogenome) is an ideal model system for comparative and evolutionary genomic research. The typical mitogenome of metazoans encodes a conserved set of 37 genes for 13 protein-coding genes (PCGs), two ribosomal RNA (rRNA) genes, and 22 transfer RNA (tRNA) genes¹, with genome-level characters, such as genome size, gene content, and gene order, display high diversity in some lineages^2,3. Gene rearrangements are observed frequently in some groups, while gene duplication and loss are distributed sporadically in limited lineages such as Bivalvia, Cephalopod, and Afrobatrachia^4,5,6. These remaining duplicate genes and pseudogenes represent important data for exploring the evolutionary history and mechanisms of gene rearrangement and recruitment. For the arrangement of mitochondrial genes, the variation in relative positions of PCGs and rRNA genes are more limited compared with that of tRNA genes across organisms within a phylum⁷. The tRNA genes with characteristics of diverse changes in relative position, gene content, and secondary structure, are considered as an important tool in studying the evolution of mitogenome, in particular to the rearrangement mechanism^8,9,10. Additionally, its variation is usually linked to evolutionary relationships in a wide range of lineages at different taxonomic levels suggesting these features of tRNA could be utilized as useful phylogenetic markers¹¹.

The extensive gene rearrangements (including PCGs and RNA) of insect mitogenomes have been detected in several lineages within the Diptera (Trichoceridae, Cecidomyiidae), Hemiptera (Enicocephalidae), Hymenoptera, Thysanoptera, Psocoptera and Phthiraptera^{12,13,14,15,16,17,18}, while most of investigated mitogenomes share the same gene order with the hypothesized ancestral pancrustacean mitogenome arrangement¹⁹ or possess rare tRNA rearrangement. Previously reported dictyopteran mitogenomes consistently display the typical ancestral gene order and content, however only two species are praying mantises and the rest are cockroaches and termites. Members of the Mantodea, a separate lineage within the Dictyoptera, have evolved many unique morphological and behavioural features as the ambush and pursuit predators^20,21,22. A better understanding of the diversity of mitogenome evolution in this enigmatic order underlines the need for exploring more taxa with the diverse praying mantis.

Herein, we report eight new mitogenomes from Mantodea and describe their general characteristics. Two new gene rearrangements and reassignment of tRNA genes are described, and evolutionary mechanisms for the gene rearrangements and duplication are discussed. Further, we examine the relationship between tRNA gene duplication and codon usage, and investigate whether these tRNA features vary with phylogeny.