Lifeboat Foundation

Viruses are tiny invaders that cause a wide range of diseases, from rabies to tomato spotted wilt virus and, most recently, COVID-19 in humans. But viruses can do more than elicit sickness — and not all viruses are tiny.

Large viruses, especially those in the nucleo-cytoplasmic large DNA virus family, can integrate their genome into that of their host — dramatically changing the genetic makeup of that organism. This family of DNA viruses, otherwise known as “giant” viruses, has been known within scientific circles for quite some time, but the extent to which they affect eukaryotic organisms has been shrouded in mystery — until now.

“Viruses play a central role in the evolution of life on Earth. One way that they shape the evolution of cellular life is through a process called endogenization, where they introduce new genomic material into their hosts. When a giant virus endogenizes into the genome of a host algae, it creates an enormous amount of raw material for evolution to work with,” said Frank Aylward, an assistant professor in the Department of Biological Sciences in the Virginia Tech College of Science and an affiliate of the Global Change Center housed in the Fralin Life Sciences Institute.

Circa 2013

The Book of Genesis puts Adam and Eve together in the Garden of Eden, but geneticists’ version of the duo — the ancestors to whom the Y chromosomes and mitochondrial DNA of today’s humans can be traced — were thought to have lived tens of thousands of years apart. Now, two major studies of modern humans’ Y chromosomes suggest that ‘Y-chromosome Adam’ and ‘mitochondrial Eve’ may have lived around the same time after all^{1, 2}.

When the overall population size does not change (as is likely to have happened for long periods of human history), men have, on average, just one son. In this case, evolutionary theory predicts that for any given man there is a high probability that his paternal line will eventually come to an end. All of his male descendants will then have inherited Y chromosomes from other men. In fact, it is highly probable that at some point in the past, all men except one possessed Y chromosomes that by now are extinct. All men living now, then, would have a Y chromosome descended from that one man — identified as Y-chromosome Adam. (The biblical reference is a bit of a misnomer because this Adam was by no means the only man alive at his time.)

Continue reading “Genetic Adam and Eve did not live too far apart in time” »

A group of researchers from the Institute of Neurosciences UMH-CSIC, in Alicante, led by Dr. Eloísa Herrera, has discovered a genetic program essential for the formation of bilateral circuits, such as the one that makes possible 3D vision or the one enabling motor coordination. The finding, carried out in mice, is published today in Science Advances.

This new study not only clarifies how images are transmitted from the retina to the brain in order to see in 3D, but also helps us to understand how laterality is established in other neuronal circuits, such as the one that allows us to coordinate movements at both sides of the body, Dr. Herrera explains.

The work also reveals the important role of a protein known as Zic2 in the regulation of a signaling pathway called Wnt, which is fundamental for the correct development of the embryo and is highly conserved among species, from fruit flies to humans, including mice, in which this study has been carried out.

– and Why We Don’t Have To — A conversation with David Sinclair.

David Andrew Sinclair AO is an Australian biologist who is a professor of genetics and co-Director of the Paul F. Glenn Center for the Biology of Aging at Harvard Medical School.

Continue reading “Why We Age – and Why We Don’t Have To — A conversation with David Sinclair” »

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Most newly-discovered species are easy to classify. They have features that are very consistent with well-known organisms and they fit neatly into one category or another. Every so often, one comes along that leaves scientists wondering, “What the hell is this thing?” Case in point: Dendrogramma. This new genus represents two species of deep-sea animals that resemble mushrooms but don’t really fit in with any other known animals. As a result, this organism could bring fairly large changes to the phylogenetic tree. The research was conducted by a team of researchers from the University of Copenhagen and the paper was published in PLOS ONE.

The 18 specimens were caught during an expedition in the Bass Strait, between Australia and Tasmania back in 1986. Two samples were dredged up from depths of 400 and 1000 meters. The samples had been fixed and preserved, rendering them unable to undergo genetic analysis. However, the preservation process was not done particularly well, causing them to become bleached and shrunken. They turned brittle over time.

Continue reading “Newly-Discovered Deep Sea ‘Mushroom’ Could Re-Write Tree of Life” »

A genetic disposition that plays a role in the development of the heart in the embryo also appears to play a key role in the human immune system. This is shown by a recent study led by the University of Bonn (Germany). When the gene is not active enough, the immune defense system undergoes characteristic changes, causing it to lose its effectiveness. Doctors speak of an aging immune system, as a similar effect can often be observed in older people. In the medium term, the results may contribute to reduce these age-related losses. The study is published in the journal Nature Immunology.

The gene with the cryptic abbreviation CRELD1 has so far been a mystery to science. It was known to play an important role in the development of the heart in the embryo. However, CRELD1 remains active after birth: Studies show that it is regularly produced in practically all cells of the body. For what purpose, however, was previously completely unknown.

The Bonn researchers used a novel approach to answer this question. Nowadays, scientific studies with human participants often include so-called transcriptome analyses. By these means, one can determine which genes are active to what extent in the respective test subjects. Researchers are also increasingly making the data they obtain available to colleagues, who can then use it to work on completely different matters. “And this is exactly what we did in our study,” says Dr. Anna Aschenbrenner from the LIMES Institute at the University of Bonn and member of the ImmunoSensation² Cluster of Excellence.

Circa 2019

In the past decade, remarkable progress has been made in reprogramming terminally differentiated somatic cells and cancer cells into induced pluripotent cells and cancer cells with benign phenotypes. Recent studies have explored various approaches to induce reprogramming from one cell type to another, including lineage-specific transcription factors-, combinatorial small molecules-, microRNAs- and embryonic microenvironment-derived exosome-mediated reprogramming. These reprogramming approaches have been proven to be technically feasible and versatile to enable re-activation of sequestered epigenetic regions, thus driving fate decisions of differentiated cells. One of the significant utilities of cancer cell reprogramming is the therapeutic potential of retrieving normal cell functions from various malignancies. However, there are several major obstacles to overcome in cancer cell reprogramming before clinical translation, including characterization of reprogramming mechanisms, improvement of reprogramming efficiency and safety, and development of delivery methods. Recently, several insights in reprogramming mechanism have been proposed, and determining progress has been achieved to promote reprogramming efficiency and feasibility, allowing it to emerge as a promising therapy against cancer in the near future. This review aims to discuss recent applications in cancer cell reprogramming, with a focus on the clinical significance and limitations of different reprogramming approaches, while summarizing vital roles played by transcription factors, small molecules, microRNAs and exosomes during the reprogramming process.

The Sterile Insect Technique (SIT) is based on the mass release of sterilized male insects to reduce the pest population size via infertile mating. Critical for all SIT programs is a conditional sexing strain to enable the cost-effective production of male-only populations. Compared to current female-elimination strategies based on killing or sex sorting, generating male-only offspring via sex conversion would be economically beneficial by doubling the male output. Temperature-sensitive mutations known from the D. melanogaster transformer-2 gene (tra2^ts) induce sex conversion at restrictive temperatures, while regular breeding of mutant strains is possible at permissive temperatures. Since tra2 is a conserved sex determination gene in many Diptera, including the major agricultural pest Ceratitis capitata, it is a promising candidate for the creation of a conditional sex conversion strategy in this Tephritid. Here, CRISPR/Cas9 homology-directed repair was used to induce the D. melanogaster-specific tra2^ts SNPs in Cctra2. 100% female to male conversion was successfully achieved in flies homozygous for the tra2^ts2 mutation. However, it was not possible, to identify a permissive temperature for the mutation allowing the rearing of a tra2^ts2 homozygous line, as lowering the temperature below 18.5 °C interferes with regular breeding of the flies.

The p53 gene like the Rb gene, is a tumor suppressor gene, i.e., its activity stops the formation of tumors. If a person inherits only one functional copy of the p53 gene from their parents, they are predisposed to cancer and usually develop several independent tumors in a variety of tissues in early adulthood. This condition is rare, and is known as Li-Fraumeni syndrome. However, mutations in p53 are found in most tumor types, and so contribute to the complex network of molecular events leading to tumor formation.

The p53 gene has been mapped to chromosome 17. In the cell, p53 protein binds DNA, which in turn stimulates another gene to produce a protein called p21 that interacts with a cell division-stimulating protein (cdk2). When p21 is complexed with cdk2 the cell cannot pass through to the next stage of cell division. Mutant p53 can no longer bind DNA in an effective way, and as a consequence the p21 protein is not made available to act as the ‘stop signal’ for cell division. Thus cells divide uncontrollably, and form tumors.

Help with unraveling the molecular mechanisms of cancerous growth has come from the use of mice as models for human cancer, in which powerful ‘gene knockout’ techniques can be used. The amount of information that exists on all aspects of p53 normal function and mutant expression in human cancers is now vast, reflecting its key role in the pathogenesis of human cancers. It is clear that p53 is just one component of a network of events that culminate in tumor formation.