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The effect of a TE on its host can be classified analogous to the effect of point mutations. In the majority of cases, the consequences of a TE their activity (transposition to a new genomic site) is either neutral or deleterious. The latter occurs, when TEs disrupt genes and their functions, or when, they trigger de-novo genomic instability by transposition or TE-mediated chromosomal rearrangements, which can lead to disease^{1, 3}. TEs can occasionally have a positive impact on the host genome, for example, by impacting gene regulatory networks. In the British peppered moth (Biston betularia), a TE inserted within the first intron of the cortex gene, resulted in increased transcription levels, subsequently affecting cell cycle regulation during wing-disc development through the amount of cortex protein product, resulting in the iconic melanic form⁴. However, more research is needed to understand these different evolutionary impacts that TEs can have when interacting with their host genome.

The increased accessibility to high throughput sequencing technologies has greatly increased our ability to analyse genetic differences caused by changes at the nucleotide level, and patterns of natural selection on coding sequences, and simultaneously allowed us to disentangle phenotypic differences at the nucleotide level. Mounting evidence has started to shed light on non-coding regions having important effects on genomic variation³. While TEs can be found in the genomes of virtually all organisms, large proportions of TEs are often absent from reference genomes, as their repetitive nature impedes their assembly and can result in collapsed regions within the reference genome^{2, 5}. These difficulties have led to an increased demand for reference genomes that are of a higher quality and are more complete. More importantly, a new demand for high-quality annotations of non-coding regions in reference genomes has surfaced. Annotations of non-coding regions are imperative to study the evolution of these regions between and within species. Improvements in sequencing techniques, especially the addition of long-read sequencing, and improved bioinformatic analytical tools are resulting in the assembly of increasingly gapless reference genomes, enabling the curation of high-quality TE annotations.

The current efforts of large consortia, such as the VGP⁶ and the B10K⁷ to create high-quality references for a wide variety of organisms provide invaluable data to improve our endeavours for a better understanding of TEs. With these new resources we can take our research into TEs and their effects on host genomes further, for example, to better understand the evolution of complex traits across phylogenomic scales. One such a complex trait is seasonal bird migration and recent research across a migratory divide in willow warblers identified a diagnostic TE correlated with migratory direction⁸. Here we focus on the Eurasian blackcap (Sylvia atricapilla), another iconic model species for bird migration, and consequently, the resource published here may be able to add insight to the quest to resolve the genetic background of migratory behaviour.

A new CRISPR-based gene-editing tool has been developed which could lead to better treatments for patients with genetic disorders. The tool is an enzyme, AsCas12f, which has been modified to offer the same effectiveness but at one-third the size of the Cas9 enzyme commonly used for gene editing. The compact size means that more of it can be packed into carrier viruses and delivered into living cells, making it more efficient.

Researchers created a library of possible AsCas12f mutations and then combined selected ones to engineer an AsCas12f enzyme with 10 times more editing ability than the original unmutated type. This engineered AsCas12f has already been successfully tested in mice and has the potential to be used for new, more effective treatments for patients in the future.

By now you have probably heard of CRISPR, the gene-editing tool which enables researchers to replace and alter segments of DNA. Like genetic tailors, scientists have been experimenting with “snipping away” the genes that make mosquitoes malaria carriers, altering food crops to be more nutritious and delicious, and in recent years begun human trials to overcome some of the most challenging diseases and genetic disorders.

Ageing has always been inevitable but fasting, epigenetic reprogramming and parabiosis are just some of the scientific techniques that seem to help people stay young. Might the Peter Pan dream become real?

00:00 — Can science turn back the clock?
01:01 — Centenarians.
02:51 — What is ageing?
04:51 — Dietary restriction.
06:00 — Roundworms.
07:55 — Epigenetics.
09:43 — Blood and guts.
11:40 — Senolytics.
12:38 — Metformin.
13:51 — Anti-ageing treatments are coming.

Continue reading “Longevity: can ageing be reversed?” »

Ribonucleic acid (RNA) is a molecule which is present in cells and made of genetic material to help build proteins necessary for cell function. RNA provides a template for the construction of proteins and is essential for cell and organism life. Immune cells rely on these proteins, including CD8⁺ or cytotoxic T cells which are responsible for killing invading pathogens. Importantly, cytotoxic T cells are a major component of the memory immune response. A pool of T cells specifically designed to recognize an invader is stored for future invasion of that particular pathogen. For example, once these cells are exposed to an invading antigen or protein, the immune system will expand T cells specific to that antigen and remember the antigen next time it enters the body. Vaccines work in a similar way by introducing a foreign antigen to the body, so the immune system is ready if the pathogen ever enters your body in the future. Only a small set of T cells that expand survive and it is unclear how this process occurs.

Recently a team of researchers at the University of Massachusetts Amherst (UMass) demonstrated that a single strand of RNA governs a T cells ability to recognize and kill tumors. The single strand of RNA is known as let-7 and is a microRNA, which is responsible for gene expression regulation. The recent discovery may improve vaccine development and cellular memory to enhance immunotherapy against cancers. Immunotherapy is a general term referring to cancer therapies that try to activate the immune system to kill the tumor compared to other drugs that try to directly kill the tumor with chemicals, such as chemotherapy.

The report published in Nature Communications identified that the microRNA, let-7, may enhance memory of T cells. Researchers led by Dr. Leonid Pobezinsky, Associate Professor of Veterinary and Animal Sciences at UMass, further built on our understanding of how T cells form immune memory. Pobezinsky and colleagues found that a small piece of microRNA that has been present throughout evolution is expressed in memory cells. Additionally, they found that more let-7 a cell has, the more likely that cell will recognize a cancer cell and kill it. The increased let-7 also indicates that the cell will turn into a memory cell after being exposed to an antigen. The regulation of enhanced memory T cells by let-7 is an integral process key to fight infections. This is a critical finding, especially because memory cells retain stem-like characteristics and can survive for decades.

Summary: Scientists made a novel discovery using zebrafish with a genetic mutation. These ‘deep-blind’ fish lack connections between the retina and brain yet retain functional brain circuits.

Remarkably, despite their inability to see, direct brain stimulation through optogenetics triggers normal visual behavior. This suggests that much of the zebrafish brain’s wiring is innate and doesn’t rely heavily on visual experience.

Hospital nurseries routinely place soft bands around the tiny wrists of newborns that hold important identifying information such as name, sex, mother, and birth date. Researchers at Rockefeller University are taking the same approach with newborn brain cells—but these neonates will keep their ID tags for life, so that scientists can track how they grow and mature, as a means for better understanding the brain’s aging process.

As described in a new paper in Cell, the new method developed by Rockefeller geneticist Junyue Cao and his colleagues is called TrackerSci (pronounced “sky”). This low-cost, high-throughput approach has already revealed that while newborn cells continue to be produced through life, the kinds of cells being produced greatly vary in different ages. This groundbreaking work, led by co-first authors Ziyu Lu and Melissa Zhang from Cao’s lab, promises to influence not only the study of the brain but also broader aspects of aging and disease across the human body.

“The cell is the basic functional unit of our body, so changes to the cell essentially underlie virtually every disease and the aging process,” says Cao, head of the Laboratory of Single-Cell Genomics and Population Dynamics. “If we can systematically characterize the different cells and their dynamics using this novel technique, we may get a panoramic view of the mechanisms of many diseases and the enigma of aging.”

Early-life stress (ELS) is one of the strongest lifetime risk factors for depression, anxiety, suicide, and other psychiatric disorders, particularly after facing additional stressful events later in life. Human and animal studies demonstrate that ELS sensitizes individuals to subsequent stress. However, the neurobiological basis of such stress sensitization remains largely unexplored. We hypothesized that ELS-induced stress sensitization would be detectable at the level of neuronal ensembles, such that cells activated by ELS would be more reactive to adult stress. To test this, we leveraged transgenic mice to genetically tag, track, and manipulate experience-activated neurons. We found that in both male and female mice, ELS-activated neurons within the nucleus accumbens (NAc), and to a lesser extent the medial prefrontal cortex, were preferentially reactivated by adult stress. To test whether reactivation of ELS-activated ensembles in the NAc contributes to stress hypersensitivity, we expressed hM4Dis receptor in control or ELS-activated neurons of pups and chemogenetically inhibited their activity during experience of adult stress. Inhibition of ELS-activated NAc neurons, but not control-tagged neurons, ameliorated social avoidance behavior following chronic social defeat stress in males. These data provide evidence that ELS-induced stress hypersensitivity is encoded at the level of corticolimbic neuronal ensembles.

SIGNIFICANCE STATEMENT Early-life stress enhances sensitivity to stress later in life, yet the mechanisms of such stress sensitization are largely unknown. Here, we show that neuronal ensembles in corticolimbic brain regions remain hypersensitive to stress across the life span, and quieting these ensembles during experience of adult stress rescues stress hypersensitivity.

Once we fully we understand intelligence it could be essentially increased to nearly infinite levels once everything is quantified like this article talks about 😗😁.

Modern humans have a gene mutation that boosts the growth of neurons in the brain neocortex, a brain region associated with higher intelligence.

By Michael Le Page

Continue reading “A single gene mutation may have made us smarter than Neanderthals” »

Mothers who eat apples and herbs in early pregnancy could be protecting the brain health of their children and grandchildren, a Monash University study using genetic models has found.

The discovery is part of a project that found a mother’s diet can affect not just her child’s brain but also those of her grandchildren.

Published in Nature CellBiology, the Monash Biomedicine Discovery Institute study found that certain foods could help protect against the deterioration of brain function.

Continue reading “A mother’s diet can protect her grandchildren’s brains: genetic model study” »