Lifeboat Foundation

De-extinction grabbed our imagination in the 90s with Jurassic Park. Scientists have since asked: how possible is it?

According to a new study, nearly impossible. But wait—it’s not all bad news. While bringing back a faithful copy of an extinct species may be impossible, we could bring back a hybrid species that’s a genetic mix between an extinct species and its modern descendant.

Published in Current Biology, the study eschews the grandiose mammoth, instead focusing on a tiny test case: the Christmas Island rat. Hefty in size and loudly vocal when invading docked ships and their cargo, the rodents were last seen in the 1900s. With a stroke of luck, the team recovered DNA from two well-preserved museum samples and compared them against a close relative: the Norway brown rat, a popular lab model for genetic studies today.

Immortal jellyfish could actually be the key to immortality and regeneration. This article talks more in depth of its importance in the search of immortality.

Turritopsis nutricula (T. nutricula) is the one of the known reported organisms that can revert its life cycle to the polyp stage even after becoming sexually mature, defining itself as the only immortal organism in the animal kingdom. Therefore, the animal is having prime importance in basic biological, aging, and biomedical researches. However, till date, the genome of this organism has not been sequenced and even there is no molecular phylogenetic study to reveal its close relatives. Here, using phylogenetic analysis based on available 16s rRNA gene and protein sequences of Cytochrome oxidase subunit-I (COI or COX1) of T. nutricula, we have predicted the closest relatives of the organism. While we found Nemopsis bachei could be closest organism based on COX1 gene sequence; T. dohrnii may be designated as the closest taxon to T. nutricula based on rRNA. Moreover, we have figured out four species that showed similar root distance based on COX1 protein sequence.

Keywords: Turritopsis nutricula, immortal jellyfish, trans-differentiation, phylogeny, relativeness.

Continue reading “The conserved mitochondrial gene distribution in relatives of Turritopsis nutricula, an immortal jellyfish” »

Marine Biological Laboratory finds gene captured from bacteria more than 60 million years ago.

Your DNA holds the blueprint to build your body, but it’s a living document: Adjustments to the design can be made by epigenetic marks. Cataloguing these marks and how they work is important for understanding biology and genetics—and coming up with therapies to address diseases and disorders.

In humans and our fellow eukaryotes, two principal epigenetic marks are known. But a team from the University of Chicago-affiliated Marine Biological Laboratory has discovered a third, novel epigenetic mark—one formerly known only in bacteria—in small freshwater animals called bdelloid rotifers.

Summary: Histone H4 mutations in the spool cause intellectual disabilities and developmental delays, a new study reports.

Source: University of Otago.

University of Otago-led research has identified a new rare genetic mutation which will finally give families around the world answers as to what is affecting their loved one.

A Stanford University-led research team has set a new Guinness World Record for the fastest DNA sequencing technique using AI computing to accelerate workflow speed.

The research, led by Dr Euan Ashley, professor of medicine, genetics and biomedical data science at Stanford School of Medicine, in collaboration with Nvidia, Oxford Nanopore Technologies, Google, Baylor College of Medicine, and the University of California, achieved sequencing in just five hours and two minutes.

The study, published in The New England Journal of Medicine, involved speeding up every step of genome sequencing workflow by relying on new technology. This included using nanopore sequencing on Oxford Nanopore’s PromethION Flow Cells to generate more than 100 gigabases of data per hour, and Nvidia GPUs on Google Cloud to speed up the base calling and variant calling processes.

An international team of researchers claim to have slowed the signs of aging in mice by resetting their cells to younger states, using a genetic treatment.

To the scientists, The Guardian reports, it’s a breakthrough in cell regeneration and therapeutic medicine that doesn’t seem to cause any unexpected issues in mice.

“We are elated that we can use this approach across the life span to slow down aging in normal animals,” said Juan Carlos Izpisua Belmonte, Salk Institute professor and co-corresponding author of a new study published in the journal Nature Aging, in a statement. “The technique is both safe and effective in mice.”

To date, scientists have largely been in the dark with regard to how individual circuits operate in the highly branched networks of the brain. Mapping these networks is a complicated process, requiring precise measurement methods. For the first time, scientists from the Max Planck Institute for Biological Cybernetics in Tübingen, Germany, together with researchers from the Ernst Strüngmann Institute in Frankfurt and Newcastle University in England, have now functionally proven a so far poorly understood neural connection in the visual system of monkeys using optogenetic methods. To this end, individual neurons were genetically modified so that they became sensitive to a light stimulus.

For decades microstimulation was the method of choice for activating neurons – the method proved to be reliable and accurate. That is why it is also used medically for deep brain stimulation. The Tübingen-based scientists were now able to show that optogenetics, a biological technique still in its infancy, delivers comparable results.

With optogenetics it is possible to directly influence the activity of neurons by light. To do this individual neurons are genetically modified with the help of viruses to express light-sensitive ion channels in their cell membrane. Through blue light pulses delivered directly into the brain, the modified neurons can then be systematically activated.

From the time of Hippocrates, physicians have suspected a link between epilepsy and depression. Now, for the first time, scientists at Rutgers University-New Brunswick and Columbia University have found evidence that seizures and mood disorders such as depression may share the same genetic cause in some people with epilepsy, which may lead to better screening and treatment to improve patients’ quality of life.

The scientists studied dozens of unusual families with multiple relatives who had epilepsy, and compared the family members’ lifetime prevalence of mood disorders with that of the U.S. population.

They found an increased incidence of mood disorders in persons who suffer from a type of the condition called focal epilepsy, in which seizures begin in just one part of the brain. But mood disorders were not increased in people with generalized epilepsy, in which seizures start on both sides of the brain.

Researchers created a mathematical framework to examine the genome and detect signatures of natural selection, deciphering the evolutionary past and future of non-coding DNA.

Despite the sheer number of genes that each human cell contains, these so-called “coding” DNA sequences comprise just 1% of our entire genome. The remaining 99% is made up of “non-coding” DNA — which, unlike coding DNA, does not carry the instructions to build proteins.

One vital function of this non-coding DNA, also called “regulatory” DNA, is to help turn genes on and off, controlling how much (if any) of a protein is made. Over time, as cells replicate their DNA to grow and divide, mutations often crop up in these non-coding regions — sometimes tweaking their function and changing the way they control gene expression. Many of these mutations are trivial, and some are even beneficial. Occasionally, though, they can be associated with increased risk of common diseases, such as type 2 diabetes, or more life-threatening ones, including cancer.