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A research team from the Hefei Institutes of Physical Science of the Chinese Academy of Sciences (CAS) has developed an analysis service platform called CRISPRimmunity, which was an interactive web server for identifying important molecular events related to CRISPR and regulators of genome editing systems. The study is published in Nucleic Acids Research.

The new CRISPRimmunity platform was designed for integrated analysis and prediction of CRISPR-Cas and anti-CRISPR systems. It includes customized databases with annotations for known anti-CRISPR proteins, anti-CRISPR-associated proteins, class II CRISPR-Cas systems, CRISPR array types, HTH structural domains and mobile genetic elements. These resources allow the study of molecular events in the co-evolution of CRISPR-Cas and anti-CRISPR systems.

To improve prediction accuracy, the researchers used strategies such as homology analysis, association analysis and self-targeting in prophage regions to predict anti-CRISPR proteins. When tested on data from 99 experimentally validated Acrs and 676 non-Acrs, CRISPRimmunity achieved an accuracy of 0.997 for anti-CRISPR protein prediction.

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Cell toxicity and genomic instability are potential side effects from the use of CRISPR-Cas9. The gene editing tool can also cause large rearrangements of DNA through retrotransposition to theoretically trigger tumor development.

While rare, the fact that CRISPR is used to edit millions of cells for some therapies means precautionary steps are warranted given the potential increase in cancer risk. However, retrotransposition is much rarer during base editing, a more precise technique that chemically changes just one “letter” of the genetic code without causing a double-strand break in DNA.

Although MHRA decided that the benefits of Casgevy outweigh its risks, the U.K. regulator granted a one-year conditional marketing authorization of the world-first gene therapy based on the findings of two global clinical trials, noting that no significant safety concerns were identified during the trials.

An algorithm that can analyse hundreds of millions of genetic sequences has identified DNA-cutting genes and enzymes that are extremely rare in nature.

Human chromosomes are long polymer chains that store genetic information. The nucleus of each cell contains the entire human genome (DNA) encoded on 46 chromosomes with a total length of about 2 meters. To fit into the microscopic cell nucleus and at the same time provide constant access to genetic information, chromosomes are folded in the nucleus in a special, predetermined way. DNA folding is an urgent task at the intersection of polymer physics and systems biology.

A few years ago, as one of the mechanisms of chromosome folding, researchers put forward a hypothesis of active extrusion of loops on chromosomes by molecular motors. Although the ability of motors to extrude DNA in vitro has been demonstrated, observing loops in a living cell experimentally is a technically very difficult, almost impossible, task.

A team of scientists from Skoltech, MIT, and other leading scientific organizations in Russia and the U.S. have presented a physical model of a polymer folded into loops. The analytical solution of this model allowed scientists to reproduce the universal features of chromosome packing based on the experimental data—the image shows the peak-dip derivative curve of the contact probability.

Two Eötvös Loránd University researchers have made an exciting breakthrough in understanding how we age.

Researchers Dr. Ádám Sturm and Dr. Tibor Vellai from Eötvös Loránd University in Hungary have achieved a significant discovery in the study of aging. Their research centered on “transposable elements” (TEs) in our DNA

DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

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The sleep-wake cycle is among the most well-known circadian rhythms in the body and is severely affected in Alzheimer’s disease (AD). “Eighty percent of patients with AD suffer dysregulation or disruption of circadian rhythms, and the obvious clinical manifestations are the sleep-wake reversals,” Desplats said. “These patients are very sleepy during the day, agitated during the night, more confused, and sometimes aggressive.”

The feeding-fasting cycle is one of the strongest signals you can send the body to entrain the circadian clock.-Paula Desplats, University of California, San Diego

In a recent study published in Cell Metabolism, Desplats’s team used mice that are genetically engineered to develop AD to test whether intermittent fasting improves circadian rhythm abnormalities.³ Rather than restricting calories or making dietary changes, they simply limited food access to a defined six-hour daily window. They found that time-restricted eating improved sleep, metabolism, memory, and cognition, and reduced brain amyloid deposits and neuroinflammatory gene expression. “Many of the genes that are affected in AD are rhythmically expressed in the brain, meaning that they are in direct relation with the circadian clock and are involved in functions that are fundamental to AD pathology,” Desplats said. Intermittent fasting restored the rhythmic activity of these genes, but the real surprise was the extent to which it mitigated brain amyloid deposits and improved cognition and sleep-wake behaviors. “I didn’t expect that it will have such a dramatic impact on pathology,” Desplats said.

The regulation of genetic diversity resulting from polyploidization and its impact on environmental adaptability remain unclear. Here, the authors show that