Lifeboat Foundation

A new CRISPR-Cas toolkit, dubbed “pAblo·pCasso,” is set to transform the landscape of bacterial genome editing, offering unprecedented precision and flexibility in genetic engineering. The new technology, developed by researchers at The Novo Nordisk Foundation Center for Biosustainability (DTU Biosustain), expands the range of genome sites available for base-editing and dramatically accelerates the development of bacteria for a wide range of bioproduction applications.

PAblo·pCasso sets a new standard in CRISPR-Cas technologies. A key innovation is to enable precise and reversible DNA edits within Gram-negative bacteria, a feat not achievable with previous CRISPR systems. The toolkit utilizes specialized fusion enzymes, modified Cas9 coupled with editor modules CBE or ABE, which act like molecular pencils to alter specific DNA nucleotides, thus accurately controlling gene function.

The development of pAblo·pCasso involved overcoming significant challenges. Traditional CRISPR-Cas systems were limited by their need for specific DNA sequences (PAM sequences) near the target site and were less effective in making precise, single-nucleotide changes. pAblo·pCasso transcends these limitations by incorporating advanced Cas-fusion variants that do not require specific PAM sequences, thereby expanding the range of possible genomic editing sites.

When young, these neurons signal fatty tissues to release energy fueling the brain. With age, the line breaks down. Fat cells can no longer orchestrate their many roles, and neurons struggle to pass information along their networks.

Using genetic and chemical methods, the team found a marker for these neurons—a protein called Ppp1r17 (catchy, I know). Changing the protein’s behavior in aged mice with genetic engineering extended their life span by roughly seven percent. For an average 76-year life span in humans, the increase translates to over five years.

The treatment also altered the mice’s health. Mice love to run, but their vigor plummets with age. Reactivating the neurons in elderly mice revived their motivation, transforming them from couch potatoes into impressive joggers.

Discovery opens window to more effective treatment. Meet MYC, the shapeless protein responsible for making the majority of human cancer cases worse. UC Riverside researchers have found a way to rein it in, offering hope for a new era of treatments.

In healthy cells, MYC helps guide the process of transcription, in which genetic information is converted from DNA into RNA and, eventually, into proteins.

“Normally, MYC’s activity is strictly controlled. In cancer cells, it becomes hyperactive, and is not regulated properly,” said UCR associate professor of chemistry Min Xue.

FactorBioscience Announces U.S. Department of Defense Grant to Develop Gene-Edited Cell Therapies Read the latest here.

Factor Bioscience Inc. announced the award of a U.S. Department of Defense grant to develop next-generation cell therapy candidates using Factor’s patented mRNA, cell-reprogramming, and gene-editing technologies. The project will be led by Factor’s Co-Founder and Chief Technology Officer, Dr. Christopher Rohde.

Under the award, Factor will generate the first scalable cell therapy specifically targeting muscle inflammation in DMD patients. To carry out the work, Factor will utilize its extensively patented technologies for engineering cells, including methods for reprogramming and gene-editing cells using mRNA.

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The repair of damage to genetic material (DNA) in the human body is carried out by highly efficient mechanisms that have not yet been fully researched. A scientific team led by Christian Seiser from MedUni Vienna’s Center for Anatomy and Cell Biology has now discovered a previously unrecognized control point for these processes.

This discovery could lead to a new approach for the development of cancer therapies aimed at inhibiting the repair of damaged cancer cells. The research work was recently published in the journal Nucleic Acids Research.

GSE1-CoREST is the name of the newly discovered complex that contains three enzymes that control DNA repair processes and could form the basis for novel cancer therapeutics. “In research, these proteins are already associated with cancer, but not in the context that we have now found,” emphasizes Seiser, who led the study in close collaboration with researchers from the Max Perutz Labs Vienna.

Interactions between RNA and proteins are the cornerstone of many important biological processes from transcription and translation to gene regulation, yet little is known about the ancient origin of said interactions. We hypothesized that peptide amyloids played a role in the origin of life and that their repetitive structure lends itself to building interfaces with other polymers through avidity. Here, we report that short RNA with a minimum length of three nucleotides binds in a sequence-dependent manner to peptide amyloids. The 3′–5′ linked RNA backbone appears to be well-suited to support these interactions, with the phosphodiester backbone and nucleobases both contributing to the affinity. Sequence-specific RNA–peptide interactions of the kind identified here may provide a path to understanding one of the great mysteries rooted in the origin of life: the origin of the genetic code.

DNA obtained from the bones and teeth of ancient Europeans who lived up to 34,000 years ago is providing insight into the origin of the often-disabling neurological disease multiple sclerosis, finding that genetic variants that now increase its risk once served to protect people from animal-borne diseases.

A previously unidentified genetic mutation in a small protein provides significant protection against Parkinson’s disease and offers a new direction for exploring potential treatments, according to a new USC Leonard Davis School of Gerontology study.

The variant, located in a mitochondrial microprotein dubbed SHLP2, was found to be highly protective against Parkinson’s disease; individuals with this mutation are half as likely to develop the disease as those who do not carry it. The variant form of the protein is relatively rare and is found primarily in people of European descent.

The findings appear in the journal Molecular Psychiatry.

Manolis Kellis, an accomplished Computer Science Professor at MIT and member of the Broad Institute, is a trailblazer in computational biology. Renowned for leading the MIT Computational Biology Group, his impactful research spans disease genetics, epigenomics, and gene circuitry. With numerous cited publications and leadership in transformative genomics projects, Kellis has garnered prestigious accolades, including the PECASE and Sloan Fellowship, shaping the field with his international perspective from Greece and France to the US.

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