Lifeboat Foundation

A team led by UT Southwestern Medical Center researchers has discovered a new way that cells regulate senescence, an irreversible end to cell division. The findings, published in Cell, could one day lead to new interventions for a variety of conditions associated with aging, including neurodegenerative and cardiovascular diseases, diabetes, and cancer, as well as new therapies for a collection of diseases known as ribosomopathies.

“There is great interest in reducing senescence to slow or reverse aging or aging-associated diseases. We discovered a noncoding RNA that when inhibited strongly impairs senescence, suggesting that it could be a therapeutic target for conditions associated with aging,” said Joshua Mendell, M.D., Ph.D., Professor of Molecular Biology and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. He is also a Howard Hughes Medical Institute Investigator.

Dr. Mendell led the study with co-first authors Yujing Cheng, Ph.D., a recent graduate of the Genetics, Development, and Disease graduate program; and Siwen Wang, M.D., a former postdoctoral researcher, both in the Mendell Lab.

Leading The Next Wave Of Innovation In Drug Discovery, To Modulate Any Target, Every Time — Dr. P. Ryan Potts, Ph.D., VP and Head, Induced Proximity Platform, Amgen.

Dr. Ryan Potts, Ph.D. is Vice President and Head, Induced Proximity Platform at Amgen (https://www.amgen.com/science/researc…) which is focused on novel ways to bring two or more molecules in close proximity to each other to tackle drug targets that are currently considered “undruggable.” He also leads Amgen’s Research \& Development Postdoctoral Fellows Program (https://www.amgen.com/science/scienti…).

Continue reading “Dr. Ryan Potts, Ph.D. — VP and Head, Induced Proximity Platform, Amgen — Any Target, Every Time” »

He Jiankui, who went to prison for three years for making the world’s first gene-edited babies, talked to MIT Technology Review about his new research plans.

Programmable and reversible CRISPRi-based genetic circuits function in a variety of plants.

Researchers at Cold Spring Harbor Laboratory have traced the domestication of maize back to its origins 9,000 years ago, highlighting its crossbreeding with teosinte mexicana for cold adaptability.

The discovery of a genetic mechanism known as Teosinte Pollen Drive by Professor Rob Martienssen provides a critical link in understanding maize’s rapid adaptation and distribution across America, shedding light on evolutionary processes and potential agricultural applications.

Cold Spring Harbor Laboratory (CSHL) scientists have begun to unravel a mystery millennia in the making. Our story begins 9,000 years ago. It was then that maize was first domesticated in the Mexican lowlands. Some 5,000 years later, the crop crossed with a species from the Mexican highlands called teosinte mexicana. This resulted in cold adaptability. From here, corn spread across the continent, giving rise to the vegetable that is now such a big part of our diets. But how did it adapt so quickly? What biological mechanisms allowed the highland crop’s traits to take hold? Today, a potential answer emerges.

Building upon groundbreaking research demonstrating how the SARS-CoV-2 virus disrupts mitochondrial function in multiple organs, researchers from Children’s Hospital of Philadelphia (CHOP) demonstrated that mitochondrially-targeted antioxidants could reduce the effects of the virus while avoiding viral gene mutation resistance, a strategy that may be useful for treating other viruses.

The preclinical findings were published in the journal Proceedings of the National Academy of Sciences.

Last year, a multi-institutional consortium of researchers found that the genes of the mitochondria, the energy producers of our cells, can be negatively impacted by the virus, leading to dysfunction in multiple organs beyond the lungs.

This is because the species undergoes a process called polyploidization, which is when a single chromosome is duplicated multiple times.

“It has amazing genetic diversity,” study co-author Tim O’Hara, a senior marine curator at Museums Victoria in Australia, told Newsweek.

“Instead of evolving into separate species over time, lineages readily hybridize with each other, so building up a great amount of genetic diversity. But not only that, they sometimes add their genomes together, so end up with four or more copies of each gene,” O’Hara said.

Researchers led by the University of California, Irvine have discovered how the TREM2 R47H genetic mutation causes certain brain areas to develop abnormal protein clumps, called beta-amyloid plaques, associated with late-onset Alzheimer’s disease. Leveraging single-cell Merfish spatial transcriptomics technology, the team was able to profile the effects of the mutation across multiple cortical and subcortical brain regions, offering first-of-their-kind insights at the single-cell level.

The study, published in Molecular Psychiatry, compared the brains of normal mice and special mouse models that undergo changes like those in humans with Alzheimer’s.

Findings revealed that the TREM2 mutation led to divergent patterns of beta-amyloid plaque accumulation in various parts of the brain involved in higher-level functions such as memory, reasoning and speech. It also affected certain cell types and their gene expression near the plaques.

With the first CRISPR–Cas9 gene therapy now approved, scientists are turning to newer editing technologies to produce safer, faster and better treatments for genetic diseases.