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Category: genetics – Page 142

Scientists have found a secret ‘switch’ that lets bacteria resist antibiotics — and it’s been evading lab tests for decades

For decades, microbiologists like Weiss thought of antibiotic resistance as something a bacterial species either had or didn’t have. But “now, we are realizing that that’s not always the case,” he said.

Normally, genes determine how bacteria resist certain antibiotics. For example, bacteria could gain a gene mutation that enables them to chemically disable antibiotics. In other cases, genes may code for proteins that prevent the drugs from crossing bacterial cell walls. But that is not the case for heteroresistant bacteria; they defeat drugs designed to kill them without bona fide resistance genes. When they’re not exposed to an antibiotic, these bacteria look like any other bacteria.

Study identifies RNA molecule that Regulates Cellular Aging

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.

Dr. Ryan Potts, Ph.D. — VP and Head, Induced Proximity Platform, Amgen — Any Target, Every Time

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…).

Dr. Potts obtained his B.S. in Biology from the University of North Carolina and his Ph.D. in Cell and Molecular Biology from UT Southwestern in 2007. In 2008 he was awarded the Sara and Frank McKnight junior faculty position at UT Southwestern Medical Center. During this time his lab focused on answering a long-standing question in cancer biology regarding the cellular function of cancer-testis antigen (CTAs) proteins. In 2011 he was appointed Assistant Professor in the Departments of Physiology, Pharmacology, and Biochemistry at UT Southwestern Medical Center. His lab’s work defined a function for the enigmatic MAGE gene (Melanoma Antigen Gene) family in protein regulation through ubiquitination.

In 2016 Dr. Potts lab moved to St. Jude Children’s Research Hospital where he was an Associate Member in the Department of Cell and Molecular Biology. There his lab continued to work on CTAs, with a focus on elucidating the biochemical, cellular, physiological and pathological functions of the MAGE gene family.

In 2020 Dr. Potts moved to Amgen, Inc. in Thousand Oaks, California to build a new department called the Induced Proximity Platform (IPP).

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

“Missing Link” Uncovered: The Secret History of Corn Revealed Through RNA

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.

Preclinical Data suggest Antioxidant Strategy to address Mitochondrial Dysfunction caused by SARS-CoV-2 virus

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.

Sea creature revealed to have so much DNA it can hardly be called a species

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.

Research team reveals how TREM2 genetic mutation affects late-onset Alzheimer’s

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 and their gene expression near the plaques.

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