Category: genetics – Page 58
According to the World Health Organization, antibiotic resistance is a top public health risk that was responsible for 1.27 million deaths across the globe in 2019. When repeatedly exposed to antibiotics, bacteria rapidly learn to adapt their genes to counteract the drugs—and share the genetic tweaks with their peers—rendering the drugs ineffective.
Superpowered bacteria also torpedo medical procedures—surgery, chemotherapy, C-sections—adding risk to life-saving therapies. With antibiotic resistance on the rise, there are very few new drugs in development. While studies in petri dishes have zeroed in on potent candidates, some of these also harm the body’s cells, leading to severe side effects.
What if there’s a way to retain their bacteria-fighting ability, but with fewer side effects? This month, researchers used AI to reengineer a toxic antibiotic. They made thousands of variants and screened for the ones that maintained their bug-killing abilities without harming human cells.
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.
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…).
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).
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.