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The researchers found that long-lived organisms often exhibit high expression of genes involved in DNA repair, RNA transport, and cellular framework organization and low expression of genes involved in inflammation and energy consumption. Researchers from the University of Rochester interested in longevity genetics propose new targets to fight aging and age-related disorders. Mammals that age at very different rates have been created through natural selection. The naked mole rat, for example, can live up to 41 years, which is 10 times longer than rats and other rodents of comparable size. What causes longer life? An important component of the puzzle, according to a recent study by biologists at the University of Rochester, is found in the mechanisms that control gene expression. Vera Gorbunova, Doris Johns Cherry professor of biology and medicine, Andrei Seluanov, the publication’s first author, Jinlong Lu, a postdoctoral researcher in Gorbunova’s lab, and other researchers examined

Credit: Pixabay/CC0 Public Domain Fish help researchers trace the origins of how the brain calculates math, reports a review in Frontiers in Neuroanatomy . An international team has reviewed more than 200 publications, which together show that fish perceive quantity using parts of their brains similar to those used by mammals and birds. Research is still underway to find the specific brain circuits that enable number processing, but these findings could eventually help treat human ailments that impair math skills. “Fish is on par with other animals in terms of a sense of quantity,” said the correspondent author Prof. Giorgio Vallortigara from the University of Trento in Italy. “There are species, particularly the zebrafish, which are ideal models for studying the molecular and genetic basis of a sense of quantity. This could have important implications for neurodevelopmental diseases that affect number cognition, such as developmental dyscalc

An international team of researchers led by UC Davis geneticist Suma Shankar has discovered a new gene involved in a neurodevelopmental condition called DPH5-associated diphtamide deficiency syndrome. This syndrome is caused by a variant of the DPH5 gene that can cause embryonic death or profound neurodevelopmental delay. Findings from their study were published in Genetics in Medicine. “We are very excited about the discovery of this new gene,” said lead author Suma Shankar, professor in the Department of Pediatrics and Ophthalmology and faculty at the UC Davis MIND Institute. Shankar is director of Precision Genomics, Albert Rowe Endowed Chair in Genetics, and head of the Division of Genomic Medicine. DPH5 is essential for protein biosynthesis. It belongs to the class of genes required for the synthesis of diphtamide, a type of modified amino acid histidine, essential for the synthesis of ribosomal proteins. “We provide strong clinical, biochemical and functional evidence for DPH5

Immunotherapy, such as immune checkpoint inhibitors, has changed the treatment of advanced cancers. Unlike chemotherapy which kills cancer cells, these drugs help the immune system to find and destroy the cancer cells themselves. Unfortunately, only a subset of patients respond to immune checkpoint inhibitors in the long term; and these treatments can be expensive and with side effects. Researchers have developed a two-step approach using whole-exome sequencing to target genes and pathways that predict whether cancer patients will respond to immunotherapy. Studies published in Nature Communication and conducted by researchers at New York University, Weill Cornell Medicine, and the New York Genome Center, illustrates how using whole-exome sequencing can better predict treatment response than current laboratory tests. “Can we better predict who will benefit from immunotherapy? Scientists have developed a variety of biomarkers that help anticipate immunotherapy treatment responses, b

A study of the herpes virus infecting chickens offers new insight into the potentially problematic interactions between vaccines made from live viruses and viruses that are meant to be thwarted. Reported in the journal Virulence, the study offers direct evidence that vaccines and viruses can infect the same cells in live animals and share the molecular tools that allow the virus to infect other animals – in this case, chickens. The study focused on Marek’s disease, a viral infection that is spread when a chicken inhales flakes of dead skin or feather tissue from an infected chicken. “We’ve been trying to understand how the virus spreads from one host to another,” said University of Illinois Urbana-Champaign pathobiology professor Keith Jarosinski, who led the study. “Not only did we do it for the benefit of chickens in the poultry industry, but also because of a very similar mechanism used by the virus that causes chickenpox, where it enters through the respiratory tract and infects l

The human genome is littered with “selfish genetic elements”, which do not appear to benefit the host, but only seek to reproduce. Selfish genetic elements can wreak havoc by, for example, distorting sex ratios, impairing fertility, causing dangerous mutations, and potentially even causing population extinction. Biologists at the University of Rochester, including Amanda Larracuente, professor of biology, and Daven Presgraves, University Dean’s Professor of Biology, are using population genomics for the first time to explain the evolution and consequences of known selfish genetic elements. as Segregation Distortion ( SD ). In a paper published in the journal eLife the researchers reported that SD has led to dramatic changes in chromosomal organization and genetic diversity. Sequencing the genome first Researchers use fruit flies as model organisms to study SD , a selfish genetic element that deviates from the rules of just genetic transmission. Fruit flies share about 70 percent of

A team led by the University of Minnesota Twin Cities has developed a new technique to image mRNA molecules in the brains of live mice. By genetically modifying the mice to produce mRNA labeled with the green fluorescent protein (shown above), the researchers were able to see when and where the mouse brain produced Arc mRNA. Credit: Hye Yoon Park, University of Minnesota’s Twin Cities A team led by the University of Minnesota’s Twin Cities has developed a new technique that allows scientists and engineers, for the first time, to visualize mRNA molecules in the brains of living mice. This research reveals new insights into how memories are formed and stored in the brain and could provide scientists with new information about diseases like Alzheimer’s. This paper was published in Proceedings of the National Academy of Sciences (PNAS) . There are still many mysteries surrounding the process of how me

A team led by the University of Minnesota’s Twin Cities has developed a new technique that allows scientists and engineers, for the first time, to visualize mRNA molecules in the brains of living mice. This research reveals new insights into how memories are formed and stored in the brain and could provide scientists with new information about diseases like Alzheimer’s. The paper is published in the Proceedings of the National Academy of Sciences of the United States of America (PNAS), a peer-reviewed, multidisciplinary, high-impact scientific journal. There are still many mysteries surrounding the process of how memories are physically created and stored in the brain. It is well known that mRNA—a type of RNA involved in making proteins—is produced during the processes of memory formation and storage, but the technology for studying this process at the cellular level is still limited. Previous research has often involved dissecting mice to examine their brains. A research team led b