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Category: genetics

Protein aggregation is linked to altered RNA processing

Neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease, are devastating and incurable diseases. Although many neurodegenerative diseases are characterized by abnormal protein aggregation in the brain, a limited understanding of whether and how aggregated proteins cause brain cell dysfunction and death represents a major barrier to developing effective treatments.

Inspired by similar approaches in cardiovascular disease and cancer, the researchers focused on rare genetic forms of neurodegeneration as a powerful way to uncover fundamental mechanisms tying protein aggregation to brain disease. Thier work unexpectedly linked protein aggregation in genetic forms of neurodegeneration to disrupted processing of transfer RNAs (tRNAs), revealing an important mechanism that might be therapeutically targeted in these disorders.

The authors were interested in genetic forms of neurodegeneration caused by GGC trinucleotide repeat expansions (DNA sequence mutations caused by copying this 3-letter sequence too many times in a row). These mutations produce aggregation-prone proteins with long stretches of a single repeated amino acid (glycine).

Reversing The Age-Related DHEA-S Decline: Cholesterol, Gut Bacteria

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Study reveals hidden regulatory roles of ‘junk’ DNA

A new international study suggests that ancient viral DNA embedded in our genome, which were long dismissed as genetic “junk,” may actually play powerful roles in regulating gene expression. Focusing on a family of sequences called MER11, researchers from Japan, China, Canada, and the US have shown that these elements have evolved to influence how genes turn on and off, particularly in early human development.

The findings are published in the journal Science Advances.

Transposable elements (TEs) are repetitive DNA sequences in the genome that originated from ancient viruses. Over millions of years, they spread throughout the genome via copy-and-paste mechanisms.

A common food additive solves a sticky neuroscience problem

An interdisciplinary team working on balls of human neurons called organoids wanted to scale up their efforts and take on important new questions. The solution was all around them.

For close to a decade now, the Stanford Brain Organogenesis Program has spearheaded a revolutionary approach to studying the brain: Rather than probe intact brain tissues in humans and other animals, they grow three-dimensional brain-like tissues in the lab from , creating models called human neural organoids and assembloids.

Beginning in 2018 as a Big Ideas in Neuroscience project of Stanford’s Wu Tsai Neurosciences Institute, the program has brought together neuroscientists, chemists, engineers, and others to tackle the neural circuits involved in pain, genes that drive neurodevelopmental disorders, new ways to study brain circuits, and more.

Different Bacterial Genes Have Different Turn-Ons

Not all genes respond in the same way to regulation by the same molecule—a property that might enable cells to produce complex genetic responses.

Genes in living cells may become active or may be suppressed in response to environmental stimuli such as heat or the availability of nutrients. For bacteria, this gene regulation often appears to be a simple “on-off switch” controlled by regulatory proteins called transcription factors (TFs). But researchers have now found that different genes might respond differently to the same stimulus even if they are regulated by the same TF [1]. The team activated genes involved in DNA repair and observed gene-to-gene variations in their protein production patterns. Such differences might have been exploited by evolution to achieve complex responses with relatively few molecular components, the researchers suggest.

In the typical scenario, a TF binds to a region of a so-called promoter, a DNA sequence next to a gene. If the TF is the type that blocks gene expression, it prevents the enzyme RNA polymerase from binding and thus from beginning the process of producing the protein that the gene encodes. Because of thermal fluctuations (noise), the TF may spontaneously unbind, allowing gene expression to proceed until it rebinds. The rate of TF binding depends on its concentration, so fluctuations in concentration will cause changes in gene expression.

Extracellular vesicles from antler blastema progenitor cells reverse bone loss and mitigate aging-related phenotypes in mice and macaques

Antler blastema progenitor cells (ABPCs) are a distinct population of skeletal mesenchymal stem cells found in regenerating deer antlers, with strong stemness and renewal capacity in vitro. Stem cell-derived extracellular vesicles (EVs) are emerging as potential therapeutic candidates that can mediate donor cells’ beneficial effects. Here, we tested the effects of ABPC-derived EVs (EVsABPC) on aging in mice and rhesus macaques (Macaca mulatta). We identified a variety of unique factors in EVsABPC and showed that in vitro, EVsABPC attenuated phenotypes of senescence in bone marrow stem cells. In aged mice and macaques, EVsABPC substantially increased femoral bone mineral density. Further, intravenous EVsABPC improved physical performance, enhanced cognitive function and reduced systemic inflammation in aged mice, while reversing epigenetic age by over 3 months. In macaques, EVABPC treatment was also neuroprotective, reduced inflammation, improved locomotor function and reduced epigenetic age by over 2 years. Our findings position ABPCs as an emerging and practical source of EVs with translational value for healthy aging interventions.

Inspired by the regenerative capacity of deer antlers, Hao and colleagues report that antler blastema progenitor cell-derived extracellular vesicle treatment counteracts bone loss and epigenetic aging and is neuroprotective in mice and macaques.

What ever-growing incisors can teach us about genetic disease

Teeth may seem like static fixtures, but a new collaboration between engineers and clinicians is proving just how dynamic, informative and medically significant our teeth can be.

In a study, published in ACS Applied Materials & Interfaces, engineers and dentists come together to uncover how teeth, as , hold key information for understanding rare craniofacial disorders that develop during childhood.

Kyle Vining, Assistant Professor in Materials Science and Engineering (MSE) and in Preventive and Restorative Science at Penn Dental Medicine, leads this interdisciplinary team, which includes Yuchen (Tracy) Jiang, a former master’s student in MSE, Kei Katsura, a pediatric dentist and KL2 postdoctoral research scholar at Children’s Hospital of Philadelphia (CHOP) and the Institute of Translational Medicine and Therapeutics at Penn, and Elizabeth Bhoj, Assistant Professor of Pediatrics in Penn Medicine and the Division of Human Genetics at CHOP.

Gene editing offers transformative solution to saving endangered species

Gene editing technologies—such as those used in agriculture and de-extinction projects—can be repurposed to offer what an international team of scientists is calling a transformative solution for restoring genetic diversity and saving endangered species.