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Category: genetics – Page 36

Communication and coordination among different cells are fundamental aspects that regulate many functions in our body. This process, known as paracrine signaling, involves the release of signaling molecules by a cell into its extracellular matrix (ECM) or surroundings to communicate changes in its cellular processes or the local environment. These signaling molecules are then detected by neighboring cells, leading to various cellular responses.

For instance, during cell/tissue injury, the paracrine signaling process releases that signal nearby stem cells to assist in tissue repair in the form of scar tissue formation or blood clotting. Similar processes occur in the regulation of other vital functions, such as digestion, respiration, and reproduction. Additionally, paracrine signals influence the expression and activity of enzymes involved in drug metabolism and play a role in drug–drug interactions.

The signaling molecules, which may contain proteins and , are transported within tiny vesicles called exosomes. These vesicles serve as valuable biomarkers for various diseases and can even be engineered to carry drugs, making them a highly effective targeted drug delivery system. Notably, the hormone oxytocin and the neurotransmitter dopamine are paracrine messengers.

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Insecticides have been used for centuries to counteract widespread pest damage to valuable food crops. Eventually, over time, beetles, moths, flies and other insects develop genetic mutations that render the insecticide chemicals ineffective.

Escalating resistance by these mutants forces farmers and vector control specialists to ramp up use of poisonous compounds at increasing frequencies and concentrations, posing risks to human health and damage to the environment since most insecticides kill both ecologically important insects as well as pests.

To help counter these problems, researchers recently developed powerful technologies that genetically remove insecticide-resistant variant genes and replace them with genes that are susceptible to pesticides. These gene-drive technologies, based on CRISPR gene editing, have the potential to protect valuable crops and vastly reduce the amount of chemical pesticides required to eliminate pests.

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Scientists have discovered that tRNAs can determine how long mRNAs exist in a cell, causing some messages to be stabilized and translated into more protein, while directing others to be degraded and limiting how much protein can be made. They published their report in Science.

The messenger RNA (mRNA)-based vaccines developed to fight the virus SARS-CoV-2 saved lives and made the nucleic acid a household name during the COVID-19 pandemic. Suddenly, everyone knew a little bit more about the molecule that helps convert genetic information into proteins.

But in addition to determining which proteins are made, mRNAs can also specify how much protein is produced.

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A multi-institutional team of researchers, led by Georgia Tech’s Francesca Storici, has discovered a previously unknown role for RNA. Their insights could lead to improved treatments for diseases like cancer and neurodegenerative disorders while changing our understanding of genetic health and evolution.

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The drug lorlatinib (Lorbrena) is superior to crizotinib (Xalkori) as an initial treatment for people with advanced non-small cell lung cancer (NSCLC) that has changes in the ALK gene, according to new results from a global clinical trial.

The findings are the latest from the CROWN study. Participants were randomly assigned to receive either lorlatinib or crizotinib as a treatment for advanced lung tumors with ALK gene mutations, a disease called ALK-positive lung cancer.

Several years ago, study investigators reported that participants who received lorlatinib went longer without the disease worsening, known as progression-free survival, than those who received crizotinib.

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Tissues take shape during development through a series of morphogenetic movements guided by local cell-scale forces. While current in vitro approaches subjecting tissues to homogenous stresses, it is currently no possible to recapitulate highly local spatially varying forces. Here we develop a method for local actuation of organoids using embedded magnetic nanoparticles. Sequential aggregation of magnetically labelled human pluripotent stem cells followed by actuation by a magnetic field produces localized magnetic clusters within the organoid. These clusters impose local mechanical forces on the surrounding tissue in response to applied global magnetic fields. We show that precise, spatially defined actuation provides short-term mechanical tissue perturbations as well as long-term cytoskeleton remodeling. We demonstrate that local magnetically-driven actuation guides asymmetric growth and proliferation, leading to enhanced patterning in human neural organoids. We show that this approach is applicable to other model systems by observing polarized patterning in paraxial mesoderm organoids upon local magnetic actuation. This versatile approach allows for local, controllable mechanical actuation in multicellular constructs, and is widely applicable to interrogate the role of local mechanotransduction in developmental and disease model systems.

The authors have declared no competing interest.

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Choanoflagellates, animals’ closest relatives, have pluripotency genes, reshaping views on their evolution.

The research highlights how evolution repurposes existing genetic tools, turning them into versatile drivers of innovation. This adaptability underscores how foundational processes in unicellular organisms laid the groundwork for the development of complex life forms.

Beyond rewriting evolutionary biology, the findings could revolutionize regenerative medicine. Understanding how ancient genes enabled pluripotency offers new pathways to refine stem cell therapies and enhance cell reprogramming techniques.

For instance, synthetic versions of these genes might outperform native animal genes, opening possibilities for more efficient treatments for diseases or tissue damage.

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There are many processes and proteins that help the body fight a flu infection. One of them is known as IFITM3. Researchers have now shown that this protein can help prevent viruses from mutating after they have infected a new host. But some people are deficient in IFITM3, which can raise their risk of a severe flu infection. That deficiency is not unusual in some groups. For example, around twenty percent of Chinese people and four percent of people with European ancestry carry variants in IFITM3 that can interfere with the protein’s expression. This study has shown that these genetic variants can allow flu viruses to establish infections even when the virus is present at very low levels that would not usually cause infection. The findings have been reported in Nature Communications.

The IFITM3 (interferon-induced transmembrane protein 3) protein is part of the innate immune system, and is generated at high levels after the detection of a flu infection. It can sequester viral particles so that they are not able to replicate, which reduces the severity of flu infections. Mouse models that are IFITM3 deficient are extremely vulnerable to the flu.

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Continue reading “Sunlight Deficiency As A Contributor To Poor Health: Roger Seheult, M.D. (‪@Medcram‬)” | >

Summary: Autism-linked SHANK3 gene mutations disrupt not only neurons but also oligodendrocytes, essential for producing myelin, which insulates nerve fibers. This damage reduces brain signal efficiency and impairs behavior.

Using gene therapy, researchers successfully repaired these cells in a mouse model, restoring their function and myelin production. They validated their findings with human-derived stem cells, confirming similar impairments and repair mechanisms.

This discovery highlights a significant role for oligodendrocytes in autism and opens the door for innovative treatments targeting myelin dysfunction. The study underscores both the biological complexity of autism and the promise of genetic therapies for intervention.

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