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DNA repair by cooperation between proteins: A look inside the cell’s repair hub

New research from the Kind Group at the Hubrecht Institute sheds light on how cells repair damaged DNA. For the first time, the team has mapped the activity of repair proteins in individual human cells.

The study demonstrates how these proteins collaborate in so-called “hubs” to repair DNA damage. This knowledge offers opportunities to improve cancer therapies and other treatments where DNA repair is essential. The researchers published their findings in Nature Communications on November 21.

DNA is the molecule that carries our genetic information. It can be damaged by normal cellular processes as well as external factors such as UV radiation and chemicals. Such damage can lead to breaks in the DNA strand. If DNA damage is not properly repaired, mutations can occur, which may result in diseases like cancer. Cells use repair systems to fix this damage, with specialized proteins locating and binding to the damaged regions.

Unlocking The Genetic Code: AI Reveals New Insights Into Psychiatric Disorders

Recent breakthroughs in genetics research may have uncovered new genes underlying common psychiatric disorders. Schizophrenia and bipolar disorder affect more than 64 million people around the world. These disorders are strongly influenced by genetics. No one gene, however, determines one’s risk of developing schizophrenia or bipolar disorder. Rather, it is likely that a host of genes contribute to risk. Using artificial intelligence, researchers at Stanford University now have uncovered complex variants throughout the human genome that may contribute to these psychiatric disorders. This new study suggests that mutations that occur after fertilization, such as genetic mosaicism, may be responsible for a number of psychiatric disorders including bipolar disorder and schizophrenia.

Think of a genome as a living book with instructions for every cell in the body. Our genes are the chapters. We have approximately 200,000 genes that provide instructions for making proteins, the building blocks of life. The vast majority of our genes, however, are non-coding, meaning that they do not provide instructions for proteins. Nonetheless, these genes play an important role in genetics and regulating cell function.

Genetic variants, or spelling changes, in either a coding or non-coding region can interfere with how the cell translates specific instructions. A small typo may have little to no effect on how the book is read. However, larger spelling changes can lead to the deletion of a sentence or even a whole chapter. Without the correct instructions to produce specific proteins, these spelling changes can contribute to disorders that impact different aspects of our body.

MIT Longevity, AI, and Cognitive Research Hackathon: Michael Lustgarten, PhD @ekkolapto3

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Novel silica nonwoven fabric scaffold enhances understanding of cell-to-cell interactions

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.

New gene drive reverses insecticide resistance in pests… then disappears

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.

TRNAs help some mRNAs get lost in translation

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.

Lorbrena Effective as Initial Treatment of ALK-Positive NSCLC

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.

Local actuation of organoids by magnetic nanoparticles

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.

Scientists use DNA from 422-million-year-old cells to create a mouse

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.