For the first time, scientists using cryo-electron microscopy have discovered the structure and shape of key receptors connecting neurons in the brain’s cerebellum, which is located behind the brainstem and plays a critical role in functions such as coordinating movement, balance and cognition.

The research, published in Nature, provides new insight that could lead to the development of therapies to repair these structures when they are disrupted either by injury or genetic mutations affecting motor skills —sitting, standing, walking, running, and jumping—learning and memory.

The study, by scientists at Oregon Health & Science University, reveals the organization of a specific type of glutamate receptor—a chemical neurotransmitter that conveys signals between neurons and is considered the primary excitatory neurotransmitter in the brain—bound together with proteins clustered on synapses, or junctions, between neurons in the cerebellum.

CLNS1A promotes autoimmunity through epigenetic and transcriptional regulation of DNA repair and cell cycle progression in CD4 T cells.

Researchers at the Max Planck Institute for Molecular Genetics have developed a novel synthetic micropeptide termed the “killswitch” to selectively immobilize proteins within cellular condensates, unveiling crucial connections between condensate microenvironments and their biological functions.

Biomolecular condensates are specialized regions inside cells, existing without membranes, where critical biochemical reactions occur. Their importance in health and disease is well established, including roles in cancer progression and viral infection.

Methods to precisely probe and manipulate condensates in living cells remain limited. Existing strategies lack specificity, either dissolving condensates indiscriminately or requiring artificial protein overexpression, which obscures the natural behavior of native cellular proteins.

Researchers from the University of Southern Denmark and Odense University Hospital have studied tissue from patients with atherosclerosis. They found that many of the cells in the diseased tissue carried the same genetic alteration and appeared to originate from a single ancestral cell that had divided repeatedly—a pattern otherwise associated with tumor biology.

In several patients, a large proportion of the cells were derived from one single mutated cell that had undergone many rounds of cell division.

“It’s striking how many cells in the tissue share the exact same genetic change. In several samples, more than 10% of the cells—hundreds of thousands cells—carried the same alteration. It’s difficult to interpret this as anything other than all these cells originating from a shared ancestral cell that, at some point during disease development, acquired the mutation,” says Lasse Bach Steffensen, Associate Professor at the Department of Molecular Medicine at the University of Southern Denmark.

The human brain is made up of billions of interconnected cells that are constantly talking to each other. A new study published in Nature zooms in to the single-cell level to see how this cellular communication may be going wrong in brains affected by post-traumatic stress disorder (PTSD).

Until recently, researchers did not have the technology to study genetic variation within individual cells. But now that it’s available, a team led by Matthew Girgenti, Ph.D., assistant professor of psychiatry at Yale School of Medicine, has been analyzing brain cells to uncover genetic variants that might be associated with psychiatric diseases such as major depressive disorder (MDD) and PTSD.

Their latest study is one of the first to examine a major psychiatric disorder, PTSD, at the single-cell level. For years, doctors have been prescribing antidepressants to treat the condition because there are currently no drugs specifically designed for PTSD. Girgenti hopes that identifying novel molecular signatures associated with the psychiatric disease can help researchers learn how to develop new drugs or repurpose existing ones to treat it more effectively.

Researchers have released genetic and behavioral data from over 1,500 children and adolescents with autism who were hospitalized in psychiatric units across the U.S.

Modern humans have existed for more than 200,000 years, and each new generation has begun with a single cell—dividing, changing shape and function, organizing into tissues, organs, and limbs. With slight variations, the process has repeated billions of times with remarkable fidelity to the same body plan.

Researchers at Tufts have been on a quest to understand the code guiding individual cells to create the architecture of a human being, and to create a foundation for regenerative medicine. As they learn more about that code, they are also looking at how to build living structures from human cells that have totally new forms and capabilities—without genetic manipulation.

To decipher that code, they took a cell from the human body and allowed it to grow in a novel environment to observe how the rules of self-organization play out.

When Vijay Sankaran was an MD-PhD student at Harvard Medical School in the mid-2000s, one of his first clinical encounters was with a 24-year-old patient whose sickle cell disease left them with almost weekly pain episodes.

“The encounter made me wonder, couldn’t we do more for these patients?” said Sankaran, who is now the HMS Jan Ellen Paradise, MD Professor of Pediatrics at Boston Children’s Hospital.

In 2008, Orkin, Sankaran, and colleagues achieved their vision by identifying a new therapeutic target for sickle cell disease.

In December 2023, through the development efforts of CRISPR Therapeutics and Vertex Pharmaceuticals, their decades-long endeavor reached fruition in the form of a new treatment, CASGEVY, approved by the U.S. Food and Drug Administration.

The decision has ushered in a new era for sickle cell disease treatment — and marked the world’s first approval of a medicine based on CRISPR/Cas9 gene-editing technology.

How a genetic insight paired with gene editing technology led to a life-changing new therapy.

Sarcomas are a group of mesenchymal malignancies which are molecularly heterogeneous. Here, the authors develop an in vivo muscle electroporation system for gene delivery to generate distinct subtypes of orthotopic genetically engineered mouse models of sarcoma, as well as syngeneic allograft models with scalability for preclinical assessment of therapeutics.

In this video, we take a deep dive into the fascinating process of binary fission, the primary mode of reproduction in prokaryotic cells like bacteria.

You’ll learn how:
DNA replication begins the cycle.
The DNA relay-ratchet mechanism ensures accurate segregation of chromosomes, and.
A septum forms to physically divide the cell into two genetically identical daughter cells.

Whether you’re a student, teacher, or just curious about microbiology, this simplified explanation breaks down complex concepts into clear, visual steps.

References & Further Reading:
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