A subtle failure during cell division can set off dramatically different outcomes, according to new research exploring whole genome duplication. A new study finds that the way a cell fails to divide after copying its DNA can shape what happens to it next. Cell division is a core process of lif
When a gene is turned on in a cell, it creates a ripple effect along the DNA strand, changing the physical structure of the strand. A new study by MIT researchers shows that these ripples can stimulate or suppress neighboring genes.
These effects, which result from the winding or unwinding of neighboring DNA, are determined by the order of genes along a strand of DNA. Genes upstream of the active gene are usually turned up, while those downstream are inhibited.
The new findings offer guidance that could make it easier to control the output of synthetic gene circuits. By altering the relative ordering and arrangement of genes, or “gene syntax,” researchers could create circuits that synergize to maximize their output, or that alternate the output of two different genes.
Mark Zuckerberg is following a path paved by fellow billionaires Bill Gates and Warren Buffet: laundering his untold billions through a health research prestige project.
Called the Chan Zuckerberg Biohub — his wife Priscilla Chan, a pediatrician, is also involved — the foundation’s stated long-term mission is to “cure and prevent all disease through AI-powered biology, frontier research, and state-of-the-art technology.”
True to those enormous goals, the Biohub recently announced a $500 million investment into AI models of human cells, specifically, in order to “accelerate the cure and prevention of all diseases,” Euronews reported.
Amyotrophic lateral sclerosis (ALS) and Huntington disease (HD) are lethal neurodegenerative diseases affecting motor function. Though their etiology and pathology are distinct, recent evidence suggests commonalities between TAR DNA-binding protein (TDP-43), which is associated with 97% of ALS cases, and huntingtin (HTT), the causative protein of HD. ALS is a heterogeneous, lethal neurodegenerative disease characterized by the progressive loss of upper and lower motor neurons, as well as brainstem and spinal cord degeneration. The causes of ALS are complex, variable, and, in some cases, unknown, but most cases involve mislocalization of the protein TDP-43. In contrast, HD is a monogenic, autosomal dominant, lethal neurodegenerative disease caused by polyglutamine expansion in HTT protein and characterized by the progressive loss of neurons in the brain, particularly in the striatum, which results in motor, cognitive, and behavioral changes. Although HD is not typically associated with motor neuron loss, recent evidence suggests a link between HTT and TDP-43 within the context of both ALS and HD, as well as links to related neurodegenerative diseases, such as frontotemporal dementia (FTD) and spinocerebellar ataxia type 2 (SCA2). Herein, we discuss confirmed cases of concurrent ALS and HD and the overlap of underlying disease mechanisms that potentially contribute to the onset and progression of these two devastating neurodegenerative diseases, with a focus on commonalities between TDP-43 and HTT. We propose that elucidating these commonalities will aid in the identification of broad-spectrum disease risk factors and potential overlapping treatment targets.
Scientists have uncovered an unexpected mechanism by which the gut’s immune system maintains balance, challenging long-standing assumptions about how immune tolerance is regulated.
Now online! A host-filtering and decontamination pipeline was benchmarked and applied to 16,369 tumor genomes, providing a high-resolution atlas of the cancer microbiome. Although most cancer types lacked a detectable microbiome, orodigestive cancers harbored complex multi-kingdom microbial communities that varied by site, subtype, and somatic mutation burden, linking the tumor microbiome to host phenotype and tumor genomic context.
Researchers at the University of Toronto have identified a protein from the quagga mussel that can stick to surfaces underwater, even though it lacks a chemical feature long thought to be essential for this kind of adhesion. The protein, called Dbfp7, is the first freshwater mussel adhesive protein to be functionally characterized.
The finding, published in PNAS, helps explain how some organisms attach themselves in wet environments and could inform the design of future medical glues—such as medical sealants and surgical adhesives—or other materials that need to work reliably in water.
Most studies of underwater adhesion have focused on marine mussels, which use proteins rich in a modified amino acid called 3,4-dihydroxyphenylalanine (DOPA) to bond to surfaces. Freshwater species have been studied less, and whether they rely on the same chemistry has not been clear.
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The world is entering an era where “technology” and “living organisms” merge into one. Most recently, in 2026, a research team from Northwestern University created a landmark breakthrough by developing “Printed Neurons.” These are not designed just to mimic biology—they can actually “transmit signals” to communicate with living brain cells!
Why is this a big deal? Typically, the silicon-based computers we use today operate entirely differently from the human brain. Computers consume massive amounts of power and are rigid. In contrast, our brains use only about 20 watts (less than some lightbulbs) and are incredibly flexible. Creating artificial neurons that “speak the same language as the brain” is the key to treating diseases that were once considered incurable.
Innovations in “Electronic Ink” and “3D Printing“ At the heart of this research lies a leap forward in materials science and engineering: • Nanomaterials (MoS₂ and Graphene): Researchers used these materials to create a specialized “ink” for printing neural networks. These materials are unique for being both flexible and excellent conductors of electricity. • Aerosol Jet Printing: This technology allows for nano-level precision printing on flexible plastic sheets, designed to contour perfectly to human tissue. • Biomimicry: These artificial cells can generate electrical signals called “Spikes,” matching the rhythm and speed of actual biological neurons.
Proven! Successful Communication with a “Mouse Brain“ The research team tested the connection between these printed neurons and mouse brain tissue. The results showed that the mouse brain cells could receive and respond to signals from the artificial device as if they were from their own kind. This is vital evidence that humans can create devices that interface seamlessly with the nervous system.