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For example, enhancers (DNA segments that promote gene expression) and gene promoters (regions that initiate transcription) can interact more readily in open, accessible regions of chromatin.

On the other hand, DNA in tightly packed chromatin regions remains less active. Through analyzing these contact points, researchers have developed models to map chromatin configurations across various species, such as humans, mice, birds, and more recently, turtles.

In a recent paper published in the journal Genome Research, Valenzuela’s team described the chromatin arrangement in the genomes of two turtle species, the spiny softshell and northern giant musk turtles, uncovering a structure previously unobserved in other organisms.

Researchers found that neural crest stem cells are uniquely capable of reprogramming, challenging current reprogramming theories and opening possibilities for stem cell-based treatments.

A research team from the University of Toronto has identified that neural crest stem cells, a group of cells found in the skin and other parts of the body, are the origin of reprogrammed neurons previously found by other scientists.

Their findings refute the popular theory in cellular reprogramming that any developed cell can be induced to switch its identity to a completely unrelated cell type through the infusion of transcription factors. The team proposes an alternative theory: there is one rare stem cell type that is unique in its ability to be reprogrammed into different types of cells.

Carbon is a gregarious little atom, bending over backwards to link with a wide variety of elements in what is collectively referred to as organic chemistry. Life itself wouldn’t be possible without carbon’s knack for making connections.

Yet even this friendly fellow has its limits. Take Bredt’s rule for instance, which says stable two-laned connections known as covalent double bonds won’t form adjacent to any V-shaped bridges that happen to form across ‘bicyclic’ molecules.

Now a team of chemists from the University of California, Los Angeles has uncovered a solution that violates Bredt’s century-old rule. This encourages future drug research to explore the use of molecules that we thought could not exist.

Google DeepMind has unexpectedly released the source code and model weights of AlphaFold 3 for academic use, marking a significant advance that could accelerate scientific discovery and drug development. The surprise announcement comes just weeks after the system’s creators, Demis Hassabis and John Jumper, were awarded the 2024 Nobel Prize in Chemistry for their work on protein structure prediction.

AlphaFold 3 represents a quantum leap beyond its predecessors. While AlphaFold 2 could predict protein structures, version 3 can model the complex interactions between proteins, DNA, RNA, and small molecules — the fundamental processes of life. This matters because understanding these molecular interactions drives modern drug discovery and disease treatment. Traditional methods of studying these interactions often require months of laboratory work and millions in research funding — with no guarantee of success.

The system’s ability to predict how proteins interact with DNA, RNA, and small molecules transforms it from a specialized tool into a comprehensive solution for studying molecular biology. This broader capability opens new paths for understanding cellular processes, from gene regulation to drug metabolism, at a scale previously out of reach.

The unexpected discovery of a geometric phase shows how math and physics are tightly intertwined.

By Manon Bischoff

I didn’t find math particularly exciting when I was in high school. To be honest, I only studied it when I went to university because it initially seemed quite easy to me. But in my very first math lecture as an undergraduate, I realized that everything I thought I knew about math was wrong. It was anything but easy. Mathematics, I soon discovered, can be really exciting—especially if you go beyond the realm of pure arithmetic.

“This paper shows a fun way to make carbon-neutral fuels and chemicals,” said Dr. Curtis P. Berlinguette. “We’ll need plastic on Mars one day, and this technology shows one way we can make it there.”


Can we use the planetary environment of Mars to help power a future colony on the Red Planet? This is what a recent study published in Device hopes to address as a team of researchers investigated how current thermoelectric generators—which can operate in a myriad of environments—on Mars could convert carbon dioxide (CO2) into fuel and other chemicals that can be used for a future Mars colony. This study holds the potential to help scientists, engineers, and the public better understand how a future Mars colony could be managed and operated without constant need for resupply from Earth.

“This is a harsh environment where large temperature differences could be leveraged to not only generate power with thermoelectric generators, but to convert the abundant CO2 in Mars’ atmosphere into useful products that could supply a colony,” said Dr. Abhishek Soni, who is a postdoctoral research fellow at the University of British Columbia (UBC) and lead author of the study.

For the study, the researchers conducted laboratory experiments with a CO2 electrolyzer, which are powered by thermoelectric generators, and a hot plate and ice bath, which obviously provide a wide range of temperatures to see how the CO2 electrolyzer converts CO2 to useful chemicals. In the end, the researchers found when the temperature difference between the ice bath and hot plate was 104 degrees Fahrenheit (40 degrees Celsius), the electrolyzer was still able to successfully convert CO2 to carbon monoxide (CO).

It is the first time that synaptic density has been measured in living people with autism.


Furthermore, the research team found that the fewer synapses an individual had, the more features of autism they exhibited.

The findings appear in Molecular Psychiatry.

As simple as our findings sound, this is something that has eluded our field for the past 80 years, says James McPartland, a professor in the Yale Child Study Center and the study’s principal investigator.

How organisms age is a question with broad implications for human health. In mammals, DNA methylation is a biomarker for biological age, which may predict age more accurately than date of birth. However, limitations in mammalian models make it difficult to identify mechanisms underpinning age-related DNA methylation changes. Here, we show that the short-lived model plant Arabidopsis thaliana exhibits a loss of epigenetic integrity during aging, causing heterochromatin DNA methylation decay and the expression of transposable elements. We show that the rate of epigenetic aging can be manipulated by extending or curtailing lifespan, and that shoot apical meristems are protected from this aging process. We demonstrate that a program of transcriptional repression suppresses DNA methylation maintenance pathways during aging, and that mutants of this mechanism display a complete absence of epigenetic decay. This presents a new paradigm in which a gene regulatory program sets the rate of epigenomic information loss during aging.

The authors have declared no competing interest.