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A team of Chinese scientists has used targeted gene editing to develop rice that produces coenzyme Q10 (CoQ10), a vital compound for human health.

Led by Prof. Chen Xiaoya from the CAS Center for Excellence in Molecular Plant Sciences/Shanghai Chenshan Research Center and Prof. Gao Caixia from the Institute of Genetics and Developmental Biology of the Chinese Academy of Sciences (CAS), the researchers used targeted gene editing to modify just five amino acids of the Coq1 rice enzyme, creating new rice varieties capable of synthesizing CoQ10.

The study is published in Cell.

In a new study published in Science, a Belgian research team explores how genetic switches controlling gene activity define brain cell types across species. They trained deep learning models on human, mouse, and chicken brain data and found that while some cell types are highly conserved between birds and mammals after millions of years of evolution, others have evolved differently.

The findings not only shed new light on evolution; they also provide powerful tools for studying how shapes different cell types, across species or different disease states.

Our brain, and by extension our entire body, is made up of many different types of cells. While they share the same DNA, all these cell types have their own shape and function. What makes each cell type different is a complex puzzle that researchers have been trying to put together for decades from short DNA sequences that act like switches, controlling which genes are turned on or off.

University of Queensland researchers have for the first time introduced genetic material into plants via their roots, opening a potential pathway for rapid crop improvement. The research is published in Nature Plants.

Professor Bernard Carroll from UQ’s School of Chemistry and Molecular Biosciences said nanoparticle technology could help fine-tune plant genes to increase crop yield and improve food quality.

“Traditional plant breeding and take many generations to produce a new crop variety, which is time-consuming and expensive,” Professor Carroll said.

Synthetic biologists from Yale successfully rewrote the genetic code of an organism—a novel genomically recoded organism (GRO) with a single stop codon—using a cellular platform they developed that enables the production of new classes of synthetic proteins. Researchers say these synthetic proteins offer the promise of innumerable medical and industrial applications that can benefit society and human health.

A new study published in the journal Nature describes the creation of the landmark GRO, known as “Ochre,” which fully compresses redundant (or “degenerate”) codons into a single codon. A codon is a sequence of three nucleotides in DNA

DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

If the coordination of DNA and RNA epigenetics gets thrown off, you may end up with too much or too little of a protein, Fuk suggested. “Now, a key protein will be expressed at a too high level,” he said.” This could be detrimental for a cell and contribute to tumorigenesis,” or the formation of tumors.

There are already approved therapies that inhibit the methylation of DNA, and there’s an early-phase clinical trial testing RNA methylation inhibition as a cancer treatment. Fuks and his team are testing the potential of combining these existing therapies to improve patients’ outcomes. Preliminary data from their laboratory studies hint this strategy could be useful for patients with leukemia.

Mice learn best when the opponent opposing forces of dopamine and serotonin work together, a new study shows, helping to resolve long-standing questions about the neuromodulators’ relationship.

In the intricate dance of learning and motivation, two key brain chemicals—dopamine (DA) and serotonin (5HT)—play opposing yet deeply interconnected roles. Scientists have long speculated how these neuromodulators work together to shape our ability to form new associations, but testing these theories directly has been a challenge.

Now, researchers have developed a new mouse model that allows them to simultaneously study both dopamine and serotonin neurons in the brain. Their experiments focused on the nucleus accumbens (NAc), a region known for processing rewards. By monitoring neural activity, they found that receiving a reward boosts dopamine signals while simultaneously suppressing serotonin signals.

To understand how this dynamic affects learning, the team used optogenetics—a technique that uses light to control brain activity. They found that disrupting dopamine or serotonin alone caused only mild learning impairments. However, when both signals were suppressed together, the mice struggled significantly to learn from rewards. On the flip side, artificially recreating both dopamine and serotonin responses helped the mice learn more effectively than manipulating either signal alone.

These findings reveal that dopamine and serotonin work in opposition to control reinforcement and learning. Instead of acting in isolation, they create a delicate balance that shapes how we associate actions with rewards—providing new insights into how the brain learns and adapts.

While most animals reproduce sexually, some species rely solely on females for parthenogenetic reproduction. Even in these species, rare males occasionally appear. Whether these males retain reproductive functions is a key question in understanding the evolution of reproductive strategies.

A new study published in Ecology by a research team led by Assistant Professor Tomonari Nozaki from the National Institute for Basic Biology, Professor Kenji Suetsugu from Kobe University, and Associate Professor Shingo Kaneko from Fukushima University provides insight into this question. The researchers focused on the rare males of Ramulus mikado, a stick insect species in Japan, where parthenogenesis is predominant. Their analysis of male reproductive behavior reveals new findings.

Washington State University scientists have developed genetically engineered mice that could help accelerate anti-aging research.

Globally, researchers are striving to unlock the secrets of extending human lifespan at the cellular level, where aging occurs gradually due to the shortening of telomeres—the protective caps at the ends of chromosomes that function like shoelace tips, preventing unraveling. As telomeres shorten over time, cells lose their ability to divide for healthy growth, and some eventually begin to die.

However, studying telomeres at the cellular level has been challenging in humans.

Microbial life in Yellowstone’s Lower Geyser Basin may hold clues to the evolution of life’s exploitation of oxygen, according to a recent analysis by researchers from Montana State University.

T he inhabitants of the basin’s Octopus and Conch Springs live in kelp-like, gelatinous ‘streamer’ structures that wiggle furiously in superheated currents, which hover around 88 degrees Celsius (190 degrees Farenheit). Genetically similar to ancient bacteria and archaea, t heir existence is a window into the primordial soup from which life emerged.

While these microbial communities share many traits, the springs’ environments are different in a few fundamental ways.

Researchers at Washington University School of Medicine in St. Louis have conducted a longitudinal study on an individual carrying the presenilin 2 (PSEN2) p. Asn141Ile mutation, a genetic variant known to cause dominantly inherited Alzheimer’s disease (DIAD). The high risk individual, despite being 18 years past the expected age of clinical onset, has remained cognitively intact. Researchers investigated genetic, neuroimaging, and biomarker data to understand potential protective mechanisms.

Unlike typical DIAD progression, in this case was confined to the occipital lobe without spreading, suggesting a possible explanation for the lack of cognitive decline.

DIAD results from highly penetrant mutations in (APP), presenilin 1 (PSEN1), or PSEN2, which lead to abnormal amyloid-β processing and early-onset Alzheimer’s disease. The Dominantly Inherited Alzheimer Network (DIAN) was established to track DIAD mutation carriers and assess clinical, cognitive, and biomarker changes over time.