DNA can be thought of as a vast library that stores all genetic information. Cells do not use this information all at once. Instead, they copy only the necessary parts into RNA, which is then used to produce proteins—the essential building blocks of life. This copying process is called transcription, and it is carried out by a molecule known as RNA polymerase II.
When RNA polymerase II begins actively transcribing DNA, a specific site called Ser2 on its tail region is marked with a small chemical group known as a phosphate. This phosphate acts as a sign that transcription is in progress. Until now, observing this sign required stopping cellular activity and chemically treating the cells to visualize the phosphate. As a result, it was impossible to see how transcription changes dynamically in living cells.
To overcome this limitation, a research team led by Professor Hiroshi Kimura at Institute of Science Tokyo (Science Tokyo) chose a different approach. Instead of freezing cells at a single moment, they aimed to track transcription continuously without stopping cellular activity.
Transparent electrodes transmit light while conducting electricity and are increasingly important in bioelectronic and optoelectronic devices. Their combination of high optical transparency, low electrical resistance, and mechanical flexibility makes them well suited for applications such as displays, solar cells, and wearable or implantable technologies.
In a significant advancement, researchers led by Professor Wonsuk Jung at Chungnam National University in the Republic of Korea have introduced a new fabrication technique called one-step free patterning of graphene, or OFP-G, which enables high-resolution patterning of large-area monolayer graphene with feature sizes smaller than 5 micrometers, without the use of photoresists or chemical etching.
Published Microsystems & Nanoengineering, the method addresses a key limitation of conventional microelectrode fabrication, where lithographic processes often damage graphene and degrade its electrical performance.
There’s still so much we don’t know about Alzheimer’s disease, but the link between poor sleep and worsening disease is one that researchers are exploring with gusto.
A study published in 2023 found that using sleeping pills to get some shut-eye could reduce the buildup of toxic clumps of proteins in fluid that washes the brain clean every night.
People who took suvorexant, a common treatment for insomnia, for two nights at a sleep clinic experienced a slight drop in amyloid-beta and tau, two proteins that pile up in Alzheimer’s disease.
Omer et al. design a DNA origami box with a lid held closed by an elastic single-stranded DNA spring. The box may selectively open in blood vessels with pathological levels of shear flow, facilitating drug delivery to sites of thrombosis while minimizing off-target toxicity. It should be noted that this paper focused entirely on the box’s design and mechanical validation (via optical tweezers) and did not perform any experiments to show drug delivery. Nonetheless, this is a good start and I’m glad to see people thinking about DNA origami for therapeutic applications. [ https://pubs.acs.org/doi/10.1021/acs.nanolett.5c04066](https://pubs.acs.org/doi/10.1021/acs.nanolett.5c04066)
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Misha Ahrens’ team at Janelia Research Campus placed zebra fish in virtual reality where swimming produced no progress. Normally, fish give up after ~20 seconds. The researchers found astrocytes were “counting” swim attempts via accumulating calcium. When calcium reached a threshold, astrocytes released adenosine to suppress swimming circuits. When researchers disabled astrocytes with a laser, the fish never stopped swimming; when they artificially activated astrocytes, the fish stopped immediately. This showed astrocytes actively mediate the transition from hope to hopelessness.
Marc Freeman’s lab showed norepinephrine doesn’t just activate astrocytes—it changes their “hearing.” At low norepinephrine (low arousal), astrocytes ignore synaptic activity. At high norepinephrine (high arousal), astrocytes suddenly “listen” to every synapse and modulate neuronal response accordingly. This creates a dynamic gain control system layered atop neuronal networks.
“We did expect that, in large part, the effect of norepinephrine on synapses would be mediated by astrocytes,” Papouin said. “But we did not expect all of it to be!”
The finding of parallel molecular pathways in such distinct species as fruit flies, zebra fish, and mice points to “an evolutionarily conserved way in which astrocytes can profoundly affect neural circuits,” Freeman said.
The results suggest a gaping hole in previous theories of neuromodulation. “In the past, neuroscientists studied neuromodulators and knew they were important in regulating neural circuit function, but none of their thinking, none of their diagrams, none of their models had anything in them other than neurons,” Fields said. “Now we see that they missed a big part of the story.”
Huang et al. identify the mechanosensitive channel PIEZO1 as a plant immune hub that decodes insect-feeding-derived mechanical forces and Ca2+-activated defense responses. They characterize a self-amplifying immune circuit and identify that Bsp9, an evolutionarily conserved insect salivary effector, subverts this pathway. This work provides a framework for engineering plant disease resistance.