Scientists have connected two organoids together with an axon bundle, to study how brain areas communicate. They sent signals back and forth and responded to external stimulation. This could be a step toward biocomputing.
CORRECTIONS/CLARIFICATIONS: As the pinned comment points out, there are many different kinds of neurons, and two pairs of organoids may not have the same cellular makeup. This natural variation between neurons might also account for the different post-stimulation behavior of the organoids from different cell lines.
In multicellular organisms, many biological pathways exhibit a curious structure, involving sets of protein variants that bind or interact with one another in a many-to-many fashion. What functions do these seemingly complicated architectures provide? And can similar architectures be useful in synthetic biology? Here, Dr. Elowitz discusses recent work in his lab that shows how many-to-many circuits can function as versatile computational devices, explore the roles these computations play in natural biological contexts, and show how many-to-many architectures can be used to design synthetic multicellular behaviors.
About Michael Elowitz. Michael Elowitz is a Howard Hughes Medical Institute Investigator and Roscoe Gilkey Dickinson Professor of Biology and Biological Engineering at Caltech. Dr. Elowitz’s laboratory has introduced synthetic biology approaches to build and understand genetic circuits in living cells and tissues. As a graduate student with Stanislas Leibler, Elowitz developed the Repressilator, an artificial genetic clock that generates gene expression oscillations in individual E. coli cells. Since then, his lab has continued to design and build synthetic genetic circuits, bringing a “build to understand” approach to bacteria, yeast, and mammalian cells. He and his group have shown that gene expression is intrinsically stochastic, or ‘noisy’, and revealed how noise functions to enable probabilistic differentiation, time-based regulation, and other functions. Currently, Elowitz’s lab is bringing synthetic approaches to understand and program multicellular functions including multistability, cell-cell communication, epigenetic memory, and cell fate control, and to provide foundations for using biological circuits as therapeutic devices. His lab also co-develops systems such as “MEMOIR” that allows cells to record their own lineage histories and tools for RNA export, and precise gene expression. Elowitz received his PhD in Physics from Princeton University and did postdoctoral research at Rockefeller University. Honors include the HFSP Nakasone Award, MacArthur Fellowship, Presidential Early Career Award, Allen Distinguished Investigator Award, the American Academy of Arts and Sciences, and election to the National Academy of Sciences.
The Monthly Seminar on Physical Genomics is a public lecture series sponsored by the Center for Physical Genomics at Northwestern University, the Robert H. Lurie Comprehensive Cancer Center, and NIH Grants T32GM142604 and U54CA268084.
Summary: Researchers have discovered how glial cells can be reprogrammed into neurons through epigenetic modifications, offering hope for treating neurological disorders. This reprogramming involves complex molecular mechanisms, including the transcription factor Neurogenin2 and the newly identified protein YingYang1, which opens chromatin for reprogramming.
The study reveals how coordinated epigenome changes drive this process, potentially leading to new therapies for brain injury and neurodegenerative diseases.
Researchers have significantly improved gene-editing techniques. This new method, called eePASSIGE, can insert or replace entire genes in human cells with much higher efficiency than previous methods. This advancement could lead to a single gene therapy for diseases caused by various mutations in a single gene, like cystic fibrosis. Traditionally, gene therapy required a different treatment for each mutation.
EePASSIGE combines prime editing, which edits small stretches of DNA, with new enzymes that insert large pieces of DNA. This allows scientists to introduce a healthy copy of a gene directly where it belongs in the genome.
“This is one of the first examples of targeted gene integration with potential for therapeutic applications,” said Dr. David Liu, senior author of the study. “If these efficiencies translate to patients, many genetic diseases could be treated.”
Learn more about the Cognitive Science Student Association and the California Cognitive Science Conference at https://cssa.berkeley.edu.
Amy Arnsten — Yale University.
Abstract. The recently evolved prefrontal cortex (PFC) subserves many of our highest-order cognitive functions, generating and sustaining the mental representations that underlie working memory, abstract reasoning, and top-down control of thought, action, and emotion. Due to the pioneering research of Patricia Goldman-Rakic, we have learned much about the neural basis underlying the ability of the dorsolateral prefrontal cortex (dlPFC) to generate mental representations, where microcircuits in deep layer III have extensive recurrent excitatory connections to maintain neuronal firing in the absence of sensory stimulation, while GABAergic interneurons provide lateral inhibition to refine the contents of working memory. However, these dlPFC circuits are also tremendously dependent on arousal state, with a narrow inverted U response to levels of acetylcholine, dopamine and norepinephrine. Even quite mild uncontrollable stress increases the release of dopamine and norepinephrine in the PFC, which rapidly impairs PFC functioning by 1) stimulating D1 and alpha-1-receptors, respectively, 2) these, in turn, activate feedforward calcium-cAMP signaling within spines, which then 3) open nearby potassium channels to disconnect PFC networks and take the PFC “off-line”. With chronic stress exposure, there is actual atrophy of PFC dendrites and spines. Understanding the neural events that weaken vs. strengthen PFC connectivity and function has led to the development of treatments for patients with stress-related PFC dysfunction, e.g. guanfacine and prazosin. This knowledge is also helping to illuminate the etiology of cognitive disorders, as genetic insults in schizophrenia often increase the activity of these stress signaling pathways, and the molecules that regulate the stress signaling pathways are lost with advancing age, leading to tau pathology as seen in Alzheimer’s disease.
Restraining or slowing ageing hallmarks at the cellular level have been proposed as a route to increased organismal lifespan and healthspan. Consequently, there is great interest in anti-ageing drug discovery. However, this currently requires laborious and lengthy longevity analysis. Here, we present a novel screening readout for the expedited discovery of compounds that restrain ageing of cell populations in vitro and enable extension of in vivo lifespan.
Using Illumina methylation arrays, we monitored DNA methylation changes accompanying long-term passaging of adult primary human cells in culture. This enabled us to develop, test, and validate the CellPopAge Clock, an epigenetic clock with underlying algorithm, unique among existing epigenetic clocks for its design to detect anti-ageing compounds in vitro. Additionally, we measured markers of senescence and performed longevity experiments in vivo in Drosophila, to further validate our approach to discover novel anti-ageing compounds. Finally, we bench mark our epigenetic clock with other available epigenetic clocks to consolidate its usefulness and specialisation for primary cells in culture.
We developed a novel epigenetic clock, the CellPopAge Clock, to accurately monitor the age of a population of adult human primary cells. We find that the CellPopAge Clock can detect decelerated passage-based ageing of human primary cells treated with rapamycin or trametinib, well-established longevity drugs. We then utilise the CellPopAge Clock as a screening tool for the identification of compounds which decelerate ageing of cell populations, uncovering novel anti-ageing drugs, torin2 and dactolisib (BEZ-235). We demonstrate that delayed epigenetic ageing in human primary cells treated with anti-ageing compounds is accompanied by a reduction in senescence and ageing biomarkers. Finally, we extend our screening platform in vivo by taking advantage of a specially formulated holidic medium for increased drug bioavailability in Drosophila. We show that the novel anti-ageing drugs, torin2 and dactolisib (BEZ-235), increase longevity in vivo.
Researchers have developed a genetic algorithm for designing phononic crystal nanostructures, significantly advancing quantum computing and communications.
The new method, validated through experiments, allows precise control of acoustic wave propagation, promising improvements in devices like smartphones and quantum computers.
Treating cancer can sometimes feel like a game of Whac-A-Mole. The disease can become resistant to treatment, and clinicians never know when, where and what resistance might emerge, leaving them one step behind. But a team led by Penn State researchers has found a way to reprogram disease evolution and design tumors that are easier to treat.
They created a modular genetic circuit that turns cancer cells into a “Trojan horse,” causing them to self-destruct and kill nearby drug-resistant cancer cells. Tested in human cell lines and in mice as proof of concept, the circuit outsmarted a wide range of resistance.
The findings were published today, July 4, in the journal Nature Biotechnology. The researchers also filed a provisional application to patent the technology described in the paper.
The advent of quantum computers promises to revolutionize computing by solving complex problems exponentially more rapidly than classical computers. However, today’s quantum computers face challenges such as maintaining stability and transporting quantum information.
Phonons, which are quantized vibrations in periodic lattices, offer new ways to improve these systems by enhancing qubit interactions and providing more reliable information conversion. Phonons also facilitate better communication within quantum computers, allowing the interconnection of them in a network.
Nanophononic materials, which are artificial nanostructures with specific phononic properties, will be essential for next-generation quantum networking and communication devices. However, designing phononic crystals with desired vibration characteristics at the nano-and micro-scales remains challenging.
A team of scientists from the University of Sharjah say they have invented a biosensor capable of detecting the gene mutations responsible for the loss of hearing.
