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Category: genetics – Page 91

Stanford and McMaster University researchers created an artificial intelligence (AI) model to design molecules that inhibit the growth of Acinetobacter baumannii, a common drug-resistant bacteria. They synthesized and validated six structurally novel molecules that demonstrated antibacterial activity against A. baumannii and other phylogenetically diverse bacterial pathogens. This study represents a significant step toward the practical application of generative AI approaches for antibiotic discovery and drug discovery in general.

The research article, “Generative AI for designing and validating easily synthesizable and structurally novel antibiotics,” was published in Nature Machine Intelligence.

Among the most critical issues in contemporary medicine is the worldwide spread of factors contributing to antibiotic resistance. In 2019, drug-resistant infections were responsible for an estimated 4.95 million deaths. As new antibiotics are being developed slower than the spread of antimicrobial resistance determinants, this figure is expected to reach 10 million annually by 2050.

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A recent study published in Nature reveals a potential link between a type of bacteria associated with dental plaque and treatment-resistant colorectal cancer. The Gram-negative, anaerobic bacterium, Fusobacterium nucleatum, was found in 50% of tumors tested, suggesting it may protect tumor cells from cancer-fighting drugs. This discovery opens avenues for new treatments and screening methods. Colorectal cancer, a leading cause of cancer deaths in the United States, is increasingly affecting younger demographics, with cases doubling among those younger than age 55 between 1995 and 2019. While the study doesn’t directly tie the bacterium to this trend, its implications raise questions about its role in rising cases among younger individuals. F. nucleatum has been suspected in colorectal cancer growth. It possesses two subspecies, one of which is capable of evading immune response and promoting tumor formation. These findings suggest a potential mechanism for its journey from the oral cavity to the colon, defying stomach acid’s toxic effects. Future research may explore developing antibiotics targeting specific bacterial subtypes or using genetically modified bacteria for targeted drug delivery into tumors. Understanding the microbiome’s role in cancer risk represents a crucial frontier in cancer research. Click here to read more.

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Humans have always been storytellers. Weaving tales, exchanging knowledge, and planning for the future are quintessentially human endeavors that have shaped the course of our species. But when did this remarkable ability to communicate through language first emerge? Recent research suggests a far earlier origin than previously thought, shedding light on the fascinating journey of human evolution.

Dr. Steven Mithen, an esteemed archaeologist from the University of Reading, has delved deep into the annals of prehistory to uncover the roots of human speech. Contrary to conventional wisdom, which pegged the advent of language to around 200,000 years ago, Mithen’s groundbreaking analysis suggests a much more ancient beginning—approximately 1.6 million years ago, in the cradle of humanity, somewhere nestled in the vast expanse of eastern or southern Africa.

In his quest to unveil the origins of language, Mithen meticulously examined a plethora of evidence spanning archaeology, genetics, neurology, and linguistics. The culmination of his research paints a vivid picture of our ancestors’ journey towards spoken communication.

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A research team led by Professor Yuanliang ZHAI at the School of Biological Sciences, The University of Hong Kong (HKU) collaborating with Professor Ning GAO and Professor Qing LI from Peking University (PKU), as well as Professor Bik-Kwoon TYE from Cornell University, has recently made a significant breakthrough in understanding how the DNA copying machine helps pass on epigenetic information to maintain gene traits at each cell division. Understanding how this coupled mechanism could lead to new treatments for cancer and other epigenetic diseases by targeting specific changes in gene activity. Their findings have recently been published in Nature.

Background of the Research.

Our bodies are composed of many differentiated cell types. Genetic information is stored within our DNA which serves as a blueprint guiding the functions and development of our cells. However, not all parts of our DNA are active at all times. In fact, every cell type in our body contains the same DNA, but only specific portions are active, leading to distinct cellular functions. For example, identical twins share nearly identical genetic material but exhibit variations in physical characteristics, behaviours and disease susceptibility due to the influence of epigenetics. Epigenetics functions as a set of molecular switches that can turn genes on or off without altering the DNA sequence. These switches are influenced by various environmental factors, such as nutrition, stress, lifestyle, and environmental exposures.

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For the first time, scientists have developed artificial nucleotides, the building blocks of DNA, with several additional properties in the laboratory. The DNA carries the genetic information of all living organisms and consists of only four different building blocks, the nucleotides. Nucleotides are composed of three distinctive parts: a sugar molecule, a phosphate group and one of the four nucleobases adenine, thymine, guanine and cytosine. The nucleotides are lined up millions of times and form the DNA double helix, similar to a spiral staircase. Scientists from the UoC’s Department of Chemistry have now shown that the structure of nucleotides can be modified to a great extent in the laboratory.

The researchers developed so-called threofuranosyl nucleic acid (TNA) with a new, additional base pair. These are the first steps on the way to fully artificial nucleic acids with enhanced chemical functionalities. The study ‘Expanding the Horizon of the Xeno Nucleic Acid Space: Threose Nucleic Acids with Increased Information Storage’ was published in the Journal of the American Chemical Society.

Artificial nucleic acids differ in structure from their originals.

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Researchers at Rutgers and Emory University are gaining insights into how schizophrenia develops by studying the strongest-known genetic risk factor.

When a small portion of chromosome 3 is missing—known as 3q29 deletion syndrome—it increases the risk for by about 40-fold.

Researchers have now analyzed overlapping patterns of altered gene activity in two models of 3q29 deletion syndrome, including mice where the deletion has been engineered in using CRIPSR, and , or three-dimensional tissue cultures used to study disease. These two systems both exhibit impaired . This dysfunction can cause energy shortfalls in the brain and result in psychiatric symptoms and disorders.

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A time question and answer starting at 32:22 (5−6 years)

Is aging a disease that can be cured? Neil deGrasse Tyson and cohosts Chuck Nice and Gary O’Reilly discover the field of epigenetics, the Information Theory of Aging, and curing blindness for mice with Professor of Genetics at Harvard Medical School, David Sinclair.

What is epigenetics? Discover the difference between genetics and epigenetics. We discuss whether aging is a disease and if there have been any changes in aging throughout the centuries. David breaks down the information theory of aging and how epigenetic inheritance works. Plus, Chuck tells us about some of the studies he’s reading and how behaviors during your lifetime can be epigenetically passed onto your children.

Could we someday cure death? What does aging look like in the broader animal kingdom? We look at aging from an evolutionary standpoint, restoring vision in blind mice, and what the length of your telomeres tells you. We break down conflicting information regarding diet and how to not just live longer but live younger, longer. What are the genes that control aging?

We break down what anti-aging medicine would look like and whether it would be affordable for everyday people. Learn about the world’s oldest mice with the youngest eyes. We discuss the Yamanaka genes and how they can be utilized to turn back time on a cellular level. Is DNA destiny?

Continue reading “Is Aging a Disease? Epigenetics with David Sinclair & Neil deGrasse Tyson” | >

In the past 10 years, gene-editing and organoid culture have completely changed the process of biology. Congenital nervous system malformations are difficult to study due to their polygenic pathogenicity, the complexity of cellular and neural regions of the brain, and the dysregulation of specific neurodevelopmental processes in humans. Therefore, the combined application of CRISPR-Cas9 in organoid models may provide a technical platform for studying organ development and congenital diseases. Here, we first summarize the occurrence of congenital neurological malformations and discuss the different modeling methods of congenital nervous system malformations. After that, it focuses on using organoid to model congenital nervous system malformations. Then we summarized the application of CRISPR-Cas9 in the organoid platform to study the pathogenesis and treatment strategies of congenital nervous system malformations and finally looked forward to the future.

Keywords: organoid, CRISPR-Cas9, congenital nervous system malformation, central nervous system, 3D

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Brain organoids have become increasingly used systems allowing 3D-modeling of human brain development, evolution, and disease. To be able to make full use of these modeling systems, researchers have developed a growing toolkit of genetic modification techniques. These techniques can be applied to mature brain organoids or to the preceding embryoid bodies (EBs) and founding cells. This review will describe techniques used for transient and stable genetic modification of brain organoids and discuss their current use and respective advantages and disadvantages. Transient approaches include adeno-associated virus (AAV) and electroporation-based techniques, whereas stable genetic modification approaches make use of lentivirus (including viral stamping), transposon and CRISPR/Cas9 systems. Finally, an outlook as to likely future developments and applications regarding genetic modifications of brain organoids will be presented.

The development of brain organoids (Kadoshima et al., 2013; Lancaster et al., 2013) has opened up new ways to study brain development and evolution as well as neurodevelopmental disorders. Brain organoids are multicellular 3D structures that mimic certain aspects of the cytoarchitecture and cell-type composition of certain brain regions over a particular developmental time window (Heide et al., 2018). These structures are generated by differentiation of induced pluripotent stem cells (iPSCs) or embryonic stem cells (ESCs) into embryoid bodies followed by, or combined, with neural induction (Kadoshima et al., 2013; Lancaster et al., 2013). In principle, two different classes of brain organoid protocols can be distinguished, namely: (i) the self-patterning protocols which produce whole-brain organoids; and (ii) the pre-patterning protocols which produce brain region-specific organoids (Heide et al., 2018).

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