In the murky depths of the ocean live some of the smartest and most unusual creatures to inhabit the earth. Octopuses are known for their sucker covered tentacles and chameleon-like abilities to change color, pattern and shape to blend it with their environment. The changes aren’t limited to just their appearance. A new study published in Cell reveals that they can change their brains as well (1). The study found that octopuses recode their brain in response to environmental temperature changes using RNA editing.
In early 2023, a type 2 diabetes medication, semaglutide (brand names Ozempic, Rybelsus), drew huge amounts of attention on social media and in popular culture. The reason? People were getting off-label (that is, not for treating type 2 diabetes) prescriptions of Ozempic to take advantage of one of its common side effects—measurable weight loss.
How does semaglutide and other drugs of its type manage diabetes on a molecular level, and what drives the weight loss effects?
According to the National Human Genome Research Institute, synthetic biology is “a field of science that involves redesigning organisms for useful purposes by engineering them to have new abilities”. Synthetic biology has a broad range of applications, from manufacturing pharmaceuticals and other biologically active chemicals and biofuels, to accelerating the adoption of plant-based burgers (1).
At the heart of the synthetic biology revolution is the rapid technological advancement—and accompanying drop in costs—of DNA oligonucleotide synthesis. Typically, synthetic biology researchers use oligonucleotides as building blocks to assemble genes of interest that are then introduced into, and expressed by, a different organism. For example, to create the plant-based Impossible Burger, the soy leghemoglobin gene (normally found in the root nodules of leguminous plants) was synthesized and expressed in yeast cells (1). This component gives the burger its meaty flavor and appearance of “bleeding” when cooked.
Promega R&D Scientists were recently honored for publishing papers and patents between 2019-2023
“We are a company that is built upon innovation, and R&D is one of the main drivers of that,” says Frank Fan, Director of Biology at Promega.
Promega Research and Development is focused on developing reliable tools that address the biggest problems facing life scientists. However, our R&D scientists do much more than just develop products. Promega scientists regularly pursue basic research to curate new skills and knowledge and collaborate extensively with researchers across academia and industry. This work fuels major advancements in areas like targeted genome editing, drug discovery, and genetic identity.
In June 2023, our Research and Development department gathered to recognize Promega scientists who have published peer-reviewed papers or patents. This was the first time the department had held this event since 2019, and in that time 71 scientists have published research in journals like Nature and Cell. 16 of those scientists published 10 or more times, and several were also invited to contribute review articles and book chapters.
In addition, Promega also recognized seven researchers with the title “Distinguished Scientist.” This award was intended to recognize scientists who are at the top of their game in both advancing and communicating science. Their work includes protein engineering, chemical biology, neuroscience and much more.
The Distinguished Scientists were selected for having an i10 index above 25 since 2018. This indicates that the scientist has more than 25 publications that have been cited 10+ times in the past five years, as measured by Google Scholar. As VP of R&D Poncho Meisenheimer said, “This award is truly from the scientific community. This is a recognition that your scientific peers see your work as valuable.”
Here is the list of Promega researchers recognized as Distinguished Scientists and some of their recent high-impact papers.
Global pandemics, such as COVID-19, have taught us to abhor viruses. The emergence of new, highly infectious viruses is—rightfully so—a cause for concern. However, despite the average human body harboring 380 trillion viruses, most of them simply coexist with us and are harmless. When it comes to an ancient lineage of viruses within the realm Duplodnaviria, researchers are even using them as weapons in the battle against infectious diseases.
We share this planet with approximately 8.7 million species of plants and animals. Within such a diverse environment, it’s only natural that many complex relationships have developed among different species. Some relationships are mutually beneficial, some are parasitic—and some are lethal.
Natural toxins and venoms are biologically active compounds produced by normal metabolic processes in an organism but are harmful to other organisms. Typically, toxins are encountered passively or ingested by the affected organisms, and have a specific mode of action and binding site within a cell. In contrast, venoms are introduced directly into the victim through a specialized delivery mechanism, and they may consist of a mixture of compounds that affect a range of cell types and tissues (1). Both types of poisons are produced for predation, defense, or to offer a competitive advantage (1).
Cells, commonly considered the smallest unit of life, provide structure and function for all living things (3).
Eye of a fruit fly, Drosophila melanogaster, scanning electron microscopy
Because cells contain the fundamental molecules of life, in some situations such as yeast, a single cell can be considered the complete organism. In other situations, for more complex multicellular organisms, a multitude of cells can mature and acquire different, specialized functions (3).
Cells developing specificity are undergoing differentiation, a process where a cell’s genes are either turned “on” or “off” resultant in a more specific cell type. As these differentiated cells start to exhibit their identity, they organize themselves into the tissues, organs, and organ systems integral to the functioning of a multicellular, developing organism. This process in which order and form is created within a developing organism is referred to as morphogenesis (5).
Our cells, and the DNA they contain, are under constant attack from external factors such as ionizing radiation, ultraviolet light and environmental toxins. Internal cellular processes can also generate metabolites, such as reactive oxygen species, that damage DNA. In most cases, DNA damage results in permanent changes to DNA molecules, including DNA mismatches, single-strand breaks (SSBs), double-strand breaks (DSBs), crosslinking, or chemical alteration of bases or sugars. If left unchecked, DNA damage can cause genome instability, mutations and aberrant transcription, and oncogenic transformation.
Fortunately, our cells have also evolved multiple pathways to repair damaged DNA, collectively known as the DNA damage response (DDR). The type of repair mechanism depends on the nature of the damage, and whether the damage occurs in mitochondrial or nuclear DNA. These mechanisms have been reviewed extensively (1,2). Recently, considerable attention has focused on pathways for repairing SSBs and DSBs, mediated by the ADP-ribosylating enzyme known as poly (ADP-ribose) polymerase 1, or PARP-1.
Alzheimer’s disease is a devastating, progressive degenerative brain condition that starts with mild dementia symptoms like memory issues and gradually worsens to the point where you can no longer communicate or care for yourself. For anyone with personal experience with it, Alzheimer’s looms like a specter over the natural process of aging.
In the beginning phase of Alzheimer’s, abnormal plaques of the protein, amyloid-β, develop. These protein clumps can accumulate for decades with no detectable impact on cognitive ability or brain health. Eventually, a second protein, tau, begins to gather and form intercellular, fibrous, tangles. It is with the formation of these tau tangles that symptoms first appear. The combined presence of these extracellular plaques and intercellular tangles are the hallmarks of Alzheimer’s disease.
Cancer cells can be distinguished from normal cells by a variety of features including their ability to inappropriately activate signals for cell proliferation, evade growth suppression from contact inhibition or tumor suppressor activity, evade cell death signals, replicate DNA continually, induce angiogenesis, invade new tissues, reprogram their metabolism to provide energy for rapid proliferation, and evade immune detection (1) . Several biological processes are responsible for these features including genomic instability, inflammation, and the creation of a tumor microenvironment.
The tumor microenvironment is the network of non-malignant cells, connective tissue and blood vessels that surround and infiltrate the tumor. These surrounding “normal” cells interact with each other and the cancer cells and are important players in tumorigenesis. One cell type that is often found in the tumor microenvironment are nerve cells. In fact, cancer cells often express proteins that encourage nerve growth into the tumor microenvironment such as growth factors and axon-guidance molecules (2). Crosstalk between nerve cells and tumor cells can facilitate development of several cancer types (2) including pancreatic, head and neck, oral, prostate, and colorectal cancers.
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