Engineered microorganisms are widely used in industrial biotechnology and biopharmaceutical applications, including the production of biofuels, sustainable chemicals, and therapeutic compounds. However, concerns remain regarding the unintended environmental release and uncontrolled proliferation of genetically engineered microbes. For this reason, biocontainment technologies, which are designed to prevent microorganisms from surviving outside controlled environments, have become increasingly important in both academia and industry.
Conventional biocontainment strategies have relied on auxotrophy-based approaches, toxin–antitoxin systems, or DNA cleavage-based technologies such as CRISPR-Cas9. However, these methods often suffer from environmental dependency, genetic instability, and the risk of unintended mutations and cellular stress caused by DNA double-strand breaks.
In particular, DNA cleavage-based systems may compromise genomic stability and allow certain mutant cells to escape survival control. In addition, CRISPR interference (CRISPRi)-based systems are inherently reversible, posing challenges for achieving complete and permanent control of cell viability.
In a recently published review, researchers led by Prof. Wu Qingfeng at the Institute of Genetics and Developmental Biology of the Chinese Academy of Sciences explored the ongoing process of neural cell competition (NCC), a fundamental mechanism that shapes the brain across the lifespan.
The review is published in National Science Review, and provides fresh insights into how brain cells continuously “compete” for survival and how this competition impacts brain development, wiring, function, and aging.
Although neural cell competition is widely recognized for its role during early brain development, Prof. Wu’s team demonstrated that this process continues to be vital throughout life. They revealed that NCC not only helps maintain healthy brain function but also contributes to age-related cognitive decline when disrupted.
Cas12a2 enzyme is programmed to identify specific RNA sequences rather than DNA. Upon successful recognition and binding to its target RNA, the protein undergoes a conformational change that unleashes indiscriminate collateral cleavage of intracellular DNA, effectively shredding the genetic material and inducing rapid cell death. In preclinical in vitro and in vivo models, a single administration of this targeted Cas12a2 system suppressed the proliferation of KRAS-mutated cancer cells by 50% and eliminated human papillomavirus (HPV)-infected cells with an efficacy exceeding 90%. Crucially, the intervention demonstrated high specificity, displaying no significant off-target cytotoxicity or damage to healthy tissue. This RNA-triggered DNA-shredding mechanism provides a highly adaptable and potent platform for oncology and virology, shifting the CRISPR paradigm from localized genetic correction to the targeted apoptosis of diseased cells, with future applications potentially expanding to target HIV and other robust infections.
Kadin Crosby, Ryan Jackson and colleagues report newly discovered details demonstrating how CRISPR Cas12a2 can be repurposed to discriminately kill cancer cells in the petri dish and in mice.
Autoimmune diseases, where the body’s own immune system mistakenly goes on the attack, are much more common in women – and a new study analyzing more than 1.25 million blood cells goes a long way to explaining why.
The analysis, led by a team from the Garvan Institute of Medical Research in Australia, revealed over 1,000 genetic ‘switches’ in immune cells that work differently depending on sex.
In short, these variations in gene activity mean that inflammatory pathways that respond to threats are likely to be busier in women, leading to a greater risk of conditions like lupus and multiple sclerosis.
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Imagine a civilization reaches something like a Type II level, advanced enough to move through interstellar space and keep large populations alive for generations. At that stage, the challenge is developing ships that can cross the void, and also making sure the people inside them can survive radiation, isolation, and extreme travel times. That could mean heavy genetic engineering before the journey begins, changing bone density, metabolism, resistance to disease, tolerance for low gravity, or even sensory systems and respiration. But when they finally arrive, they may still find that the planet is wrong for them, maybe the air is toxic, the gravity is crushing, the temperatures are extreme, or the native chemistry is incompatible with human biology.
At that point, they face two paths. One is terraforming, which means trying to remake an entire planet into something closer to Earth. That could involve thickening or thinning an atmosphere, warming a frozen world, cooling a hot one, importing water, altering soil chemistry, introducing engineered microbes, building orbital mirrors or shades, and managing the planet for centuries or even millennia. The scale of that project is absurdly expensive, not just in money but in energy, infrastructure, labor, time, and raw materials. You are not changing a city or even a continent, you are trying to rewrite a whole world.
The other option is pantropy. Instead of forcing the planet to become Earth-like, the colonists change themselves to fit the planet. They might alter their lungs to breathe a different atmospheric mix, redesign their skin to handle harsher radiation, reduce their size for lower resource use, strengthen their bodies for higher gravity, or even become something so biologically different that they no longer look fully human. That is the core idea of pantropy, adapting the colonists to the world rather than adapting the world to the colonists.
The term was coined by James Blish, and he used it in connection with the stories collected in The Seedling Stars, especially “Surface Tension.” which was first published in 1952 in Galaxy Science Fiction.
Genetic diseases impact almost 70–80 million people worldwide. Oftentimes, there are limited treatments that doctors can provide, leaving patients with few interventions to manage symptoms.
Recently, though, gene therapy has completely shifted the potential to care for many diseases. Advances in knowledge of responsible genes and nucleic acid technology have revolutionized the ability to specifically edit regions of the genome to correct mutations.
Today (April 18), the Breakthrough Prize Foundation awarded the Life Sciences prize to two teams of five researchers who pioneered gene therapies for two different types of genetic diseases. Physician scientist Jean Bennett, retinal surgeon Albert Maguire, and physician scientist Katherine High from the University of Pennsylvania developed a treatment to cure retinal blindness that is currently in use in the US, Canada, Australia, and Switzerland. Separately, clinical investigator Swee Lay Thein, now at the National Heart, Lung, and Blood Institute, tracked down the gene responsible for continued production of fetal hemoglobin in beta thalassemia and sickle cell disease and, with the help of physician scientist Stuart Orkin at Harvard University, brought this finding from the bench to the bedside.
CcCoV-KY43 is found in heart-nosed bats, or Cardioderma cor, an ecologically important species found mainly in eastern Africa, including eastern Sudan and northern Tanzania.
The researchers say the zoonotic (animal-to-human) and pandemic potential of alphaCoVs has remained relatively unchartered – to date, only two cellular receptors have been characterized for alphaCoVs.
They screened the CcCoV-KY43 spike against a panel of human receptors, identified direct interactions with the human CEACAM proteins CEACAM3, CEACAM5 and CEACAM6. Overexpression of human CEACAM6—a protein widely expressed in the human lung—conferred permissivity to otherwise refractory human cells.
During the study, partners provided specific expertise. They identified CcCoV-KY43’s ability to infect human cells and confirmed CEACAM6 supports human cell entry.
They measured how strongly CEACAM6 binds to the spike, and solved the spike structure and receptor binding in atomic detail. They showed that the RBD binds the amino-terminal IgV-like domain of human CEACAM6.
They also made initial CcCov detection in bats and mapped it across Kenya, and showed where CEACAM6s is expressed in the human body, testing serum from people living in CcCoV areas to see if they might have previously been infected by CcCoV-KY43.
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