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Experimental vaccine forces bacteria down an evolutionary dead end

The team says that the technique could be used to develop new vaccines against antibiotic-resistant bacteria, and potentially even wipe out some dangerous strains in a similar way to how smallpox was eradicated.


Pathogens like bacteria and viruses are extremely good at evolving in response to drugs, which can render vaccines ineffective. But now, researchers at ETH Zurich have found a way to weaponize that ability against them, forcing the bugs down harmless evolutionary dead ends.

Microbes are living examples of evolution in action. Darwin’s classic theory says that when lifeforms are exposed to pressures from their environment, some of them will develop new genetic mutations that help them cope better. Since other individuals will be at a disadvantage, the mutations will eventually become the norm throughout a population.

In the world of bacteria and viruses, drugs and vaccines are the environmental pressures that they must overcome. And they do it with frustrating ease, quickly finding ways around the attacks and then swapping those genes like trading cards. The end result is the constant looming threat of antibiotic-resistant “superbugs” that render our best drugs ineffective.

Synthetic SPECIES developed for use as a confinable gene drive

CRISPR-based technologies offer enormous potential to benefit human health and safety, from disease eradication to fortified food supplies. As one example, CRISPR-based gene drives, which are engineered to spread specific traits through targeted populations, are being developed to stop the transmission of devastating diseases such as malaria and dengue fever.

But many scientists and ethicists have raised concerns over the unchecked spread of gene drives. Once deployed in the wild, how can scientists prevent gene drives from uncontrollably spreading across populations like wildfire?

Now, scientists at the University of California San Diego and their colleagues have developed a gene drive with a built-in genetic barrier that is designed to keep the drive under control. Led by molecular geneticist Omar Akbari’s lab, the researchers engineered synthetic fly that, upon release in sufficient numbers, act as gene drives that can spread locally and be reversed if desired.

Who’s to Die and Who’s to Live: Mechanical Cue Is at the Origin of Cell Death Decision

Hydraulic Instability Decides Who’s to Die and Who’s to Live

In many species including humans, the cells responsible for reproduction, the germ cells, are often highly interconnected and share their cytoplasm. In the hermaphrodite nematode Caenorhabditis elegans, up to 500 germ cells are connected to each other in the gonad, the tissue that produces eggs and sperm. These cells are arranged around a central cytoplasmic “corridor” and exchange cytoplasmic material fostering cell growth, and ultimately produce oocytes ready to be fertilized.

In past studies, researchers have found that C. elegans gonads generate more germ cells than needed and that only half of them grow to become oocytes, while the rest shrinks and die by physiological apoptosis, a programmed cell death that occurs in multicellular organisms. Now, scientists from the Biotechnology Center of the TU Dresden (BIOTEC), the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG), the Cluster of Excellence Physics of Life (PoL) at the TU Dresden, the Max Planck Institute for the Physics of Complex Systems (MPI-PKS), the Flatiron Institute, NY, and the University of California, Berkeley, found evidence to answer the question of what triggers this cell fate decision between life and death in the germline.

Ancient dog breed DNA helps unravel clues about evolution of man’s best friend

An international study led by UNSW researchers has mapped one of the most intact and complete dog genomes ever generated.

The genome sequence of the Basenji dog could have a big impact on the understanding of dog evolution, domestication and canine genetic diseases.

The Basenji—also known as the barkless dog—is an ancient African dog breed which still lives and hunts with tribesmen in the African Congo.

Researchers discover that a mechanical cue is at the origin of cell death decision

In many species including humans, the cells responsible for reproduction, the germ cells, are often highly interconnected and share their cytoplasm. In the hermaphrodite nematode Caenorhabditis elegans, up to 500 germ cells are connected to each other in the gonad, the tissue that produces eggs and sperm. These cells are arranged around a central cytoplasmic “corridor” and exchange cytoplasmic material fostering cell growth, and ultimately produce oocytes ready to be fertilized.

In past studies, researchers have found that C. elegans gonads generate more germ than needed and that only half of them grow to become oocytes, while the rest shrink and die by physiological apoptosis, a that occurs in multicellular organisms. Now, scientists from the Biotechnology Center of the TU Dresden (BIOTEC), the Max Planck Institute of molecular Cell Biology and Genetics (MPI-CBG), the Cluster of Excellence Physics of Life (PoL) at the TU Dresden, the Max Planck Institute for the Physics of Complex Systems (MPI-PKS), the Flatiron Institute, NY, and the University of California, Berkeley, have found evidence to answer the question of what triggers this cell fate decision between life and death in the germline.

Prior studies revealed the genetic basis and biochemical signals that drive physiological cell death, but the mechanisms that select and initiate apoptosis in individual germ cells remained unclear. As germ cells mature along the gonad of the nematode, they first collectively grow in size and in volume homogenously. In the study just published in Nature Physics, the scientists show that this homogenous growth suddenly shifts to a heterogenous growth where some cells become bigger and some cells become smaller.

Cities Have Unique Microbial ‘Fingerprints’, First Study of Its Kind Reveals

Each city is populated by a unique host of microbial organisms, and this microbial ‘fingerprint’ is so distinctive, the DNA on your shoe is likely enough to identify where you live, scientists say.

In a new study, researchers took thousands of samples from mass transit systems in 60 cities across the world, swabbing common touch points like turnstiles and railings in bustling subways and bus stations across the world.

Subjecting over 4700 of the collected samples to metagenomic sequencing (the study of genetic material collected from the environment), scientists created a global atlas of the urban microbial ecosystem, which they say is the first systematic catalog of its kind.

Trials begin on lozenge that rebuilds tooth enamel

Before too long, you may be able to buy a breath mint that rebuilds your tooth enamel while it whitens your teeth, thanks to a team of University of Washington researchers.

The team is preparing to launch clinical trials of a lozenge that contains a genetically engineered peptide, or chain of amino acids, along with phosphorus and calcium ions, which are building blocks of tooth enamel. The peptide is derived from amelogenin, the key protein in the formation of tooth enamel, the tooth’s crown. It is also key to the formation of cementum, which makes up the surface of the tooth root.

Each lozenge deposits several micrometers of new enamel on the teeth via the peptide, which is engineered to bind to the damaged enamel to repair it while not affecting the mouth’s soft tissue. The new layer also integrates with dentin, the living tissue underneath the tooth’s surface. Two lozenges a day can rebuild enamel, while one a day can maintain a healthy layer. The lozenge – which can be used like a mint – is expected to be safe for use by adults and children alike.

New tool activates deep brain neurons

Using a mouse model, Chen and the team delivered a viral construct containing TRPV1 ion channels to genetically-selected neurons. Then, they delivered small burst of heat via low-intensity focused ultrasound to the select neurons in the brain via a wearable device. The heat, only a few degrees warmer than body temperature, activated the TRPV1 ion channel, which acted as a switch to turn the neurons on or off.


Neurological disorders such as Parkinson’s disease and epilepsy have had some treatment success with deep brain stimulation, but those require surgical device implantation. A multidisciplinary team at Washington University in St. Louis has developed a new brain stimulation technique using focused ultrasound that is able to turn specific types of neurons in the brain on and off and precisely control motor activity without surgical device implantation.

The team, led by Hong Chen, assistant professor of biomedical engineering in the McKelvey School of Engineering and of radiation oncology at the School of Medicine, is the first to provide direct evidence showing noninvasive, cell-type-specific activation of neurons in the brain of mammal by combining ultrasound-induced heating effect and genetics, which they have named sonothermogenetics. It is also the first work to show that the ultrasound-genetics combination can robustly control behavior by stimulating a specific target deep in the brain.

Results of the three years of research, which was funded in part by the National Institutes of Health’s BRAIN Initiative, were published online in Brain Stimulation May 11, 2021.

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