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On a still night, as the air is thick with silence, the sharp, whining buzz of a mosquito shatters the calm. These blood-sucking insects that disturb people’s deep slumber are also responsible for spreading diseases such as dengue, chikungunya, malaria and Zika fever, which affect millions of people each year worldwide.

Given the harmful effects of pesticides on the environment, combined  with the emergence of mosquitoes resistant to pesticides, scientists are looking for alternative environment-friendly approaches for pest management. 

Now, researchers have developed a new population control method where male insects carrying toxic proteins can poison disease-spreading females during mating. The results, published in Nature Communications, describe a genetic biocontrol method that offers a fast and effective solution to managing pests.

Such approaches are not entirely new. In the 1950s, when researchers mated female insects with radiologically sterilized males, they did not produce offsprings, reducing the next generation’s population. More recently, scientists propagated transgenes in insects that lower the fitness of future generations, resulting in decreased insect population. Although such methods are promising, they require at least one generation to take effect: Female insects may not produce offsprings, but they can continue transmitting infections.

“As we’ve learned from COVID-19, reducing the spread of these diseases as quickly as possible is important to prevent epidemics,” said study author Samuel Beach, a graduate student in biologist Maciej Maselko’s lab at Macquarie University, in a press release.

By Sneha Khedkar

Article can be accessed on: The Scientist

Cellular communication is vital for passing information to neighboring cells. One key messenger in this process is an exosome, a nanosized particle that buds off from a progenitor cell, carrying molecular cargo. Because these small, cellular vehicles carry contents from their parent cells, exosomes can serve as snapshots for a given population of cells, including tumors.

“If you can sample a vesicle, or any entity, from blood, it gives you a huge advantage, being a low or minimally invasive strategy to monitor cancer or detect cancer,” said David Greening, a biologist who studies extracellular vesicles like exosomes at La Trobe University.

One strategy to improve the use of exosomes as cancer biomarkers is to identify surface proteins on these vesicles that reflect their originating tumor. L-type amino acid transporter 1 (LAT1), a surface protein that shuttles large amino acids into the cell, is predominantly associated with cancerous cells and correlates with tumor severity.  These characteristics made the protein an attractive target for therapeutic intervention, with one LAT1 inhibitor currently undergoing clinical trials.

In a study published in Scientific Reports, researchers demonstrated the potential of LAT1 on exosomes from pancreatic and other cancer cell lines as a biomarker. “[Now] we can detect and treat cancer using the same target,” said Ryuichi Ohgaki, a pharmacologist at Osaka University and study coauthor.

Ohgaki and his team studied the role of LAT1 in driving cancer progression for years. Inspired by previous work that measured cancer-associated proteins on exosomes, the group set out to investigate the correlation between LAT1 expression on exosomes and their originating cancer cells.

To explore this relationship, the team used ultracentrifugation to isolate these particles from human pancreatic, cervical, and bile duct tumor cell lines. In most of the tested cell lines, LAT1 expression on exosomes correlated with LAT1 expression on cell membranes.

To study exosomes in vivo, the team introduced pancreatic cancer cells into the peritoneal cavity of mice. One month later, they used immunohistochemistry to measure LAT1 expression in tumor tissue and adjacent nontumor cells, finding the protein exclusively in the tumor tissue. When they isolated exosomes from the peritoneal cavities of tumor-bearing and control mice, they detected greater LAT1 expression on the vesicles from the mice with tumors.

By Shelby Bradford, PhD

Article can be accessed on: The Scientist

The soft and squishy fat rolls on a baby serve a significant purpose. They are an important depot for brown adipocytes—fat cells that burn energy to release heat—that help keep the baby warm. As babies grow up, they lose a majority of these brown fat stores. Adults have a higher proportion of white adipose tissue (WAT), which stores fat as energy reserves for the body. However, some cells embedded within WAT can burn fat; these cells that show brown adipocyte-like properties are called beige adipocytes.

Now, researchers have found that suppressing a protein in subcutaneous WAT confers the fat-burning properties of beige adipocytes. The results, published in the Journal of Clinical Investigation, reveal that mature adipocytes exhibit plasticity, and identify a pathway that could inform the development of therapies for obesity and metabolic diseases.

Inducing fat burning by converting other cell types into those that expend energy is not a new concept; researchers have previously coaxed stem cells to become energy-burning beige adipocytes for therapeutic purposes. “But what’s sort of been a stumbling block in the field is that [adult] stem cells are rare,” said Brian Feldman an academic pediatric endocrinologist at the University of California, San Francisco and coauthor of the study. In contrast, white adipocytes are easier to come by.

Feldman and his team previously found that the transcription factor Krüppel-like factor 15(KLF15) affects adipogenesis, the process by which stem cells create fat cells. To test whether KLF15 is involved in maintaining adipocytes, Feldman’s team measured its expression in fat isolated from various parts of the bodies of mice. They observed that WAT expressed higher levels of Klf15 compared to brown adipose tissue (BAT). Deleting Klf15 from white adipocytes isolated from mice induced the expression of genes associated with brown fat identity and function. These findings led the researchers to hypothesize that decreased Klf15 levels may be required for BAT to produce heat.

Cold exposure activates BAT, which results in heat production via a beta-adrenergic signaling pathway. When the researchers deleted Klf15 in white adipocytes from mice, they observed increased expression of the gene encoding beta-1 adrenergic receptor. Treating Klf15-deleted adipocytes with a beta-adrenergic stimulant enhanced the expression of brown fat-associated genes.

By Sneha Khedkar

Article can be accessed on: The Scientist

Cells constantly face stress from infection, diseases, and aging. To detect foreign DNA threats, they use the cGAS-STING pathway, a defense mechanism that is conserved across species. The STING protein is crucial for antiviral and inflammatory responses through type I interferon production, a function recently identified in vertebrates. However, cells can also alleviate cellular stress and promote survival by removing harmful material. This led Jay Xiaojun Tan, a cellular biologist from the University of Pittsburgh, to explore whether the cGAS-STING pathway had other overlooked roles in stress management.

“We thought [this pathway] should have protective functions or stress clearance functions, in addition to the very famous inflammation function.” Tan’s team explored whether the cGAS-STING pathway interacts with lysosomes, the cell’s housekeeping organelle responsible for clearing cellular damage and promoting longevity. Their findings, published in Molecular Cell, revealed an ancient role for this pathway in lysosomal biogenesis and stress clearance, which predates type I interferons.

When STING is triggered, TANK-binding kinase (TBK1) activates and leads to interferon production. However, Tan and his team wanted to identify other transcription factors regulated by STING. On screening human cells to identify proteins that shuttled from the cytosol to the nucleus during STING activation, they identified 17 candidates.

Among these, the transcription factors EB (TFEB) and E3 (TFE3) caught Tan’s attention, because their activation coincided with genes that increased lysosome production. TFEB is also an ancient regulator of autophagy and innate immunity.

By Laura Tran, PhD

Article can be accessed on: The Scientist

Researchers from Children’s Hospital of Philadelphia (CHOP) and Stanford University have revealed the molecular structure of TRACeR-I, a protein platform for reprogramming immune responses. A better understanding of its structure may help optimize designs for the platform, which can be used to develop cancer treatments by either directly modifying immune cells or by creating proteins that help immune cells locate cancer cells. The findings were published in the journal Nature Biotechnology.

Immunotherapy presents a promising strategy for treating cancer, autoimmune diseases and viral infections, but its effectiveness depends on its ability to specifically target diseases’ cells. Monoclonal antibodies are widely used because they can target antigens proteins generated by cancer cells that trigger an immune response on the surface of diseased cells, but uniquely expressed antigens found on the surface are sparse.

Another potentially powerful target involves fragments of these proteins that may be presented on the tumor cell surface through the presentation of peptides on the major histocompatibility complex (MHC), which displays pieces of suspicious material like parts of a virus or cancer cells on the surface of our cells.

Researchers at Stanford made a breakthrough with the development of TRACeRs, platforms that recognize many different versions of these MHC proteins. TRACeRs act as “master keys” that can open a variety of “locks” posed by these MHC proteins and then treat the appropriate diseased cells while sparing healthy cells.

By  Children’s Hospital of Philadelphia

Article can be accessed on: MedicalXpress

MIT scientists have released a powerful, open-source AI model called Boltz-1 that could significantly accelerate biomedical research and drug development. Developed by a team of researchers in the MIT Jameel Clinic for Machine Learning in Health, Boltz-1 is the first fully open-source model that achieves state-of-the-art performance at the level of AlphaFold3, the model from Google DeepMind that predicts the 3D structures of proteins and other biological molecules. MIT graduate students Jeremy Wohlwend and Gabriele Corso were the lead developers of Boltz-1, along with MIT Jameel Clinic Research Affiliate Saro Passaro and MIT professors of electrical engineering and computer science Regina Barzilay and Tommi Jaakkola. Wohlwend and Corso presented the model at a Dec. 5 event at MIT’s Stata Center, where they said their ultimate goal is to foster global collaboration, accelerate discoveries, and provide a robust platform for advancing biomolecular modeling.

“We hope for this to be a starting point for the community,” Corso said. “There is a reason we call it Boltz-1 and not Boltz. This is not the end of the line. We want as much contribution from the community as we can get.”

DeepMind’s AlphaFold2, which earned Demis Hassabis and John Jumper the 2024 Nobel Prize in Chemistry, uses machine learning to rapidly predict 3D protein structures that are so accurate they are indistinguishable from those experimentally derived by scientists. This open-source model has been used by academic and commercial research teams around the world, spurring many advancements in drug development.

By Adam Zewe, Massachusetts Institute of Technology

Article can be accessed on: phys.org

A team of researchers led by professors Wybren Jan Buma at the University of Amsterdam and Vasilios Stavros at the University of Warwick (U.K.) have laid the groundwork for using urocanic acid and its derivatives as a novel class of sunscreen filters. Urocanic acid is a naturally occurring UV-A and UV-B absorbing compound found in the skin.

The team investigated the light-adsorbing, “sun-blocking” properties of urocanic acid and its derivatives, both in isolated molecules and in solutions. They present their results in two papers published in the journal Physical Chemistry Chemical Physics.

According to Wybren Jan Buma, professor of Molecular Photonics at the UvA’s Van ‘t Hoff Institute for Molecular Sciences, the two papers provide detailed insight into the light-conversion mechanism of urocanic acid.

“This is an excellent starting point for further optimization of its photoactive properties,” he says. “We envision many specific applications of urocanic acid and its derivatives, notably in safe UV filters.”

He expects that urocanic acid can meet the need for better, safer and more efficient sunscreen agents, replacing synthetic filters that are under discussion because of potential adverse effects on health and environment.

By  University of Amsterdam

Article can be accessed on: phys.org

Some sequences in the genome cause genes to be switched on or off. Until now, each of these gene switches, or so-called enhancers, was thought to have its own place on the DNA. Different enhancers are therefore separated from each other, even if they control the same gene, and switch it on in different parts of the body.

A recent study from the University of Bonn and the LMU Munich challenges this idea. The findings are also important because gene switches are thought to play a central role in evolution. The study has been published in the journal Science Advances.

The blueprint of plant and animal forms is encoded in their DNA. But only a small part of the genome—about two percent in mammals—contains genes, the instructions for making proteins. The rest largely controls when and where these genes are active: how many of their transcripts are produced, and thus how many proteins are made from these transcripts.

Some of these regulatory sequences, called “enhancers,” work like dimmer switches used to modulate the light in our living room. Indeed, they specifically increase the expression of a particular gene, where and when this gene is required. Genes controlling morphology often respond to several independent enhancers, each determining the expression of the gene in a different body part.

By University of Bonn

Article can be accessed on: phys.org

Tucked away on the kitchen countertop sits a bubbling, living goop in a jar. Each day, a mixture of flour and water feeds the beige concoction, commencing a ritualistic dance that summons wild yeast and bacteria from the air. This transformation turns simple ingredients into a tangy, fermenting marvel embraced by professional bakers and home chefs alike to create rustic bread loaves.

Cooking is deeply rooted in science. Replacing eggs in baking with aquafaba from cooked legumes or using baking soda to increase the pH of onions for faster caramelization are just a couple examples of how a deeper understanding of physical and chemical principles can transform the cooking process.

In his laboratory at Stanford University, chef-turned-scientist Vayu Hill-Maini loves to experiment with the science of food. He draws on his experiences in the kitchen and scientific training in biochemistry and microbiology to address challenges facing the food system. Specifically, his team uses filamentous fungi—molds and mushrooms—as a platform to address these goals and transform food waste into tasty meals. He believes that mastering food preservation, waste minimization, and alternative ingredients can lead to more sustainable culinary practices, reducing the environmental impact of the modern food system. For Hill-Maini, one man’s trash is another man’s dinner.

From Chef to Scientist, Food is a Common Ground

For many, the kitchen is a sacred space, a warm haven where the scents of simmering spices and baked bread mingle with laughter, familiar faces, and memories. “Food is deeply meaningful and deeply personal and deeply connected to who I am and how I see the world,” said Hill-Maini, who noted the influence of his global upbringing. Born in Stockholm to a Cuban and Norwegian father and a mother who is of Indian descent from Kenya, food became his bridge to connecting with these diverse cultures.

At the age of 18, Hill-Maini moved to the US to pursue a career as a chef. After a few years working in a sandwich shop in New York City, Hill-Maini returned to school, enrolling at Carleton College. He recalled how difficult it was to connect with the overly theoretical material taught in the introductory biology, chemistry, and physics classes; he craved more hands-on learning that would allow him to tap into his creative side. During the summer after his freshman year, he visited the Fundación Alícia, started by Ferran Adrià, a three-star Michelin chef and pioneer in molecular gastronomy, a scientific approach to cooking that explores the chemical and physical properties of food to create innovative dishes.

“It was a space that really embraced science as a way to create new food innovations,” said Hill-Maini.

He returned to university with a fresh perspective on his studies, recognizing that science served as a lens through which he could understand and connect with his passion; organic chemistry provided a foundation for understanding smell and sensation while biology was a vehicle for exploring the human experience and nutrition. His budding interests were met with support from mentors who encouraged him to continue his studies, which led him to pursue a PhD in biochemistry at Harvard University.

“I never really dreamt or considered it, until these experiences led me there,” said Hill-Maini.

There, he studied how gut bacteria break down food and drugs and explored how the emergence of cooking in human evolution may have shifted the structure and function of the gut microbiome. His graduate studies led him to a postdoctoral fellowship at the University of California, Berkeley (UC Berkeley), where he worked with bioengineer Jay Keasling to develop synthetic biology tools for manipulating microbial metabolism.

As he continued to immerse himself in the realms of biochemistry and microbiology, Hill-Maini saw an opportunity to combine his passions for science and cooking, envisioning innovative solutions to the pressing challenges facing the food system.

By Danielle Gerhard, PhD

Article can be accessed on: The Scientist

The genome serves as the blueprint for the body, influencing every trait from the shape of the face to the arches of the feet, and even the development of certain diseases. While some disorders, like cystic fibrosis, are linked to single genes and can be reliably predicted based on a person’s genetic data, many others—such as autism spectrum disorder, Alzheimer’s disease, depression, and obesity— are not.

For the past 15 years, scientists have used genome-wide association studies (GWAS) to compare genomes of large groups of people to identify hundreds of thousands of genetic variants that are associated with a trait or disease. This method has helped scientists unravel the underlying biology and risk factors of complex diseases and has also led to the discovery of novel drug targets. Despite these advancements, GWAS studies have their limitations, which scientists have tried to address with the help of artificial intelligence (AI). However, in two studies published in Nature Genetics, researchers at the University of Wisconsin-Madison identified pervasive biases these new approaches can introduce when working with large but incomplete datasets.

GWAS rely on large biobanks with extensive patient data. However, these repositories could be lacking anything from blood reports, scans, and patient history to family data. Even with a thorough survey, challenges such as the lack of data on late onset diseases in a cohort of young participants can throw a wrench into researchers’ plans.

By Sahana Sitaraman, PhD

Article can be accessed on: The Scientist