Discoveries

GLP-1s are building a reputation as “wonder drugs.” First characterized for their ability to improve insulin release and treat diabetes, the drugs were later found to promote weight loss and improve cardiovascular health. In addition to those bonus benefits, GLP-1 drugs can improve pancreatic beta cell health. But how, exactly, are they doing that?

In the lab of Marc Montminy, MD, PhD, scientists are burrowing into the mechanistic details behind how GLP-1 drugs promote viability and stress resistance in pancreatic beta cells. Since cellular performance adaptations arise from gene expression changes, the team screened for regulatory proteins that can switch on gene programs responsible for the beneficial effects of prolonged use of GLP-1 therapeutics. They identified a protein called Med14—part of a larger protein complex called Mediator—that enables the GLP-1-dependent changes in gene expression that lead to pancreatic health benefits.

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In little moments like when sipping coffee or licking an ice cream cone, it doesn’t seem like your body is pulling off a biological miracle. But it is. That ice cream is not you—yet when you put it in your mouth, your body is able to tolerate it and process it without any detriment to your health in a process called oral tolerance. 

Jamie Blum, PhD, is an oral tolerance expert, and her latest research identified new bits of food proteins that tell gut immune cells when to tolerate certain foods. They found three of these protein segments, called epitopes—one each from soybean, corn, and wheat. These epitopes interact with specialized immune cells called regulatory T cells to inform that tolerance-or-rejection decision. The findings are an enormous step forward in understanding food tolerance and may inform future immunotherapies for people with food allergies.

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Neurodegenerative diseases affect more than 57 million people globally. Though scientists know that aging is a major risk factor for neurodegenerative diseases, the mechanisms underlying its impact remain unclear. But a great place to start is epigenetic change—the way small chemical tags on top of our base genetic code shift over time to alter gene expression. Joseph Ecker, PhD, Margarita Behrens, PhD, and colleagues have created the most comprehensive single-cell atlas of epigenetic changes in the aging mouse brain to date. The new atlas represents eight brain regions and 36 distinct brain cell types, with more than 200,000 single cells profiled across methylation and chromatin conformation assays, plus nearly 900,000 cells captured with spatial transcriptomics. The contents have already revealed clear epigenetic differences across age groups and enabled the researchers to develop novel deep-learning models that predict age-related gene expression changes.

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For more than 25 years, the American Southwest has faced the severe social and economic consequences of a megadrought, including a $1.1 billion agricultural loss in California in 2021 alone. New research led by Joseph Ecker, PhD, provides a roadmap that could help researchers engineer crop varieties that get us out of this agricultural rut. 

The team profiled nearly a million cells from the leaves of Arabidopsis thaliana, a small flowering plant that serves as a laboratory stand-in for important crops like corn, wheat, and rice. They measured changes in gene expression in these cells across different drought levels and leaf developmental stages and compiled the data in a public atlas. The atlas revealed that drought conditions accelerate leaf aging, but a specific gene could be used to rescue leaf growth during drought.

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Plants can’t move to escape the heat like humans can—they are forced to adapt. As temperatures fluctuate, one key survival strategy is the ability of roots to keep growing, allowing plants to access water and nutrients farther away in the soil. Lucia Strader, PhD, asked how plants sense temperature and translate it into growth. She found her answer in a familiar plant hormone: auxin.

Auxin is at the center of plant growth, governing everything from cell elongation to root and stem development. But it’s not the center of this story—instead, the latest research found auxin’s partner proteins serve as internal plant “thermostats.” These partner proteins directly sense temperature, then change genetic programs to direct root growth accordingly. The findings could be used in future efforts to engineer plants that can withstand more extreme temperatures.

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Metabolic dysfunction-associated steatotic liver disease (MASLD) is among the most common chronic liver diseases and, when untreated, can progress to cancer, cardiovascular disease, and diabetes. A new study led by Ronald Evans, PhD, found that production of the protein FGF1 in the liver varies throughout the day to regulate the timing of fat release from the liver into the bloodstream, acting as a circadian pacemaker for liver fat metabolism. 

This liver clock ensures fat enters the bloodstream on a precise daily schedule and prevents fat accumulation seen in MASLD. The findings may also help explain why circadian disruption, from shift work to chronic sleep loss, has been linked to metabolic disease. Each mechanistic step uncovered brings scientists closer to therapies grounded not just in symptom management, but also in the fundamental biology of how the body regulates fat.

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Some of your most important life partners are the mitochondria that power all your cells. You and these little cellular powerhouses are in a 1.5-billion-year-old evolutionary relationship—but mitochondria brought some baggage. Mitochondria brought their own DNA with them when they joined with our bigger, more complex cells so long ago, and today, that mitochondrial DNA influences human health.

Ronald Evans, PhD, is asking what those influences are, and the latest study from his lab unveils a new biological platform for studying mitochondrial DNA in physiology, adaptation, disease mechanisms, and therapeutic development. They have already used the platform to generate a library of 155 mitochondrial DNA mutant cell lines and to reveal correlations between mouse development and mitochondrial function. The platform, library, and findings will accelerate therapeutic development for mitochondrial disorders and help scientists treat mitochondrial dysfunction in other diseases and conditions, such as cancer and aging. 

“The majority of human diseases come with or cause mitochondrial dysfunction. Progress in this field has been limited, but this new platform is going to fuel so much important research that points to therapeutic approaches to combat mitochondrial diseases, as well as diseases or conditions associated with mitochondrial dysfunction like cancer or aging.”

Ronald Evans 

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Fluorescent proteins have revolutionized science, enabling researchers to tag and visualize individual molecules in living cells, tissues, and animals. Using these tools, researchers have watched viruses infect cells in real time, observed cellular waste collection, and tracked the signaling that spurs tumor growth. Axel Nimmerjahn, PhD, worked with collaborators at Albert Einstein College of Medicine to advance this visualization technology. 

Their new technology, called visible-spectrum antigen-stabilizable fluorescent nanobodies (VIS-Fbs), was validated across multiple mammalian cell types and provides a powerful tool for a wide range of life science research applications. Scientists can now gain more accurate, timely insight into cellular activity—even in complex environments such as living brain tissue.

“This work establishes a versatile platform for imaging proteins with high specificity and minimal background. It opens new opportunities to study how molecular and cellular processes unfold in real time across diverse biological systems.”

Axel Nimmerjahn

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Naked mole rats keep kingdoms underground. One queen bears all the children, while other mole rats maintain complex subterranean tunnels, forage for food, take care of newborns, and perform other necessary upkeep. This society hinges on the central pillar of a singular queen. For years, the prevailing view has been that succession in naked mole rat colonies is violent and chaotic. 

New research led by Janelle Ayres, PhD, suggests it does not have to be that way. Her team found that when reproduction is impaired in an established queen, peaceful succession is possible within an established naked mole rat colony. The study illuminates a new layer of social complexity for naked mole rats, which are important models in biomedical research on socialization, aging, adaptation, fertility, and more. The findings also help answer broader questions about biological resilience, potentially revealing principles that can explain human health and disease.

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Fragile X syndrome (FXS) is an inherited genetic developmental condition that strongly impacts brain development. Its symptoms are broad and highly variable, and there is currently no cure. Existing treatments are limited to medications and therapies to help manage symptoms. Nicola Allen, PhD, and team recently discovered how star-shaped brain cells called astrocytes contribute to some FXS symptoms. They found that a protein pathway commonly upregulated in FXS astrocytes could be suppressed to lessen those symptoms, meaning less severe seizures and restored molecular balances in a mouse model of FXS. The findings validate the importance of studying astrocytes in FXS research and represent a promising step toward future therapeutics for FXS and other developmental conditions, such as Down syndrome and Rett syndrome. 

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