What Is: mRNA

The Genetic Messenger
Messenger RNA (mRNA) serves as the vital intermediary in the "central dogma" of molecular biology, bridging the gap between stable genomic DNA and the production of functional proteins. Acting as a transient transcript, mRNA carries specific genetic instructions from the cell nucleus to the ribosome, where the code is translated into precise amino acid sequences. By providing a temporary, programmable blueprint for cellular machinery, mRNA enables the dynamic regulation of life’s essential processes and stands as a cornerstone of modern biotechnological innovation.

Scientific Frontline: Extended "At a Glance" Summary

The Core Concept: Messenger RNA (mRNA) acts as a transient biological intermediary that conveys specific genetic instructions from cellular DNA to ribosomes, serving as a programmable blueprint for the synthesis of functional proteins.

Key Distinction/Mechanism: Unlike traditional pharmaceuticals that deliver the "hardware" (such as small molecule inhibitors or recombinant proteins), mRNA therapeutics deliver the "software" (genetic code), instructing the patient's own cells to manufacture the therapeutic agent. This process is inherently transient; the molecule degrades naturally without integrating into the host genome, eliminating the risk of insertional mutagenesis associated with DNA-based gene therapies.

Biochemistry lab at IU Bloomington finds chemical solution for tackling antibiotic resistance

“I love thinking outside the box when it comes to the antibiotic resistance problem,” said J.P. Gerdt, assistant professor of chemistry at Indiana University Bloomington.
Photo Credit: Chris Meyer, Indiana University

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Identification of a small chemical molecule that actively inhibits bacterial immune defenses, enabling bacteriophages to successfully infect and destroy bacteria that would otherwise resist viral attack.
• Methodology: Researchers screened a commercial compound library against a model bacterium to isolate specific molecules capable of suppressing the bacteria's immune response to bacteriophages.
• Key Data: The specific bacterial immune system mechanism targeted by the discovered molecule is present in approximately 2,000 distinct bacterial species.
• Significance: Offers a potential solution to antimicrobial resistance by potentiating phage therapy, allowing for the precise elimination of pathogens like Staphylococcus aureus without harming beneficial microbiomes, unlike broad-spectrum antibiotics.
• Future Application: Development of a comprehensive library of bacterial immune inhibitors over the next 10 to 15 years for use in agriculture and treating hard-to-cure human infections.
• Branch of Science: Biochemistry and Microbiology
• Additional Detail: These findings were published in the journal Cell Host and Microbe in a paper titled "Chemical inhibition of a bacterial immune system."

Shrinking Shellfish? Risks of Acidic Water in the Indian River Lagoon

FAU researchers measured aragonite saturation – a key indicator of water’s ability to support calcifying organisms like clams and oysters – throughout the Indian River Lagoon.
Photo Credit: Courtesy of Florida Atlantic University

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Elevated nutrient runoff, freshwater discharges, and harmful algal blooms are accelerating coastal acidification in Florida's Indian River Lagoon, resulting in critically low levels of aragonite saturation necessary for shell-building organisms to survive.
• Methodology: Researchers performed a comprehensive spatial survey of the entire lagoon alongside weekly monitoring at three distinct central sites—an urban canal, a river mouth, and a natural reference area—between 2016 and 2017 to measure water chemistry and correlate aragonite saturation (\(\Omega_{arag}\)) with environmental stressors.
• Key Data: The study established a strong positive correlation between aragonite saturation and salinity, with data showing that nutrient-dense northern regions and freshwater-impacted southern areas consistently exhibited saturation levels insufficient for healthy shell development.
• Significance: Depleted aragonite levels inhibit the growth and structural integrity of calcifying species like oysters and clams, making them more vulnerable to predation and disease, which threatens the stability of the entire estuarine food web and local economy.
• Future Application: These findings provide a baseline for new ecosystem management strategies focused on controlling nutrient inputs and freshwater flows, supported by real-time pH and \(\mathrm{CO_2}\) monitoring via the upgraded Indian River Lagoon Observatory Network of Environmental Sensors (IRLON).
• Branch of Science: Marine Biogeochemistry and Estuarine Ecology
• Additional Detail: This research represents the first complete documentation of aragonite saturation distribution across the entire Indian River Lagoon, identifying specific "hotspots" where local anthropogenic pressures amplify global ocean acidification trends.

Electrifying biology in a bubble

Small, naturally occurring droplets could have accelerated the development of early life.
Image Credit: Scientific Frontline

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Naturally forming coacervate droplets create a unique internal micro-environment that energetically favors spontaneous reduction-oxidation (redox) reactions, effectively functioning as "proto-enzymes" for early life.
• Methodology: Researchers synthesized coacervates using polyuridylic acid (RNA) and poly-L-lysine (peptides) and coated metal electrodes with a thin film of these droplets. They used electrochemistry to measure voltage as a direct proxy for Gibbs energy and employed Raman spectroscopy to track molecular vibrational modes and the behavior of water molecules surrounding iron ions.
• Key Data: Electrochemical analysis confirmed that the droplet interior significantly alters the thermodynamics of the \([Fe(CN)_{6}]^{3-}\)) / \([Fe(CN)_{6}]^{4-}\) redox pair compared to bulk water, making electron donation more probable. Temperature-dependent measurements allowed the team to isolate and quantify the specific entropic and enthalpic contributions driving this favorable energy shift.
• Significance: This study provides the first molecular-level explanation for how prebiotic droplets could drive chemical evolution, demonstrating that they actively alter reaction thermodynamics rather than merely concentrating reactants as previously thought.
• Future Application: These findings establish a framework for engineering synthetic cells and bioreactors, with immediate research directed toward controlling reaction kinetics (speed) and catalyzing complex biochemical pathways within artificial droplet systems.
• Branch of Science: Biochemistry, Electrochemistry, and Prebiotic Chemistry
• Additional Detail: The investigation uniquely bridges electrochemistry and biology by treating the coacervate-electrode interface as a "Gibbs energy meter," offering a new tool for probing the thermodynamic potential of prebiotic environments.

Mitochondria as Control Centers of Cell Communication

Anna Meichsner is investigating the role of mitochondria.
Photo Credit: © RUB, Marquard

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Mitochondria operate as central signaling hubs that actively control cellular communication by linking metabolic states with stress and immune responses, moving beyond their traditional role as energy producers.
• Methodology: Researchers from Ruhr University Bochum analyzed and systematized the functional roles of mitochondria in intracellular signaling and innate immunity, publishing a comprehensive review in Molecular Cell.
• Key Data: Mitochondria release specific signaling molecules including reactive oxygen species, metabolites, and nucleic acids which possess bacterial-like signatures that the cell identifies as danger signals to trigger immune activation.
• Significance: The identification of mitochondria as critical interfaces for cellular stress and immune responses explains the mechanism connecting mitochondrial dysfunction to the development of metabolic, neurodegenerative, and inflammatory diseases.
• Future Application: Clarifying these regulatory mechanisms enables the development of targeted medical interventions that modulate pathological signaling processes to treat chronic inflammation and associated disorders.
• Branch of Science: Biochemistry and Cell Biology
• Additional Detail: The study reveals a dual nature of mitochondrial signaling, where controlled release enhances immunity but unregulated release provokes chronic inflammation, marking a pivotal shift in understanding disease pathology.

Purdue team announces new therapeutic target for breast cancer

Graduate student Addison Young (left) and Kyle Cottrell, assistant professor, both in Purdue’s department of biochemistry. Young and Cottrell have reported discovering a new therapeutic target for triple-negative breast cancer in the journal RNA.
Photo Credit: Courtesy of Purdue University

Scientific Frontline: "At a Glance" Summary

• Main Discovery: A specific double-stranded RNA (dsRNA)-binding protein called PACT has been identified as a novel therapeutic target for triple-negative breast cancer (TNBC), a deadly form of the disease that currently lacks targeted therapies.
• Methodology: Researchers utilized the gene-editing tool CRISPR-Cas9 to deplete PACT in various cell lines, allowing them to observe which cellular pathways became activated and to confirm PACT's role as a suppressor of the RNA-activated protein kinase (PKR).
• Key Data: The study established that PACT functions as a dimer—requiring the fusion of two monomers to operate—and that TNBC cells are particularly sensitive to its depletion, which triggers a "viral mimicry" state that can lead to cancer cell death.
• Significance: This research resolves a scientific controversy by confirming PACT acts as a suppressor rather than an activator of PKR; blocking PACT allows PKR to sense dsRNA and initiate stress responses that kill cancer cells, offering a strategy to treat TNBC without broad chemotherapy.
• Future Application: Scientists aim to develop molecules that specifically inhibit PACT dimerization, creating precise drugs for TNBC and potentially other cancer types that depend on this protein for survival.
• Branch of Science: Biochemistry and Oncology.
• Additional Detail: Unlike many therapeutic targets which are enzymes, PACT is a structural protein; therefore, treatment strategies must focus on physically preventing the binding of its two monomers rather than blocking enzymatic activity.

Tapping the engines of cellular electrochemistry and forces of evolution

Biological condensates are clumps of molecules that condense and scatter apart based on the surrounding chemical and electrical environment in a cell. Recent work from WashU researchers shows how to design and embed these proteins into living systems to serve as electron generators.
Image Credit: AI-generated image courtesy of Dai lab

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Researchers successfully engineered "intrinsically disordered proteins" into biological condensates that function as nanoscale electrochemical "battery droplets" within living cells, capable of generating voltage and driving redox reactions.
• Methodology: The team utilized "directed evolution" in E. coli bacteria, subjecting protein sequences to selective pressures to guide the self-assembly of condensates that create interfacial electric fields similar to electrode-electrolyte boundaries in traditional batteries.
• Key Data: The engineered bio-batteries successfully drove the synthesis of gold and copper nanoparticles directly inside cells and executed redox reactions capable of killing bacteria without the use of traditional antibiotics.
• Significance: This establishes a new framework for "electrogenic protein powerhouses," proving that soft biological matter can store and release electrochemical energy on demand to power synthetic biological signals and reactions.
• Future Application: Applications include sustainable bioproduction, wastewater decontamination (via pollutant degradation), and "biohybrid" medical devices designed to fight infection or reverse antibiotic resistance.
• Branch of Science: Synthetic Biology, Biomedical Engineering, and Electrochemistry.
• Additional Detail: The study overcomes a significant hurdle in evolutionary biology by successfully applying directed evolution to non-structured (disordered) proteins, enabling the programmable design of cellular function based on survival and fitness.

Study Sheds Light on the Function of a Key Antibiotic-Producing Enzyme

Researchers have successfully replaced a section of the antibiotic-synthesizing enzyme PikAIII-M5, advancing our understanding of its structure and function and moving us closer to the creation of synthetic antibiotics.
Illustration Credit: ©Tohoku University

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Researchers successfully engineered a chimeric version of the enzyme PikAIII-M5, a key component in pikromycin biosynthesis, by swapping its beta-ketoreductase domain to control the stereochemistry of macrolide chains.
• Methodology: The team utilized a synthetic substrate evaluation system to physically replace the beta-ketoreductase domain within the PikAIII-M5 enzyme with an alternative domain, subsequently analyzing how these structural modifications altered the enzyme's biochemical output.
• Key Data: The study validated that the beta-ketoreductase domain acts as an interchangeable module; its successful replacement demonstrated that specific domain swapping can predictably dictate the structural composition of the resulting macrolactone ring.
• Significance: This research establishes a verified "design guideline" for combinatorial biosynthesis, enabling more accurate predictions of chemical structures from genomic data and facilitating the engineering of complex, non-natural drug molecules.
• Future Application: The findings will be applied to create novel macrolide antibiotics with structures not found in nature, directly addressing the global crisis of antibiotic resistance and the shrinking pipeline of effective antimicrobial drugs.
• Branch of Science: Synthetic Biology, Biochemistry, and Pharmaceutical Sciences.
• Additional Detail: The researchers describe the strategic engineering process as analogous to "swapping interchangeable parts in a machine," emphasizing the high potential for modular manipulation in antibiotic development.

Breakthrough in RNA Research Could Lead to Treatment for Neuromuscular Disorders

Danith Ly said this discovery paves the way for developing highly selective, structure-based RNA therapies with fewer side effects and broader applications.
Photo Credit: Courtesy of Carnegie Mellon University

Scientific Frontline: Extended "At a Glance" Summary

The Core Concept: Researchers have developed precise synthetic molecules, likened to "pothole fillers," that neutralize the toxic RNA repeats responsible for genetic neuromuscular disorders like myotonic dystrophy type 1 (DM1).

Key Distinction/Mechanism: Unlike traditional antisense therapies that require unwinding complex RNA structures to work, these ligands utilize "Janus" (bifacial) bases that insert themselves directly between RNA strands. This allows the molecule to bind to both sides of the toxic "hairpin" structure simultaneously, displacing harmful proteins without disturbing healthy RNA functions.

Origin/History: Published on January 15, 2026, by a team led by Professor Danith Ly at Carnegie Mellon University, this breakthrough builds upon years of research into peptide nucleic acids (PNAs) supported by the DSF Charitable Foundation since 2014.

Chemists determine the structure of the fuzzy coat that surrounds Tau proteins

MIT chemists showed they can use nuclear magnetic resonance (NMR) to decipher the structure of the fuzzy coat that surrounds Tau proteins. The findings may aid efforts to develop drugs that interfere with Tau buildup in the brain.
Image Credit: Jose-Luis Olivares, MIT; figure courtesy of the researchers
(CC BY-NC-ND 4.0)

Scientific Frontline: "At a Glance" Summary

• Discovery: MIT chemists successfully determined the atomic-level structure of the intrinsically disordered "fuzzy coat" surrounding Tau protein fibrils, a region comprising approximately 80% of the protein that was previously uncharacterizable by standard imaging.
• Methodology: The team developed a novel nuclear magnetic resonance (NMR) technique to magnetize protons within the rigid protein core and measure the transfer time to mobile segments, allowing them to map the proximity and dynamic movement of the disordered layers.
• Structural Detail: The analysis revealed a "burrito-like" architecture where the fuzzy coat wraps in layers around a rigid beta-sheet inner core, rather than extending randomly into the surrounding environment.
• Mechanism: The coat exhibits three distinct zones of mobility: a rigid core, an intermediate layer, and a highly dynamic outer layer rich in positively charged proline residues that are electrostatically repelled by the positively charged core.
• Significance: This structural model suggests that normal Tau proteins likely accumulate at the ends of existing filaments to drive fibril growth, rather than piling onto the sides, offering a precise mechanism for how Alzheimer's tangles propagate.
• Implication: Future therapeutic strategies must account for this protective layering, as small-molecule drugs intended to disaggregate Tau fibrils will need to effectively penetrate the dense fuzzy coat to reach and disrupt the toxic core.

New study shows how the cell repairs its recycling stations

Leaks in the cell's lysosomes can be life-threatening. The discovery by researchers Yaowen Wu and Dale Corkery may help to understand and prevent diseases such as Alzheimer’s.
Photo Credit: Yue Li

When the cell’s recycling stations, the lysosomes, start leaking, it can become dangerous. Toxic waste risks spreading and damaging the cell. Now, researchers at Umeå University have revealed the molecular sensors that detect tiny holes in lysosomal membranes so they can be quickly repaired – a process crucial for preventing inflammation, cell death, and diseases such as Alzheimer’s. 

Lysosomes are the cell’s recycling stations, handling cellular waste and converting it into building blocks that can be reused. Lysosomal membranes are frequently exposed to stress from pathogens, proteins, and metabolic byproducts. Damage can lead to leakage of toxic contents into the cytoplasm, which in turn may cause inflammation and cell death. Until now, the mechanism by which cells detect these membrane injuries has remained unknown. 

The Mechanical Ratchet: A New Mechanism of Cell Division Uncovered

A zebrafish embryo during the first cell division cycle, with the structural protein actin labelled, which marks the cell boundary and ingressing furrow. The image shows a time course from dark orange (before ingression) to brighter orange and finally white as ingression proceeds.
Image Credit: © Alison Kickuth, Brugués Lab

Cell division is an essential process for all life on earth, yet the exact mechanisms by which cells divide during early embryonic development have remained elusive – particularly for egg-laying species. Scientists from the Brugués group at the Cluster of Excellence Physics of Life (PoL) at Dresden University of Technology have revealed a novel mechanism that explains how early embryonic cells may divide without forming a complete contractile ring, traditionally seen as essential for this process. The findings, published in Nature, challenge the long-standing textbook view of cell division, revealing how parts of the cytoskeleton, and material properties of the cell interior (or cytoplasm) cooperate to drive division through a ‘ratchet’ mechanism.     

Exposure to natural light improves metabolic health

The research team provides the first evidence of the beneficial impact of natural light on people with this condition.
Image Credit: © Loïc Metz, UNIGE AI generated

Metabolic diseases have reached epidemic proportions in our society, driven by a sedentary lifestyle coupled with circadian misalignment - a desynchrony between our intrinsic biological clocks and environmental signals. Furthermore, we spend almost 90% of our time indoors, with very limited exposure to natural daylight. To investigate the specific role of daylight in human metabolism, particularly in glycemic control, researchers from the University of Geneva (UNIGE), the University Hospitals of Geneva (HUG), Maastricht University, and the German Diabetes Center (DDZ) conducted a controlled study with thirteen volunteers with type 2 diabetes. When exposed to natural light, participants exhibited more stable blood glucose levels and an overall improvement in their metabolic profile. These results, published in the journal Cell Metabolism, provide the first evidence of the beneficial impact of natural light on people with type 2 diabetes. 

Capturing the moment a cell shuts the door on free radicals

The moment a cell shuts the door on free radicals.
Illustration Credit: Catrin Jakobsson, Lund University

For the first time, researchers have been able to show how a cell closes the door to free radicals – small oxygen molecules that are sometimes needed, but that can also damage our cells. The study is published in Nature Communications and was led by Lund University. 

For our cells to function, they need to maintain a careful balance between beneficial and harmful oxygen molecules known as free radicals. One of the most important is hydrogen peroxide – the same substance found in disinfectants, but which our cells use in very small amounts to send important signals. However, in excessive concentrations, hydrogen peroxide can cause damage and even cell death.  

Researchers identify kidney sensor that helps control fluid balance

Rose Hill, Ph.D., second from left,studies sensory nerves within the kidneys at OHSU. Her new study identified a protein that acts as a pressure sensor in the kidneys, which helps the body control fluids and blood pressure. With her are lab team members: Taylor Krilanovich, Lily Schainker and Janelle Doyle.
 Photo Credit: OHSU/Christine Torres Hicks

A new study has identified a critical “pressure sensor” inside the kidney that helps the body control blood pressure and fluid levels. The finding helps explain how the kidneys sense changes in blood volume — something scientists for decades have known occurs but didn’t have a mechanistic explanation.

Researchers at Oregon Health & Science University and collaborating institutions discovered that a protein called PIEZO2 acts as a mechanical sensor in the kidney. When blood volume changes, this protein helps trigger the release of renin, a hormone that starts a chain reaction known as the renin-angiotensin-aldosterone system, or RAAS. The system is one of the body’s main tools for keeping blood pressure stable and making sure the body has the right balance of salt and water.

Nasal drops fight brain tumors noninvasively

Researchers at WashU Medicine have developed a noninvasive medicine delivered through the nose that successfully eliminated deadly brain tumors in mice. The medicine is based on a spherical nucleic acid, a nanomaterial (labeled red) that travels along a nerve (green) from the nose to the brain, where it triggers an immune response to eliminate the tumor.
Image Credit: Courtesy of Alexander Stegh

Researchers at Washington University School of Medicine in St. Louis, along with collaborators at Northwestern University, have developed a noninvasive approach to treat one of the most aggressive and deadly brain cancers. Their technology uses precisely engineered structures assembled from nano-size materials to deliver potent tumor-fighting medicine to the brain through nasal drops. The novel delivery method is less invasive than similar treatments in development and was shown in mice to effectively treat glioblastoma by boosting the brain’s immune response.

Glioblastoma tumors form from brain cells called astrocytes and are the most common kind of brain cancer, affecting roughly three in 100,000 people in the U.S. Glioblastoma generally progresses very quickly and is almost always fatal. There are no curative treatments for the disease, in part because delivering medicines to the brain remains extremely challenging.

What Is: Mitochondrion

Evolutionary Singularities and the Eukaryotic Dawn

The mitochondrion represents a biological singularity, a discrete evolutionary event that fundamentally partitioned life on Earth into two distinct energetic stratums: the prokaryotic and the eukaryotic. While colloquially reduced to the moniker of "cellular powerhouse," the mitochondrion is, in functional reality, a highly integrated endosymbiont that serves as the master regulator of eukaryotic physiology. It is the nexus of cellular respiration, the arbiter of programmed cell death, a buffer for intracellular calcium, and a hub for biosynthetic pathways ranging from heme synthesis to steroidogenesis. To comprehend the complexity of multicellular life, one must first dissect the intricate molecular sociology of this organelle.   

The origin of the mitochondrion is the subject of intense phylogenomic reconstruction. The prevailing consensus, the endosymbiotic theory, posits that the mitochondrion descends from a free-living bacterial ancestor—specifically a lineage within the Alphaproteobacteria—that entered into a symbiotic relationship with a host archaeal cell approximately 1.5 to 2 billion years ago. This was not a trivial acquisition but a transformative merger. The energetic capacity afforded by the internalization of a bioenergetic specialist allowed the host cell to escape the surface-area-to-volume constraints that limit prokaryotic genome size, facilitating the expansion of the nuclear genome and the development of complex intracellular compartmentalization. 

New type of DNA damage found in our cells’ powerhouses

Linlin Zhao (left) and Yu Hsuan Chen
Photo Credit: Courtesy of University of California, Riverside

A previously unknown type of DNA damage in the mitochondria, the tiny power plants inside our cells, could shed light on how our bodies sense and respond to stress. The findings of the UC Riverside-led study are published in the Proceedings of the National Academy of Sciences and have potential implications for a range of mitochondrial dysfunction-associated diseases, including cancer and diabetes. 

Mitochondria have their own genetic material, known as mitochondrial DNA (mtDNA), which is essential for producing the energy that powers our bodies and sending signals within and outside cells. While it has long been known that mtDNA is prone to damage, scientists didn't fully understand the biological processes. The new research identifies a culprit: glutathionylated DNA (GSH-DNA) adducts.

An adduct is bulky chemical tag formed when a chemical, such as a carcinogen, attaches directly to DNA. If the damage isn’t repaired, it can lead to DNA mutations and increase the risk of disease.

Scientists observe metabolic activity of individual lipid droplets in real time

LipiPB Red shows longer fluorescence lifetimes in stable lipid droplets (red) and shorter lifetimes as they undergo degradation (blue). This probe revealed that lipid droplets sequentially degrade, where lipolysis precedes lipophagy.
Image Credit: Issey Takahashi, Nagoya University

A research team has developed a fluorescent probe that allows scientists to visualize how individual lipid droplets break down inside living cells in real time. The probe changes its fluorescence properties depending on the chemical composition of each droplet, which allows researchers to observe not only their location within cells, but also their metabolic activity during lipid breakdown. The findings, published in the Journal of the American Chemical Society, may contribute to the development of new strategies to treat metabolic diseases such as obesity and diabetes, as well as cancers associated with abnormal lipid metabolism. 

“Lipid droplets are cellular organelles that not only store excess lipids but also play critical roles in lipid metabolism. However, understanding how individual droplets function has been challenging,” Professor Shigehiro Yamaguchi, from the Institute of Transformative Bio-Molecules (ITbM) at Nagoya University, explained. 

A cellular protein, FGD3, boosts breast cancer chemotherapy, immunotherapy

The research team included, front row, from left: graduate student Junyao Zhu, biochemistry professor David Shapiro, and senior researcher Chengiian Mao; back row, from left: graduate students Abigail Spaulding, Xinyi Dai and Qianjin Jiang.
Photo Credit: Fred Zwicky

A naturally occurring protein that tends to be expressed at higher levels in breast cancer cells boosts the effectiveness of some anticancer agents, including doxorubicin, one of the most widely used chemotherapies, and a preclinical drug known as ErSO, researchers report. The protein, FGD3, contributes to the rupture of cancer cells disrupted by these drugs, boosting their effectiveness and enhancing anticancer immunotherapies.

The new findings were the happy result of experiments involving ErSO, an experimental drug that killed 95-100% of estrogen-receptor-positive breast cancer cells in a mouse model of the disease. ErSO upregulates a cellular pathway that normally protects cancer cells from stress, said University of Illinois Urbana-Champaign biochemistry professor David Shapiro, who led the new work with Illinois graduate student Junyao Zhu. But when that protective pathway is ramped up, the system goes awry.