In creating a pair of new robots, Cornell University researchers cultivated an unlikely component, one found on the forest floor: fungal mycelia. By harnessing mycelia’s innate electrical signals, the researchers discovered a new way of controlling “biohybrid” robots that can potentially react to their environment better than their purely synthetic counterparts.

The team’s paper published in Science Robotics. The lead author is Anand Mishra, a research associate in the Organic Robotics Lab led by Rob Shepherd, professor of mechanical and aerospace engineering at Cornell University, and the paper’s senior author.

“This paper is the first of many that will use the fungal kingdom to provide environmental sensing and command signals to robots to improve their levels of autonomy,” Shepherd said. “By growing mycelium into the electronics of a robot, we were able to allow the biohybrid machine to sense and respond to the environment. In this case we used light as the input, but in the future it will be chemical. The potential for future robots could be to sense soil chemistry in row crops and decide when to add more fertilizer, for example, perhaps mitigating downstream effects of agriculture like harmful algal blooms.”

Mycelia are the underground vegetative part of mushrooms. They have the ability to sense chemical and biological signals and respond to multiple inputs.

“Living systems respond to touch, they respond to light, they respond to heat, they respond to even some unknowns, like signals,” Mishra said. “If you wanted to build future robots, how can they work in an unexpected environment? We can leverage these living systems, and any unknown input comes in, the robot will respond to that.”

Two biohybrid robots were built: a soft robot shaped like a spider and a wheeled bot.

The robots completed three experiments. In the first, the robots walked and rolled, respectively, as a response to the natural continuous spikes in the mycelia’s signal. Then the researchers stimulated the robots with ultraviolet light, which caused them to change their gaits, demonstrating mycelia’s ability to react to their environment. In the third scenario, the researchers were able to override the mycelia’s native signal entirely.

The research was supported by the National Science Foundation (NSF) CROPPS Science and Technology Center; the U.S. Department of Agriculture’s National Institute of Food and Agriculture; and the NSF Signal in Soil program.

In a study published on July 31 in the journal Earth’s Future, scientists, including researchers at the University of Colorado Boulder, revealed how heat waves, especially those occurring in Antarctica’s cold seasons, may impact the animals living there. The research illustrates how extreme weather events intensified by climate change could have profound implications for the continent’s fragile ecosystems.

In March 2022, the most intense heat wave ever recorded on Earth hit Antarctica, just as organisms in the southern region braced themselves for the long, harsh winter ahead. The extreme weather raised temperatures in parts of Antarctica to more than 70°F above average, melting glaciers and snow even in the McMurdo Dry Valleys, one of the planet’s coldest and driest regions.

As part of a Long-Term Ecological Research (LTER) project in Antarctica, the research team found that the unexpected melt followed by a rapid refreeze likely disrupted the life cycles of many organisms and killed a large swath of some invertebrates in the McMurdo Dry Valleys.

“It’s important that we pay attention to these signals, even if they’re coming from microscopic organisms in soils in a polar desert,” said Michael Gooseff, the paper’s senior author and professor in the Department of Civil, Environment and Architectural Engineering at CU Boulder. “They’re the early responders to changes that could cascade up to larger organisms, the landscape and even us, far away from Antarctica.”

When Gooseff arrived in Antarctica in November 2021, the continent looked much like it had for the past two decades. As a fellow of the Institute of Arctic and Alpine Research (INSTAAR), Gooseff has led the LTER at the McMurdo Dry Valleys, a National Science Foundation-funded project, for the past decade. Nearly every Antarctic summer, he travels to the southern region to study its ecosystem and how organisms survive in extreme environmental conditions.

While most animals can’t tolerate the region’s dryness and cold, some microbes and invertebrates, including roundworms and water bears, thrive in this frozen desert. Water bears, or tardigrades, are tiny, eight-legged animals measuring 0.002 to 0.05 inches long. They can survive extreme conditions — as cold as -328°F and as hot as 300 °F — that would kill most other forms of life.

In 2022, all members of the polar expedition team left the continent in February, before the Antarctic summer ended. A month later, Antarctica experienced the most extreme heat wave on record, driven by an intense storm known as an atmospheric river, which transported moist air over long distances to the polar region.

The team’s sensors in the McMurdo Dry Valleys recorded air temperatures, which typically hover around -4°F in March, rising above freezing and exceeding the average by 45°F.

Satellite imagery and stream discharge measurements showed that the sudden warming wetted the valleys’ soil more than two months after the peak summer thaw, at a time when the land is typically dry.

In two days, after the heat wave passed, temperatures plummeted and the soil froze. This event happened during a critical transition period, when organisms hunker down and get ready for the dark, cold winter. Gooseff and his colleagues were curious about how animals in the valleys responded.

“These animals invest a significant amount of energy in preparing and shutting down for the winter,” said Gooseff. “When things start to warm up the following summer, they use energy to become active again. One of our major concerns with unusual weather events like this heat wave is that these animals might start using a lot more energy, thinking it’s summer, only to have to shut down again two days later. How many times can they go through that cycle before they exhaust their energy reserves?”

He and the team returned to Antarctica the following summer, in December 2022. They sampled the soil and compared organisms living in areas that became wet to those that stayed dry during the heat wave.

They observed a 50% decrease in the population of Scottnema, a common roundworm, in areas that got wet. Scottnema is adapted to extremely cold and dry climates.

“The heat wave made the environment appear warm enough for things to get wet, creating a false start to summer. Some of the biology responding to these temperatures might be seriously disrupted by this,” Gooseff said.

Rapid swings between extremes in weather can disproportionately impact sensitive species like Scottnema, but they may have far less impact on other animals, such as tardigrades. These creatures have a higher tolerance for moisture, allowing them to proliferate as the environment becomes wetter.

“Changes in which species are in the soil and how big the populations are can have a major impact on the ecosystem’s food web and nutrient cycling,” Gooseff said.

Previous research has shown Scottnema is responsible for about 10% of the carbon processed in the Dry Valleys’ soil ecosystem.

As climate change exacerbates extreme weather events in Antarctica, larger species are also being impacted. For example, in the summer of 2013, an unusual rainfall event along the Adélie Coast of East Antarctica killed all Adélie penguin chicks in the region. In July, temperatures in parts of East Antarctica climbed up to 50 °F above the usual winter average.

Gooseff and his team plan to continue documenting extreme weather events and their impacts on the Antarctic ecosystem.

What happens in Antarctica doesn’t stay in Antarctica, Gooseff said.

“The loss of ice shelves has pretty dramatic impacts on the mass balance of our oceans, and it affects us even thousands of miles away.”

“We know of only three or four occurrences of similar gravitational lens configurations in the observable universe, which makes this find exciting, as it demonstrates the power of Webb and suggests maybe now we will find more of these,” said astronomer Guillaume Desprez of Saint Mary’s University in Halifax, Nova Scotia, a member of the team presenting the Webb results.

While this region has been observed previously with NASA’s Hubble Space Telescope, the dusty red galaxy that forms the intriguing question-mark shape only came into view with Webb. This is a result of the wavelengths of light that Hubble detects getting trapped in cosmic dust, while longer wavelengths of infrared light are able to pass through and be detected by Webb’s instruments.

Astronomers used both telescopes to observe the galaxy cluster MACS-J0417.5-1154, which acts like a magnifying glass because the cluster is so massive it warps the fabric of space-time. This allows astronomers to see enhanced detail in much more distant galaxies behind the cluster. However, the same gravitational effects that magnify the galaxies also cause distortion, resulting in galaxies that appear smeared across the sky in arcs and even appear multiple times. These optical illusions in space are called gravitational lensing.

The red galaxy revealed by Webb, along with a spiral galaxy it is interacting with that was previously detected by Hubble, are being magnified and distorted in an unusual way, which requires a particular, rare alignment between the distant galaxies, the lens, and the observer — something astronomers call a hyperbolic umbilic gravitational lens. This accounts for the five images of the galaxy pair seen in Webb’s image, four of which trace the top of the question mark. The dot of the question mark is an unrelated galaxy that happens to be in the right place and space-time, from our perspective.

In addition to producing a case study of the Webb NIRISS (Near-Infrared Imager and Slitless Spectrograph) instrument’s ability to detect star formation locations within a galaxy billions of light-years away, the research team also couldn’t resist highlighting the question mark shape. “This is just cool looking. Amazing images like this are why I got into astronomy when I was young,” said astronomer Marcin Sawicki of Saint Mary’s University, one of the lead researchers on the team.

“Knowing when, where, and how star formation occurs within galaxies is crucial to understanding how galaxies have evolved over the history of the universe,” said astronomer Vicente Estrada-Carpenter of Saint Mary’s University, who used both Hubble’s ultraviolet and Webb’s infrared data to show where new stars are forming in the galaxies. The results show that star formation is widespread in both. The spectral data also confirmed that the newfound dusty galaxy is located at the same distance as the face-on spiral galaxy, and they are likely beginning to interact.

“Both galaxies in the Question Mark Pair show active star formation in several compact regions, likely a result of gas from the two galaxies colliding,” said Estrada-Carpenter. “However, neither galaxy’s shape appears too disrupted, so we are probably seeing the beginning of their interaction with each other.”

“These galaxies, seen billions of years ago when star formation was at its peak, are similar to the mass that the Milky Way galaxy would have been at that time. Webb is allowing us to study what the teenage years of our own galaxy would have been like,” said Sawicki.

The Webb images and spectra in this research came from the Canadian NIRISS Unbiased Cluster Survey (CANUCS). The research paper is published in the Monthly Notices of the Royal Astronomical Society.

While there is substantial research into developing interventions to repair injured tissue, scientists at Washington University School of Medicine in St. Louis focused instead on developing, in mice, an immunotherapy to minimize the damage from traumatic spinal cord injury. Their findings show that immunotherapy can lessen such damage by protecting neurons at the injury site from being attacked by immune cells.

The study, published Sept. 4 in Nature, demonstrates success in mice given the immunotherapy and presents a novel approach with potential to help improve outcomes for people recovering from spinal cord injuries.

“Immune cells in the central nervous system have a reputation for being the bad guys that can harm the brain and spinal cord,” said senior author Jonathan Kipnis, PhD, the Alan A. and Edith L. Wolff Distinguished Professor of Pathology & Immunology and a BJC Investigator at WashU Medicine. “But our study shows that it’s possible to take advantage of immune cells’ neuroprotective function, while controlling their inherent detrimental abilities, to help in the recovery from central nervous system injury.”

Shortly after injury to the nervous system, immune cells flood the site. Among them is a mixture of activated T cells — a subset of immune cells — that either harm or protect the surrounding neurons. Wenqing Gao, PhD, a postdoctoral research associate in the Department of Pathology & Immunology and the study’s first author, analyzed T cells from the spinal cords of injured mice and performed a genetic analysis to decode their identities. Her goal was to separate the harmful from the protective T cells and create numerous copies of the beneficial cells with which to treat the injured mice.

But there was a catch, she found. The protective T cells that swoop into the injury site can mistakenly attack the body’s surrounding tissues when activated for too long, causing autoimmune disease. To improve the therapy’s safety, Gao modified the cells to shut off after a few days.

Mice given the modified T cells had better mobility than did the untreated mice. The researchers saw the biggest improvements when the mice were infused with T cells within a week of the injury. None of the mice receiving immunotherapy developed a destructive autoimmune reaction.

“There are no effective treatments for traumatic injuries to the central nervous system,” explained Gao. “We developed immunotherapy for such injuries by taking advantage of the protective immune cells that infiltrate the injury site and found that it dramatically improved mobility in mice.”

In collaboration with WashU Medicine’s Wilson Zachary Ray, MD, a spinal cord surgeon and the Henry G. & Edith R. Schwartz Professor of Neurosurgery, the researchers also looked every day for a week for T cells in the cerebral spinal fluid of patients with spinal cord injuries. They found a significant expansion of the T cells, confirming the feasibility of expanding protective T cells from such patients to generate the immunotherapy.

“Our future goal is to devise a clinical trial to test the therapy in people with such injuries, while expanding this work to neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) as well as Alzheimer’s and Parkinson’s diseases,” Gao said.

Added Kipnis: “Although the initial trigger in neurodegenerative diseases is different, the subsequent death of neurons may very well be mediated by similar processes, opening an opportunity for adapting our engineered cells for use as a therapy in neurodegeneration.”

This work was supported by the BJC Investigators Program at WashU.

A new study from MIT offers an explanation for how collagen can survive for so much longer than expected. The research team found that a special atomic-level interaction defends collagen from attack by water molecules. This barricade prevents water from breaking the peptide bonds through a process called hydrolysis.

“We provide evidence that that interaction prevents water from attacking the peptide bonds and cleaving them. That just flies in the face of what happens with a normal peptide bond, which has a half-life of only 500 years,” says Ron Raines, the Firmenich Professor of Chemistry at MIT.

Raines is the senior author of the new study, which will appear in ACS Central Science. MIT postdoc Jinyi Yang PhD ’24 is the lead author of the paper. MIT postdoc Volga Kojasoy and graduate student Gerard Porter are also authors of the study.

Water-resistant

Collagen is the most abundant protein in animals, and it is found in not only bones but also skin, muscles, and ligaments. It’s made from long strands of protein that intertwine to form a tough triple helix.

“Collagen is the scaffold that holds us together,” Raines says. “What makes the collagen protein so stable, and such a good choice for this scaffold, is that unlike most proteins, it’s fibrous.”

In the past decade, paleobiologists have found evidence of collagen preserved in dinosaur fossils, including an 80-million-year-old Tyrannosaurus rex fossil, and a sauropodomorph fossil that is nearly 200 million years old.

Over the past 25 years, Raines’ lab has been studying collagen and how its structure enables its function. In the new study, they revealed why the peptide bonds that hold collagen together are so resistant to being broken down by water.

Peptide bonds are formed between a carbon atom from one amino acid and a nitrogen atom of the adjacent amino acid. The carbon atom also forms a double bond with an oxygen atom, forming a molecular structure called a carbonyl group. This carbonyl oxygen has a pair of electrons that don’t form bonds with any other atoms. Those electrons, the researchers found, can be shared with the carbonyl group of a neighboring peptide bond.

Because this pair of electrons is being inserted into those peptide bonds, water molecules can’t also get into the structure to disrupt the bond.

To demonstrate this, Raines and his colleagues created two interconverting mimics of collagen — the one that usually forms a triple helix, which is known as trans, and another in which the angles of the peptide bonds are rotated into a different form, known as cis. They found that the trans form of collagen did not allow water to attack and hydrolyze the bond. In the cis form, water got in and the bonds were broken.

“A peptide bond is either cis or trans, and we can change the cis to trans ratio. By doing that, we can mimic the natural state of collagen or create an unprotected peptide bond. And we saw that when it was unprotected, it was not long for the world,” Raines says.

“No weak link”

This sharing of electrons has also been seen in protein structures known as alpha helices, which are found in many proteins. These helices may also be protected from water, but the helices are always connected by protein sequences that are more exposed, which are still susceptible to hydrolysis.

“Collagen is all triple helices, from one end to the other,” Raines says. “There’s no weak link, and that’s why I think it has survived.”

Previously, some scientists have suggested other explanations for why collagen might be preserved for millions of years, including the possibility that the bones were so dehydrated that no water could reach the peptide bonds.

“I can’t discount the contributions from other factors, but 200 million years is a long time, and I think you need something at the molecular level, at the atomic level in order to explain it,” Raines says.

The research was funded by the National Institutes of Health and the National Science Foundation.

Many different types of cells work together in the brain. In humans, nerve cells (neurons) make up less than half of the cells. The rest are called “glia.” The most common glial cells are astrocytes. They supply the neurons with nutrients, form part of the blood-brain barrier, regulate the synapses and support the immune cells.

However, a small proportion of astrocytes are able to produce nerve cells and other types of brain cells. These special astrocytes are therefore also known as brain stem cells. Brain stem cells and ordinary astrocytes hardly differ in their gene expression, i.e. in the activity of their genes. “How they can perform such different functions and what makes up the stem cell properties was previously completely unclear,” explains Ana Martin-Villalba, stem cell researcher at the DKFZ.

Methylation is the key

To solve this puzzle, the teams led by Martin-Villalba and Simon Anders (University of Heidelberg) isolated both ordinary astrocytes and brain stem cells from one of the regions of the brain where young neurons still develop in adult mice, the “ventricular-subventricular zone” (vSVZ). The researchers analyzed gene expression at the level of individual cells using mRNA sequencing as well as the patterns of methylation (“methylome”) in the entire genome. They used a specially developed tool to analyze the methylation data*.

DNA methylation refers to chemical “markers” with which the cell can switch off unused parts of its DNA. Methylation is therefore crucial for the identity of the cells.

During this study, the stem cell experts noticed that brain stem cells have a special DNA methylation pattern that distinguishes them from other astrocytes. “Unlike normal astrocytes, certain genes are demethylated in brain stem cells that are otherwise only used by nerve precursor cells. This allows the brain stem cells to activate these genes in order to produce nerve cells themselves,” explains Lukas Kremer, first author of the current publication. Co-first author Santiago Cerrizuela adds: “This pathway is denied to ordinary astrocytes, as the required genes are blocked by DNA methylation.”

Lack of blood supply triggers reprogramming of astrocytes to stem cells and increases new nerve formation

Could methylation also be used to convert astrocytes into brain stem cells in other regions of the brain, outside the vSVZ? “This would be an important step for regenerative medicine to repair damaged areas of the brain,” says Ana Martin-Villalba.

Earlier studies had already shown that a lack of blood supply, such as occurs in brain injuries or stroke, increases the number of newborn nerve cells. Do altered methylation profiles play a role in this process?

To investigate this, the researchers interrupted the blood supply to the brain of mice for a short time. As a result, astrocytes with the typical stem cell methylation profile could be detected even outside the vSVZ, as well as an increased number of nerve progenitor cells.

“Our theory is that normal astrocytes in the healthy brain do not form nerve cells because their methylation pattern prevents them from doing so,” explains study head Martin-Villalba. “Techniques to specifically alter the methylation profile could represent a new therapeutic approach to generate new neurons and treat nerve diseases.”

“The lack of blood supply apparently causes astrocytes in certain areas of the brain to redistribute the methyl marks on their DNA in such a way that their stem cell program becomes accessible. The reprogrammed cells then begin to divide and form precursors for new neurons,” summarizes Simon Anders and adds: “If we understand these processes better, we may be able to specifically stimulate the formation of new neurons in the future. For example, after a stroke, we could strengthen the brain’s self-healing powers, so that the damage can be repaired.”

Why studies on mice are necessary for this research

Strokes or accidents can lead to damage to the brain that is generally irreparable at present and often has dramatic consequences for those affected. As of today, there is no way to replace lost nerve cells. The aim of this work is to find ways to stimulate the regeneration of nerves in the adult brain.

This requires a profound understanding of how and under what circumstances brain stem cells can be induced to provide a supply of young nerve cells. To do this, the researchers need to study developmental processes that only take place in the brains of highly developed mammals. Epigenetic reprogramming cannot be observed in living animals using imaging techniques, but requires studies at the level of individual cells. The investigations cannot be carried out on cells from the culture dish, as the methylation profile of the astrocytes changes as soon as they are taken into culture, so that the epigenetic reprogramming can no longer be traced.