Starving bacteria (cyan) use a microscopic harpoon—called the Type VI secretion system—to stab and kill neighboring cells (magenta). The prey burst, turning spherical and leaking nutrients, which the killers then use to survive and grow. (Image Credit: Glen D'Souza/ASU/Screen shot from video)NewsletterSign up for our email newsletter for the latest science newsBacteria are bad neighbors. And we’re not talking noisy, never-take-out-the-trash bad neighbors. We’re talking has-a-harpoon-gun-and-points-it-at-you bad neighbors. According to a new study in Science, some bacteria hunt nearby bacterial species when they’re hungry. Using a special weapon system called the Type VI Secretion System (T6SS), these bacteria shoot, spill, and then absorb the nutrients from the microbes they harpoon. “The punchline is: When things get tough, you eat your neighbors,” said Glen D’Souza, a study author and an assistant professor at Arizona State University, according to a press release. “We’ve known bacteria kill each other, that’s textbook. But what we’re seeing is that it’s not just important that the bacteria have weapons to kill, but they are controlling when they use those weapons specifically for situations to eat others where they can’t grow themselves.” According to the study authors, the research doesn’t just have implications for bacterial neighborhoods; it also has implications for human health and medicine. By harnessing these bacterial weapons, it may be possible to build better targeted antibiotics, designed to overcome antibiotic resistance. Ruthless Bacteria Use HarpoonsResearchers have long known that some bacteria can be ruthless, using weapons like the T6SS to clear out their competition. A nasty tool, the T6SS is essentially a tiny harpoon gun with a poison-tipped needle. When a bacterium shoots the weapon into another bacterium from a separate species, the needle pierces the microbe without killing it. Then, it injects toxins into the microbe that cause its internal nutrients to spill out.Up until now, researchers thought that this weapon helped bacteria eliminate their competition for space and for food, but after watching bacteria use the T6SS to attack their neighbors when food was scarce, the study authors concluded that these tiny harpooners use the weapon not only to remove rivals, but also to consume their competitors’ leaked nutrients.“Watching these cells in action really drives home how resourceful bacteria can be,” said Astrid Stubbusch, another study author and a researcher who worked on the study while at ETH Zurich, according to the press release. “By slowly releasing nutrients from their neighbors, they maximize their nutrient harvesting when every molecule counts.” Absorbing Food From NeighborsTo show that the bacteria used this system to eat when there was no food around, the study authors compared their attacks in both nutrient-rich and nutrient-poor environments. When supplied with ample resources, the bacteria used their harpoons to kill their neighbors quickly, with the released nutrients leaking out and dissolving immediately. But when resources were few and far between, they used their harpoons to kill their neighbors slowly, with the nutrients seeping out and sticking around. “This difference in dissolution time could mean that the killer cells load their spears with different toxins,” D’Souza said in another press release. While one toxin could eliminate the competition for space and for food when nutrients are available, another could create a food source, allowing bacteria to “absorb as many nutrients as possible” when sustenance is in short supply.Because of all this, this weapon system is more than ruthless; it’s also smart, and important to some species’ survival. When genetically unedited T6SS bacteria were put in an environment without food, they survived on spilled nutrients. But when genetically edited T6SS bacteria were placed in a similar environment, they died, because their ability to find food in their neighbors had been “turned off.”Harnessing Bacterial HarpoonsAccording to the study authors, the T6SS system is widely used by bacteria, both in and outside the lab. “It’s present in many different environments,” D’Souza said in one of the press releases. “It’s operational and happening in nature, from the oceans to the human gut.” The study authors add that their research could change the way we think about bacteria and could help in our fight against antibiotic resistance. In fact, the T6SS could one day serve as a foundation for targeted drug delivery systems, which could mitigate the development of broader bacterial resistance to antibiotics. But before that can happen, however, researchers have to learn more about bacterial harpoons, and about when and how bacteria use them, both to beat and eat their neighbors.Article SourcesOur writers at Discovermagazine.com use peer-reviewed studies and high-quality sources for our articles, and our editors review for scientific accuracy and editorial standards. Review the sources used below for this article:Sam Walters is a journalist covering archaeology, paleontology, ecology, and evolution for Discover, along with an assortment of other topics. Before joining the Discover team as an assistant editor in 2022, Sam studied journalism at Northwestern University in Evanston, Illinois.1 free article leftWant More? Get unlimited access for as low as $1.99/monthSubscribeAlready a subscriber?Register or Log In1 free articleSubscribeWant more?Keep reading for as low as $1.99!SubscribeAlready a subscriber?Register or Log In

Bacteria wouldn’t be so bad if we could tell them what to do. “Stop spreading! Stop sticking together! Stop fending off our antibiotics!” A new method is starting to allow scientists to do just that, letting them use light to control certain functions of bacteria. Introduced in a paper published in The European Physical Journal Plus, the preliminary approach could have several potential applications, including a possible avenue for combating antibiotic resistance.The Problem of Antibacterial Resistance Bacteria are behind a variety of diseases, from strep to staph to pneumonia and meningitis, and they attack our bodies in a variety of ways, as well, including through the production of toxins that damage and disrupt our cells. Some of these infections stop on their own, but others are too stubborn, or too serious, to leave untreated. These are the infections that we target with antibiotics — that is, as long as our antibiotics are working.But, because bacteria are constantly changing, they can develop defenses against the antibiotics that we use to stave them off, making these treatments much less effective. That’s the gist of the growing threat posed by antibiotic resistance, which has contributed to millions of deaths since 1990 and is anticipated to contribute to millions more by 2050. Setting out to find a new solution to this growing problem, scientists from the Italian Institute of Technology and the Polytechnic University of Milan embarked on the Engineering of Bacteria to See Light (EOS) project. The project aims to use light to control bacteria, primarily for the fight against antibiotic resistance. And the new method pushes the project closer to achieving that aim. Using light and light-sensitive molecules to adjust the electrical signals that are transmitted across the bacterial membrane, the method impacts the biological activity of bacteria without any alterations to their genetic makeup.“This interplay between light and electrical [signaling] allows us to control key biological processes such as movement, biofilm formation, and antibiotic sensitivity,” said Giuseppe Maria Paternò, a study author and a professor at the Polytechnic University of Milan, according to a press release. “We can influence antibiotic uptake and restore or even enhance the effectiveness of treatments against resistant strains.”Coating Bacteria to Curb Antibiotic ResistanceTo control bacteria, the method takes advantage of a light-sensitive molecule called Ziapin2, which sticks to the bacterial surface. By covering bacteria with this light-sensitive molecule and by subjecting the covered bacteria to light, the scientists were able to modify the electrical signals that were transmitted across their bacterial membranes, transforming the bacteria’s basic functioning. Testing their method on one of the most studied bacterial species, the scientists changed the electrical signaling across the membranes of Bacillus subtilis, a popular model organism that’s often used as a stand-in for Staphylococcus aureus, the bacterium that causes staphylococcus, or staph, infections.When tested, the method modulated the bacteria’s susceptibility to Kanamycin, an intracellular antibiotic that’s frequently used as a treatment for severe bacterial infections after other treatments fail. “Under blue light,” Paternò said in the release, “the effectiveness of Kanamycin was significantly reduced,” indicating that the electrical signaling on the bacterial membrane “plays a crucial role in the drug’s uptake.”Additional research is required to tailor the method to increase the effectiveness of Kanamycin and other antibiotics against bacteria. But for now, it seems that such an outcome could be possible. “This initial assessment […] represents a first step in a completely new field of study,” the scientists state in their paper. “This proof-of-concept study underscores the potential of non-genetic, light-based interventions to modulate bacterial susceptibility in real time. Future work will expand this approach […] ultimately advancing our understanding of bacterial bioelectric regulation and its applications in antimicrobial therapies.”This article is not offering medical advice and should be used for informational purposes only.Article SourcesOur writers at Discovermagazine.com use peer-reviewed studies and high-quality sources for our articles, and our editors review for scientific accuracy and editorial standards. Review the sources used below for this article:The European Physical Journal Plus. Photocontrol of Bacterial Membrane Potential Regulates Antibiotic Persistence in B. SubtilisSam Walters is a journalist covering archaeology, paleontology, ecology, and evolution for Discover, along with an assortment of other topics. Before joining the Discover team as an assistant editor in 2022, Sam studied journalism at Northwestern University in Evanston, Illinois.

Great star corals in the grip of disease have been saved with probiotics — beneficial bacteria that attack or displace invading pathogens or possibly trigger immune responses to them. What’s causing this deadly disease remains unidentified. But researchers at the Smithsonian Marine Station in Fort Pierce, Fla., were able to successfully halt progression of the disease’s symptoms, the team reports June 5 in Frontiers in Marine Science. The condition is called stony coral tissue loss disease and is characterized by white lesions that lead to the loss of polyps — tiny soft-bodied organisms similar to sea anemones — blanketing coral. Eventually, nothing but the white coral skeleton is left behind. The disease emerged in Florida in 2014 and has spread rampantly throughout the Florida Keys and the Caribbean. A great star coral (M. cavernosa) colony is infected with stony coral tissue loss disease on the coral reef in Fort Lauderdale. The lesion, where the white band of tissue occurs, typically moves across the coral, killing coral tissue along the way. Kelly Pitts/Smithsonian Researchers suspect that the disease is bacterial in nature. Antibiotic treatments can offer a quick fix, but these drugs do not prevent reinfection and carry the risk of the mysterious pathogen building resistance against them. So, in late 2020, the Smithsonian group tried for a more sustainable solution, giving probiotics to 30 infected great star coral colonies. The helpful microbes came from corals tested in the lab that showed resistance to the disease. “We noticed that one of the coral fragments would not get infected … so one of the first things we did was try to culture the microbes that are on this coral,” says microbiologist Blake Ushijima, who developed the probiotic used in the team’s experiment. “These microbes produce antibacterial compounds … and one had a high level of activity against bacteria from diseased corals,” acting as a “pro” biotic, by somehow neutralizing pathogens. The identified microbe, a bacterium called McH1-7, became the active ingredient in a paste delivered by divers to several infected colonies. They covered these colonies with plastic bags to immerse them in the probiotic solution, injecting the paste into the bags using a syringe. They also applied the paste directly to other colonies, slathering lesions caused by the disease. A probiotic paste of McH1-7 is applied to the disease lesion of a great star coral (M. cavernosa) colony infected with stony coral tissue loss disease. The paste was then smoothed flat with a gloved hand so that all apparently infected tissue was covered by the lesion-specific treatment.Kelly Pitts/Smithsonian For two and a half years, the team monitored the corals’ health. The probiotics slowed or stopped the disease from spreading in all eight colonies treated inside bags. On average, the disease’s ugly advance was held to only 7 percent of tissue, compared with an aggressive 30 percent on untreated colonies. The paste put directly on the coral had no beneficial effect. The results are encouraging, but coauthor Valerie Paul cautions against declaring the probiotic a cure. She doubts the practicality of swimming around with heavily weighted plastic bags and putting them on corals. And, she points out, the study was limited to one species of coral, when the disease plagues over 30. Sponsor Message Still, Ushijima considers the study a proof of concept. “The idea of coral probiotics has been thrown around for decades, but no one has directly shown their effects on disease in the wild,” he says. “I think it’s very exciting because it’s actually opening the door to a new field.”

A Deadly Disease Is Eating Away at Caribbean Corals and Wreaking Havoc on Reefs. Could Probiotics Be the Solution? New research suggests the probiotic McH1-7 could help stop the spread of stony coral tissue loss disease among wild corals near Fort Lauderdale, Florida Scientists determined the most effective method of halting the disease was covering a coral colony with a weighted plastic bag, then injecting a seawater solution that contains the probiotic. They left the colony covered for two hours to allow the probiotic bacteria to colonize the coral. Hunter Noren Probiotics can be good for human health. Now, new research suggests they might also help protect coral reefs. A bacterial probiotic helped slow the advance of stony coral tissue loss disease—a fast-spreading and deadly condition—among wild corals in Florida, researchers report today in a new study published in the journal Frontiers in Marine Science. The probiotic may be a good alternative to antibiotics like amoxicillin, which temporarily curb the spread of the disease but must be reapplied frequently. In addition, scientists fear stony coral tissue loss disease may one day become resistant to these antibiotic treatments—just as “superbugs” that infect humans are building resistance to our own drugs. Antibiotics are meant to kill microorganisms, but probiotics are beneficial living microbes. The idea is that a probiotic can be incorporated into corals’ natural microbiomes, ideally offering them longer-lasting protection. First discovered in Florida in 2014, stony coral tissue loss disease attacks the soft tissue of more than 30 different species of coral. Without treatment, the disease eventually kills the corals, and their soft tissue falls off, revealing the white calcium carbonate skeleton below. In just weeks or months, it can devastate a whole colony. Stony coral tissue loss disease can be spread by fish that eat coral, as well as by boaters and divers who do not disinfect their gear. The condition has since expanded its range beyond Florida to reefs throughout the Caribbean. Several years ago, researchers looking at the great star coral (Montastraea cavernosa) discovered a probiotic called Pseudoalteromonas sp. strain McH1-7. Laboratory tests showed McH1-7 stopped or slowed the progression of stony coral tissue loss disease in infected corals. It also helped prevent the disease from spreading to healthy corals. But that was in the lab. Would McH1-7 be similarly effective in the ocean? Researchers were eager to find out, so they set up an experiment on a shallow reef off the coast of Fort Lauderdale. Study co-author Kelly Pitts, a research technician with the Smithsonian Marine Station, applies a paste containing the probiotic directly onto the disease lesion of an infected coral. Hunter Noren Experimenting with wild corals For the study, the scientists focused on 40 great star coral colonies that were showing symptoms of stony coral tissue loss disease. In one experimental condition, the researchers made a paste that contained McH1-7 and applied it directly onto the disease lesions. For comparison, they also applied the same paste, minus the probiotic, to some corals. In another condition, they covered infected coral colonies with weighted plastic bags, then filled the bags with seawater solutions made with and without McH1-7. They left the corals covered for two hours. “This created a little mini-aquarium that kept the probiotics around each coral colony,” says study co-author Valerie Paul, head scientist at the Smithsonian Marine Station at Fort Pierce, Florida, in a statement. The scientists completed all the treatments within the first 4.5 months of the project. Then, they returned periodically to gather tissue and mucus samples from the corals to measure changes to their microbiomes. Over the next 2.5 years, they took photos from a variety of different angles, which they then used to create 3D models that could track the disease’s progression. In the end, the results suggest covering the corals with plastic bags filled with the probiotic seawater solution was the most effective method. More than two years post-treatment, the colonies that received the probiotic bag had lost just 7 percent of their tissue, while colonies in the control bag condition faced 35 percent tissue loss. Scientists applied a probiotic paste directly to disease lesions on some corals. Kelly Pitts The probiotic paste, by contrast, appears to have made the situation worse: The corals that had the probiotic paste applied directly to their lesions lost more tissue than those treated with the control paste, which did not contain McH1-7. “We do not really know what is going on with the probiotic paste treatment,” Paul tells Smithsonian magazine in an email. But she has a few theories. It’s possible the high concentrations of McH1-7 contributed to localized hypoxia, or low-oxygen conditions that further harmed the already stressed corals, she says. Or, the probiotic could have changed the microbiome at the lesion site in some negative way. Another possibility is that McH1-7 produces antibiotics or other substances that were harmful at high concentrations. Amanda Alker, a marine microbiologist at the University of Rhode Island who was not involved with the study, wonders if this finding suggests McH1-7 is beneficial at specific dosages—a question future laboratory research might be able to answer, she tells Smithsonian magazine in an email. She’s also curious to know which specific molecular components of the probiotic are responsible for the increased tissue loss when applied as a paste. More broadly, Alker would like to see additional experiments validating the bag treatment method, but she says this “inventive” technique seems promising. “Their approach is a safer solution than antibiotic treatment methods that have been deployed to combat [stony coral tissue loss disease] in the field so far,” she says. “Further, this is a practical solution that could be implemented widely because it doesn’t require highly specialized equipment and has the ability to be used with any type of microbial solution.” Looking ahead to save reefs Probiotics are likely not a silver bullet for protecting corals. For one, researchers still don’t know exactly what causes stony coral tissue loss disease, which makes it difficult to determine how or why the probiotic works, Paul says. In addition, since the disease has spread to many different parts of the Caribbean, it might be challenging to use the bag treatment technique on all affected colonies. “We would need to develop better methods of deploying the probiotic through time release formulations or other ways to scale up treatments,” Paul says. “Right now, having divers swim around underwater with weighted bags is not a very scalable method.” The researchers have also conducted similar experiments on infected corals located farther south, in the Florida Keys. However, these tests have produced mixed results, probably because of regional differences in stony coral tissue loss disease. This is another hurdle scientists will likely need to overcome if they hope to expand the use of probiotics. “We probably need to develop different probiotics for different coral species and different regions of the Caribbean,” Paul says. Researchers returned to gather samples of tissues and mucus to see how the corals' microbiomes had changed. Hunter Noren Even so, scientists are heartened by the results of the experiments conducted near Fort Lauderdale. With more research, the findings suggest probiotics could be a promising tool for combatting the disease elsewhere. “Coral probiotics is a challenging field, because there are hundreds of different types of bacteria that associate with corals, and there are limitless experiments that need to be performed,” Amy Apprill, a marine chemist at Woods Hole Oceanographic Institution who was not involved with the research, tells Smithsonian magazine in an email. “These researchers made a major advance with their study by demonstrating the utility of whole colony treatment as well as the specific probiotic tested.” Apprill adds that, while antibiotics have been widely used to control stony coral tissue loss disease, scientists haven’t conducted much research to see how these treatments are affecting the plants and creatures that live nearby. “Using a naturally occurring bacterium for disease treatment may result in lessened impacts to other members of the coral reef ecosystem,” she says. Amid rising ocean temperatures, scientists expect to find even more diseased coral colonies in the future. Warmer waters may also allow other pathogens to thrive and proliferate. Against that backdrop, Apprill adds, probiotics and the different methods of applying them will be “major allies” in the fight to save coral reefs. Paul is also optimistic. Through research and field studies, she’s confident researchers will be able to develop interventions that can “help corals better survive changing environments and respond better to diseases and bleaching,” she says. Get the latest stories in your inbox every weekday.

Co-lead author Ravneet Sidhu examines an ancient human tooth at the McMaster Ancient DNA Centre. (Image Credit: McMaster University)NewsletterSign up for our email newsletter for the latest science newsA new study in Science suggests that changes in a gene in Yersinia pestis, the bacterium that causes plague, could’ve added to the length of two plague pandemics, including the pandemic that started with the “Black Death.” “Ours is one of the first research studies to directly examine changes in an ancient pathogen, one we still see today, in an attempt to understand what drives the virulence, persistence, and eventual extinction of pandemics,” said Hendrik Poinar, a study author and the director of the McMaster Ancient DNA Centre, according to a press release.The study suggests that less virulent plague bacteria could’ve caused longer plague pandemics — thanks to the fact that infected rodents lived (and spread plague) for longer periods of time before dying from their infections. Read More: Scientists Reveal the Black Death’s Origin StoryThe Three Plague PandemicsThe bacterium Y. pestis infects rodents and humans alike and has caused three main plague pandemics in humans, all of which continued for centuries after their initial outbreaks. The first began in the 500s; the second began in the 1300s; and the third started in the 1800s (and still continues in certain areas in Asia, Africa, and the Americas today). Although all three pandemics were devastating at their outset, the second pandemic was by far the most severe. The Black Death, its initial outburst, killed around 30 to 50 percent of the population of Europe between 1347 and 1352 and — to this day — represents the deadliest disease wave in recorded history.To learn more about how these plague pandemics changed over time, scientists at McMaster University in Canada and the Institut Pasteur in France turned to a Y. pestis virulence gene known as pla. This gene is repeated many times throughout the Y. pestis genome, and it allows the bacterium to spread undetected throughout the bodies of infected individuals. A Gene and the PlagueTo investigate this gene, the scientists studied historical strains of Y. pestis from human remains and found that the number of repetitions of pla decreased over the course of the first and second plague pandemics. Then, the scientists tested Y. pestis bacteria from the third pandemic, infecting mice with three strains that had reduced repetitions of pla. “These three samples enabled us to analyze the biological impact of these pla gene deletions,” said Javier Pizarro-Cerdá, another study author and the director of the Yersinia Research Unit at the Institut Pasteur, according to the release.The results revealed that pla depletion decreases the virulence and increases the length of plague infections in mice. According to the study authors, these changes could have caused rodents to live longer in the later stages of the first and second pandemics, allowing them to spread their infections for a longer period. “It’s important to remember that plague was an epidemic of rats, which were the drivers of epidemics and pandemics. Humans were accidental victims. ” Poinar added in another press release.The Continued Threat of Y. PestisThough the pla depletion occurred around 100 years after the first and second pandemics began, the scientists stress that both changes were random and unrelated.“Our research sheds light on an interesting pattern in the evolutionary history of the plague. However, it is important to note that the majority of strains which continue to circulate today in Africa, the Americas, and Asia are highly virulent strains,” said Ravneet Sidhu, another study author and a Ph.D. student at the McMaster Ancient DNA Centre.Though still a threat to current populations, Y. pestis infections are much more manageable now as a result of modern diagnostics and treatments.“Today, the plague is a rare disease, but one that remains a public health concern and serves as a model for gaining a broad understanding of how pandemics emerge and become extinct. This example illustrates the balance of virulence a pathogen can adopt in order to spread effectively,” Pizarro-Cerdá said in the press release.Article SourcesOur writers at Discovermagazine.com use peer-reviewed studies and high-quality sources for our articles, and our editors review for scientific accuracy and editorial standards. Review the sources used below for this article:Science. Sam Walters is a journalist covering archaeology, paleontology, ecology, and evolution for Discover, along with an assortment of other topics. Before joining the Discover team as an assistant editor in 2022, Sam studied journalism at Northwestern University in Evanston, Illinois.1 free article leftWant More? Get unlimited access for as low as $1.99/monthSubscribeAlready a subscriber?Register or Log In1 free articleSubscribeWant more?Keep reading for as low as $1.99!SubscribeAlready a subscriber?Register or Log In

Scientists have discovered a previously unknown bacterium aboard China's Tiangong space station. "It has been named Niallia tiangongensis, and it inhabited the cockpit controls on the station, living in microgravity conditions," reports Wired. From the report: According to China Central Television, the country's national broadcaster, taikonauts (Chinese astronauts) collected swab samples from the space station in May 2023, which were then frozen and sent back to Earth for study. The aim of this work was to investigate the behavior of microorganisms, gathered from a completely sealed environment with a human crew, during space travel, as part of the China Space Station Habitation Area Microbiome Program (CHAMP). A paper published in the Journal of Systematic and Evolutionary Microbiology describes how analysis of samples from the space station revealed this previously unseen bacterial species, which belongs to the genus Niallia. Genomic sequencing showed that its closest terrestrial relative is the bacterium Niallia circulans, although the Tiangong species has substantial genetic differences. [...] It is unclear whether the newly discovered microbe evolved on the space station or whether it is part of the vast sea of as yet unidentified microorganisms on Earth. To date, tens of thousands of bacterial species have been cataloged, although there are estimated to be billions more unclassified species on Earth. The discovery of Niallia tiangongensis will provide a better understanding of the microscopic hazards that the next generation of space travelers will face and help design sanitation protocols for extended missions. It is still too early to determine whether the space bacterium poses any danger to taikonauts aboard Tiangong, although it is known that its terrestrial relative, Niallia circulans, can cause sepsis, especially in immunocompromised people. Read more of this story at Slashdot.

In May 2023, Chinese astronauts swabbed several surfaces of their space station Tiangong (Mandarin for "Heavenly Place"), then sent the samples back to Earth for analysis. The results are now in: the sample contained one bacterium never before seen, according to a report in the International Journal of Systemic and Evolutionary Microbiology.New Bacteria in Space Station The samples were taken, according to the paper, to help keep astronauts healthy in subsequent missions. “Understanding the characteristics of microbes during long-term space missions is essential for safeguarding the health of astronauts and maintaining the functionality of spacecraft,” according to the paper.There are multiple plausible explanations for both the bacteria’s presence and novelty. It could have hitch-hiked with the astronauts and remained more or less the same (although thousands have been identified, there are potentially billions of unknown bacterium on our planet). It could have taken that same route, but mutated and evolved. Or it could be a strain only found in space.Bacteria Similarities and AbilitiesTo get a better picture of the possibilities, it might be best to parse the knowns from the unknowns. First, and perhaps most importantly, it is not completely novel. The bacteria shares enough genetic similarities (two significant stretches of DNA match or are conserved) with Niallia circulans for it to be considered the same genus. Therefore, the authors named it Niallia tiangongensis.Its general appearance also doesn’t appear to be completely out of this world. The paper described it as an “[…] aerobic, spore-forming, rod-shaped strain.”It does appear to have some interesting abilities, though. According to the paper, it shows “a unique ability to hydrolyse gelatin.” This means it can break down some compounds and add components of water to them, perhaps as a way to feed themselves in an environment with little available food.Adaptations to SpaceDifferences in two proteins that resemble those in its cousin hint that it has evolved enhanced abilities to protect itself from some conditions specific to space. Those include tools to create a biofilm it could perhaps hide beneath, and the means to repair damage from radiation, among other abilities.Its terrestrial cousin has one concerning ability. It can cause infection — even sepsis. Knowing whether N. tiangongensis can do the same, and if so, at what level, will likely be the subject of further investigation, since such understanding is a key part of the China Space Station Habitation Area Microbiome Program (CHAMP) that led to its collection, return, and analysis.Article SourcesOur writers at Discovermagazine.com use peer-reviewed studies and high-quality sources for our articles, and our editors review for scientific accuracy and editorial standards. Review the sources used below for this article:International Journal of Systemic and Evolutionary Microbiology. Niallia tiangongensis sp. nov., isolated from the China Space Station Before joining Discover Magazine, Paul Smaglik spent over 20 years as a science journalist, specializing in U.S. life science policy and global scientific career issues. He began his career in newspapers, but switched to scientific magazines. His work has appeared in publications including Science News, Science, Nature, and Scientific American.

May 20, 2025Could Mitochondria Be Rewriting the Rules of Biology?New discoveries about mitochondria could reshape how we understand the body’s response to stress, aging, and illness. Scientific AmericanSUBSCRIBE TO Science QuicklyRachel Feltman: Mitochondria are the powerhouse of the cell, right? Well, it turns out they might be way more complicated than that, and that could have implications for everything from diet and exercise to treating mental health conditions.For Scientific American’s Science Quickly, I’m Rachel Feltman.Our guest today is Martin Picard, an associate professor of behavioral medicine at Columbia University. He’s here to tell us all about our mitochondria, what they do for us and how they can even talk to each other. If you like to watch your pods instead of just listening, you can check out a video version of my conversation with Martin over on our YouTube page. Plus, you’ll get to see some of the aligning mitochondria we’re about to talk about in action.On supporting science journalismIf you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today.Martin, would you tell us a little bit about who you are and where you work?Martin Picard: Sure, I work at Columbia University; I’m a professor there, and I lead a team of mitochondrial psychobiologists, so we try to understand the, the mind-mitochondria connection, how energy and those little living creatures that populate our cells, how they actually feed our lives and allow us to, to be and to think and to feel and to experience life.Feltman: Before we get into the details, most people know mitochondria as the “powerhouse of the cell”—which, fun fact, Scientific American actually coined in the 1950s—but what are mitochondria, to start us off with a really basic question?Picard: [Laughs]Yes, 1957 is the “powerhouse of the cell.” That was momentous.That shaped generations of scientists, and now the powerhouse analogy is expired, so it’s time for a new perspective.Really, mitochondria are, are small living organelles, like little organs of the cell, and what they do is they transform the food we eat and the oxygen that we breathe. Those two things converge inside the mitochondria, and that gets transformed into a different kind of energy. Energy is neither created nor destroyed, right? It’s a fundamental law of thermodynamics. So mitochondria, they don’t make energy; they transform the energy that’s stored in food from the plants and from the energy of the sun and then the oxygen combining this, and then they transform this into a little electrical charge. They dematerialize food—energy stored in food—into this very malleable, flexible form of energy that’s membrane potential, so they become charged like little batteries and then they power everything in our cells, from turning on genes and making proteins and cellular movement; cellular division; cell death, aging, development—everything requires energy. Nothing in biology is free.Feltman: Well, I definitely wanna get into what you said about the powerhouse analogy not working anymore ’cause that seems pretty huge, but before we get into that: you recently wrote a piece for Scientific American, and you referred to yourself as, I think, a “mitochondriac.” I would love to hear what you mean by that and how you got so interested in these organelles.Picard: Yeah, there’s a famous saying in science: “Every model is wrong, but some are useful.” And the model that has pervaded the world of biology and the health sciences is the gene-based model (the central dogma of biology, as it’s technically called): genes are the blueprint for life, and then they drive and determine things. And we know now [it] to be misleading, and it forces us to think that a lot of what we experience, a lot of, you know, health or diseases, is actually determined by our genes. The reality is a very small percentage [is].Whether we get sick or not and when we get sick is not driven by our genes, but it’s driven by, you know, emergent processes that interact from our movement and our interaction with other people, with the world around us, with what we eat, how much we sleep, how we feel, the things we do. So the gene-based model was very powerful and useful initially, and then, I think, its, its utility is dwindling down.So the powerhouse analogy powered, you know, a few [laughs] decades of science, and then what started to happen, as scientists discovered all of these other things that mitochondria do, we kept getting surprised. Surprise is an experience, and when you feel surprised about something, like, it’s because your internal model of what that thing is, it was wrong, right?Feltman: Right.Picard: And when there’s a disconnect between your internal model and the, the reality, then that feels like surprise. And I grew up over the last 15 years as a academic scientist, and, like, every month there’s a paper that’s published: “Mitochondria do this. Mitochondria make hormones.” Surprise! A, a powerhouse should have one function: it should make, or transform, energy, right? This is what powerhouses do. Mitochondria, it turns out, they have a life cycle. They make hormones. They do transform energy, but they also produce all sorts of signals. They turn on genes; they turn off genes. They can kill the cell if they deem that’s the right thing to do.So there are all of these functions, and, and I think, as a community, we keep being surprised as we discover new things that mitochondria do. And then once you realize the complexity and the amazing beauty of mitochondria and their true nature, then I think you have to become a mitochondriac [laughs]. You have to, I think, be impressed by the beauty of—this is just a—such a beautiful manifestation of life. I fell in love with mitochondria, I think, is what happened [laughs].Feltman: Yeah, well, you touched on, you know, a few of the surprising things that mitochondria are capable of, but could you walk us through some of your research? What surprises have you encountered about these organelles?Picard: One of the first things that I saw that actually changed my life was seeing the first physical evidence that mitochondria share information ...Feltman: Mm.Picard: With one another. The textbook picture and the powerhouse analogy suggests that mitochondria are these, like, little beans and that they, they kind of float around and they just make ATP, adenosine triphosphate, which is the cellular energy currency, and once in a while they reproduce: there’s more mitochondria that come from—mitochondria, they can grow and then divide. So that’s what the powerhouse predicts.And what we found was that when—if you have a mitochondrion here and another mitochondrion here, inside the mitochondria, they’re these membranes ...Feltman: Mm.Picard: They’re, like, little lines. They look, in healthy mitochondria, look like radiators, right? It’s, like, parallel arrays. And it’s in these lines that the oxygen that we breathe is consumed and that the little charge—the, the food that we eat is converted into this electrical charge. These are called cristae.And in a normal, healthy mitochondria the cristae are nicely parallel, and there’s, like, a regularity there that’s just, I think, intuitively appealing, and it, it looks healthy. And then if you look at mitochondria in a diseased organ or in a diseased cell, often the cristae are all disorganized. That’s a feature of “something’s wrong,” right?And I’ve seen thousands of pictures and I’ve taken, you know, several thousands of pictures on the electron microscope, where you can see those cristae very well, and I’d never seen in the textbooks or in articles or in presentations, anywhere, that the cristae could actually, in one mitochondrion, could be influenced by the cristae in another mitochondrion.And what I saw that day and that I explained in the [laughs], in the article was that there was this one mitochondrion there—it had beautifully organized cristae here, and here the cristae were all disorganized. And it turns out that the part of this mitochondrion that had beautifully organized cristae is all where that mitochondria was touching other mitochondria.Feltman: Mm.Picard: So there was something about the mito-mito contact, right? Like, a unit touching another unit, an individual interacting with another individual, and they were influencing each other ...Feltman: Yeah.Picard: And the cristae of one mitochondrion were bending out of shape. That’s not thermodynamically favorable [laughs], to bend the lipid membrane, so there has to be something that is, you know, bringing energy into the system to bend the membrane, and then they were meeting to be parallel with the cristae of another mitochondrion. So there was these arrays that crossed boundaries between individual mitochondria ...Feltman: Wow.Picard: And this was not [laughs] what I, I learned or this was not what I was taught or that I’d read, so this was very surprising.The first time we saw this, we had this beautiful video in three dimension, and I was with my colleague Meagan McManus, and then she realized that the cristae were actually aligning, and we did some statistics, and it became very clear: mitochondria care about mitochondria around them ...Feltman: Yeah.Picard: And this was the first physical evidence that there was this kind of information exchange.When you look at this it just looks like iron filings around a magnet.Feltman: Mm.Picard: Sprinkle iron filings on the piece of paper and there’s a magnet underneath, you see the fields of force, right? And fields are things that we can’t see, but you can only see or understand or even measure the strength of a field by the effect it has on something. So that’s why we sprinkle iron filings in a magnetic field to be able to see the field.Feltman: Right.Picard: It felt like what we were seeing there was the fingerprint of maybe an underlying electromagnetic field, which there’s been a lot of discussion about and hypothesis and some measurements in the 1960s, but that’s not something that most biologists think is possible. This was showing me: “Maybe the powerhouse thing is, is, is, is not the way to go.”Feltman: Did you face any pushback or just general surprise from your colleagues?Picard: About the cristae alignment?Feltman: Yeah.Picard: I did a lot of work. I took a lot of pictures and did a lot of analysis to make sure this was real ...Feltman: Mm.Picard: So I think when I presented the evidence, it was, it was, you know, it was clear [laughs].Feltman: Right.Picard: This was real.Feltman: Yeah.Picard: Whether this is electromagnetic—and I think that’s where people have kind of a gut reaction: “That can’t be real. That can’t be true.”Feltman: Mm.Picard: The cristae alignment is real, no questioning this, but whether this—there’s a magnetic field underlying this, we don’t have evidence for that ...Feltman: Sure.Picard: It’s speculation, but I think it, it hits some people, especially the strongly academically trained people that have been a little indoctrinated—I think that tends to happen in science ...Feltman: Sure.Picard: I think if we wrote a grant, you know, to, to [National Institutes of Health] to study the magnetic properties of mitochondria, that’d be much harder to get funded. But there was no resistance in accepting the visual evidence of mitochondria exchanging information ...Feltman: Yeah.Picard: What it means, then, I think, is more work to be done to—towards that.Feltman: If, if we were seeing an electromagnetic field, what would the implications of that be?Picard: I think the implications is that the model that most of biomedical sciences is based on, which is “we’re a molecular soup and we’re molecular machines,” that might not be entirely how things work. And if we think that everything in biology is driven by a lock-and-key mechanism, right—there’s a molecule that binds a receptor and then this triggers a conformational change, and then there’s phosphorylation event and then signaling cascade—we’ve made a beautiful model of this, a molecular model of how life works.And there’s a beautiful book that came out, I think last year or end of 2023, How Life Works, by Philip Ball, and he basically brings us through a really good argument that life does not work by genetic determinism, which is how most people think and most biologists think that life works, and instead he kind of brings us towards a much more complete and integrative model of how life works. And in that alternate model it’s about patterns of information and information is carried and is transferred not just with molecules but with fields. And we use fields and we use light and we use, you know, all sorts of other means of communication with technology; a lot of information can be carried through your Bluetooth waves ...Feltman: Mm.Picard: Right? Fields. Or through light—we use fiber optic to transfer a lot of information very quickly. And it seems like biology has evolved to, to harness these other ways of, of nonmolecular mechanisms of cell-cell communication or organism-level communication.There’s an emerging field of quantum biology that is very interested in this, but this clashes a little bit with the molecular-deterministic model that science has been holding on to [laughs]—I think against evidence, in, in some cases—for a while. Nobody can propose a rational, plausible molecular mechanism to explain what would organize cristae like this across mitochondria. The only plausible mechanism seems to be that there’s a—there’s some field, some organizing electromagnetic field that would bend the cristae and organize them, you know, across organelles, if that’s true.Feltman: Right.Picard: It was a bit of an awakening for me, and it turned me into a mitochondriac because it made me realize that this is the—this whole thing, this whole biology, is about information exchange and mitochondria don’t seem to exist as little units like powerhouses; they exist as a collective.Feltman: Yeah.Picard: The same way that you—this body. It’s a bunch of cells; either you think it’s a molecular machine or you think it’s an energetic process, right? There’s energy flowing through, and are you more the molecules of your body or are you more the, the energy flowing through your body?Feltman: Mm.Picard: And if you go down this, this line of questioning, I think, very quickly you realize that the flow of energy running through the physical structure of your body is more fundamental. You are more fundamentally an energetic process ...Feltman: Hmm.Picard: Than the physical molecular structure that you also are. If you lose part of your anatomy, part of your structure, right—you can lose a limb and other, you know, parts of your, of your physical structure—you still are you ...Feltman: Right.Picard: Right? If your energy flows differently or if you change the amount of energy that flows through you, you change radically. Three hours past your bedtime you’re not the best version of your, the best version of yourself. When you’re hangry, you haven’t eaten, and you, like, also, you’re not the best version of yourself, this is an energetic change. Right?Feltman: Yeah.Picard: Many people now who have experienced severe mental illness, like schizophrenia and bipolar disease, and, and who are now treating their symptoms and finding full recovery, in some cases, from changing their diets.Feltman: Mm.Picard: And the type of energy that flows through their mitochondria, I think, opens an energetic paradigm for understanding health, understanding disease and everything from development to how we age to this whole arc of life that parallels what we see in nature.Feltman: Yeah, so if we, you know, look at this social relationship between mitochondria, what are, in your mind, the most, like, direct, obvious implications for our health and ...Picard: Mm-hmm.Feltman: And well-being?Picard: Yeah, so we can think of the physical body as a social collective. So every cell in your body—every cell in your finger, in your brain, in your liver, in your heart—lives in some kind of a social contract with every other cell. No one cell knows who you are, or cares [laughs], but every cell together, right, makes up who you are, right? And then together they allow you to feel and to have the experience of who you are. That kind of understanding makes it clear that the key to health is really the coherence between every cell.Feltman: Mm.Picard: If you have a few cells here in your body that start to do their own thing and they kind of break the social contract, that’s what we call cancer. So you have cells that stop receiving information from the rest of the body, and then they kind of go rogue, they go on their own. Their purpose in life, instead of sustaining the organism, keeping the whole system in coherence, now these cells have as their mind, like, maybe quite literally, is, “Let’s divide, and let’s make more of ourselves,” which is exactly what life used to be before mitochondria came in ...Feltman: Mm.Picard: Into the picture 1.5 billion years ago, or before endosymbiosis, the origin of, of multicellular life. So cancer, in a way, is cells that have broken the social contract, right, exited this social collective, and then to go fulfill their own little, mini purpose, which is not about sustaining the organism but sustaining themselves. So that principle, I think, has lots of evidence to, to support it.And then the same thing, we think, happens at the level of mitochondria, right? So the molecular-machine perspective is that mitochondria are little powerhouses and they’re kind of slaves to the cell: if the cell says, “I need more energy,” then the mitochondria provide and they kind of obey rules. The mito-centric perspective [laughs] is that mitochondria really drive the show. And because they’re in charge of how energy flows, they have a veto on whether the cell gets energy and lives and divides and differentiates and does all sorts of beautiful things or whether the cell dies.And most people will know apoptosis, programmed cell death, which is a normal thing that happens. The main path to apoptosis in, in our bodies is mitochondria calling the shot, so mitochondria have a veto, and they can decide, “Now, cell, it’s time to die.” And mitochondria make those decisions not based on, like, their own little powerhouse [laughs] perception of the world; they make these decisions as social collectives. And you have the hundreds, thousands of mitochondria in some cells that all talk to each other and they integrate dozens of signals—hormones and metabolites and energy levels and temperature—and they integrate all this information; they basically act like a mini brain ...Feltman: Hmm.Picard: Inside every cell. And then once they have a, a—an appropriate picture of what the state of the organism is and what their place in this whole thing is, then they actually, I think, make decisions about, “Okay, it’s time to divide,” right? And then they send signals to, to the nucleus, and then there’re genes in the nucleus that are necessary for cell division that gets turned on, and then the cell enters cell cycle, and we and others have shown in, in, in the lab, you can prevent a cell from staying alive [laughs] but also from differentiating—a stem cell turning into a neuron, for example, this is a major life transition for a cell. And people have asked what drives those kind of life transitions, cellular life transitions, and it’s clear mitochondria are one of the main drivers of this ...Feltman: Hmm.Picard: And if mitochondria don’t provide the right signals, the stem cell is never gonna differentiate into a specific cell type. If mitochondria exists as a social collective, then what it means for health [laughs] is that what we might wanna do is to promote sociality, right, to promote crosstalk between different parts of our bodies.Feltman: Hmm.Picard: And I suspect this is why exercise is so good for us.Feltman: Yeah, that was—that’s a great segue to my next question, which is: How do you think we can foster that sociality?Picard: Yeah. When times are hard, right, then people tend to come together to solve challenges. Exercise is a, a big challenge for the organism, right?Feltman: Mm.Picard: You’re pushing the body, you’re, like, contracting muscles, and you’re moving or, you know, whatever kind of exercise you’re doing—this costs a lot of energy, and it’s a big, demanding challenge for the whole body. So as a result you have the whole body that needs to come together to survive this moment [laughs]. And if you’re crazy enough to run a marathon, to push your body for three, four hours, this is, like, a massive challenge.Feltman: Sure.Picard: The body can only sustain that challenge by coming together and working really coherently as a unit, and that involves having every cell in the body, every mitochondria in the body talking to each other. And it’s by this coherence and this kind of communication that you create efficiency, and the efficiency is such a central concept and principle in all of biology. It’s very clear there, there have been strong evolutionary forces that have pushed biology to be evolved towards greater and greater efficiency.The energy that animals and organisms have access to is finite, right? There’s always a limited amount of food out there in the world. If there’s food and there are other people with you, your social group, do you need to share this? So if biology had evolved to just eat as much food as possible, we would’ve gone extinct or we wouldn’t have evolved the way we have. So it’s clear that at the cellular level, at the whole organism level, in insects to very large mammals, there’s been a drive towards efficiency.You can achieve efficiency in a few ways. One of them is division of labor. Some cells become really good at doing one thing, and that’s what they do. Like muscles, they contract [laughs]; they don’t, you know, release hormones—or they release some hormones but not like the liver, right?Feltman: Sure.Picard: And the liver feeds the rest of the body, and the liver is really good at this. But the liver’s not good at integrating sensory inputs like the brain. The brain is really good at integrating sensory inputs and kind of managing the rest of the body, but the brain is useless at digesting food or, you know, feeding the rest of the body. So every organ specializes, and this is the reason we’re so amazing [laughs]. This is the reason complex multicellular animals that, you know, that, that have bodies with organs can do so many amazing things: because this whole system has harnessed this principle of division of labor. So you have a heart that pushes blood, and you have lungs that take in oxygen, and that’s the main point: [it’s] the cooperation and the teamwork, the sociality between cells and mitochondria and, and organs that really make the whole system thrive.So exercise does that.Feltman: Yeah.Picard: It forces every cell in the body to work together. Otherwise you’re just not gonna survive. And then there are other things that happen with exercise. The body is a predictive instrument, right ...Feltman: Mm.Picard: That tries to make predictions about what’s gonna happen in the future, and then you adapt to this. So when you exercise and you start to breathe harder the reason you breathe harder, the reason, you know, you need to bring in more oxygen in your body, is because your mitochondria are consuming the oxygen. And when that happens every cell has the ability to feel their energetic state, and when they feel like they’re running out of energy, like if you’re exercising hard and your muscles are burning, your body says, “Next time this happens I’ll be ready.” [Laughs] And it gets ready—it mobilizes this program, this preparatory program, which, which we call exercise adaptation, right—by making more mitochondria. So the body can actually make more mitochondria after exercise.So while you’re exercising, the mitochondria, they’re transforming food and oxygen very quickly, making ATP, and then cells—organs are talking to one another; then you’re forcing this great social collective. Then when you go and you rest and you go to sleep, you lose consciousness [laughs], and then the natural healing forces of the body can work. Now the body says, “Next time this happens I’ll be ready,” and then it makes more mitochondria. So we know, for example, in your muscles you can double the amount of mitochondria you have ...Feltman: Wow.Picard: With exercise training. So if you go from being completely sedentary to being an elite runner, you will about double the amount of mitochondria in, in your muscle. And ...Feltman: That’s really cool.Picard: Yeah. And this seems to happen in other parts of the body as well, including the brain.Feltman: I know that your lab does some work on mitochondria and mental health as well. Could you tell us a little bit more about that?Picard: The ability to mitochondria to flow energy supports basic cellular functions, but it also powers the brain [laughs] and powers the mind, and our best understanding now of what is the mind—and consciousness researchers have been debating this for a long time—I think our, our best, most parsimonious definition of the mind is that the mind is an energy pattern. And if the flow of energy changes, then your experience also changes. And there’s emerging evidence in a field called metabolic psychiatry that mental health disorders are actually metabolic disorders ...Feltman: Hmm.Picard: Of the brain.There’s several clinical trials—some are published, many more underway—and the evidence is very encouraging that feeding mitochondria a certain type of fuel, called ketone bodies, brings coherence into the organism. And energetically we think this reduces the resistance to energy flow so energy can flow more freely through the neurons and through the structures of the brain and then through the mitochondria.And that—that’s what people report when they, they go into this medical ketogenic therapy: they feel like they have more energy, sometimes quite early, like, after a few days, sometimes after a few weeks. And then the symptoms of, of mental illness in many people get better. The website Metabolic Mind has resources for clinicians, for patients and, and guidance as to how to—for people to work with their care team, not do this on their own but do this with their medical team.Feltman: And I know that mitochondria have kind of a weird, fascinating evolutionary backstory.Picard: They used to be bacteria, and once upon a time, about two billion years ago, the only thing that existed on the planet that was alive were unicellular, right, single-cell, bacteria, a single-cell organism. And then some bacteria—there were different kinds—and then some bacteria were able to use oxygen for energy transformation; that was—those are called aerobic, for oxygen-consuming. And then there are also anaerobic, non-oxygen-consuming, bacteria that are fermenting cells.And then at some point, about 1.5 billion years ago, what happened is there was a small aerobic bacterium, an alphaproteobacterium, that either infiltrated a larger anaerobic cell or it was the larger cell that ate the small aerobic bacterium, the large one kept it in, and then the small aerobic bacterium ended up dividing and then became mitochondria. So mitochondria used to be this little bacterium that now is very much part of what we are, and what seems to have happened when this critical kind of merger happened is that a new branch of life became possible.Feltman: Yeah.Picard: And animals became possible. And somehow this acquisition, from the perspective of the larger cell, enabled cell-cell communication, a form of cell-cell communication that was not possible before. And this seems to have been the trigger for multicellular life and the development of, initially, little worms and then fishes and then animals and then eventually Homo sapiens.Feltman: Yeah, and that was really controversial when it was first proposed, right?Picard: Yeah. Lynn Margulis, who is, like, a fantastic scientist, she proposed this, and I think her paper was rejected [15] times ...Feltman: Wow.Picard: Probably by Nature and then by a bunch of [laughs] ...Feltman: [Laughs] Sure.Picard: A bunch of other journals. Fourteen rejections and then in the end she published it, and now this is a cornerstone of biology. So kudos for persistence ...Feltman: Yeah.Picard: For Lynn Margulis.Feltman: And mitochondria have just been shaking things up for, for decades [laughs], I guess.Picard: Mm-hmm, yeah, there’ve been several Nobel Prizes for understanding how mitochondria work—specifically for the powerhouse function of mitochondria [laughs].The field of [molecular] mitochondrial medicine was born in the ’80s. Doug Wallace, who was my mentor as a postdoc, discovered that we get our mitochondria from our mothers. The motherly nourishing energy [laughs] is passed down through mitochondria. There’s something beautiful about that.Feltman: Yeah. Thank you so much for coming in. This was super interesting, and I’m really excited to see your work in the next few years.Picard: Thank you. My pleasure.Feltman: That’s all for today’s episode. Head over to our YouTube page if you want to check out a video version of today’s conversation. We’ll be back on Friday with one of our deep-dive Fascinations. This one asks whether we can use artificial intelligence to talk to dolphins. Yes, really.While you’re here, don’t forget to fill out our listener survey. You can find it at sciencequickly.com/survey. If you submit your answers in the next few days, you’ll be entered to win some free Scientific American swag. More importantly, you’ll really be doing me a solid.Science Quickly is produced by me, Rachel Feltman, along with Fonda Mwangi, Kelso Harper, Naeem Amarsy and Jeff DelViscio. This episode was edited by Alex Sugiura. Shayna Posses and Aaron Shattuck fact-check our show. Our theme music was composed by Dominic Smith. Subscribe to Scientific American for more up-to-date and in-depth science news.For Scientific American, this is Rachel Feltman. See you next time!