Carbohydrate-binding proteins fill in gaps in immune defenses
Our bodies produce a family of proteins that recognize and kill bacteria whose carbohydrate coatings resemble those of our own cells too closely, scientists have discovered.
Called galectins, these proteins recognize carbohydrates from a broad range of disease-causing bacteria, and could potentially be deployed as antibiotics to treat certain infections. The results are scheduled for publication in Nature Chemical Biology.
Researchers at Emory University School of Medicine made the discovery with the aid of glass slides coated with an array of over 300 different glycans (carbohydrates found on the surfaces of cells) derived from bacteria, many of which are found in the intestine. One can think of these slides – called microbial glycan microarrays – as wardrobes displaying a variety of clothes worn by gut bacteria.
“Many microbes cover themselves with glycans that somewhat resemble our own cells,” says Richard D. Cummings, PhD, professor and chair of the Department of Biochemistry at Emory University School of Medicine. “That limits how well the immune system can use antibodies to respond to those microbes.”
To prevent auto-immune attack, our bodies usually don’t make antibodies against molecules found on our own cells. That leaves gaps in our defenses that bacteria could exploit. Several of those gaps are filled by galectins, the researchers found.
The discovery expands upon an initial finding, published in Nature Medicine in 2010, describing galectins that recognize and kill bacteria that express the human blood group B antigen.
The Emory researchers collaborated with the laboratory of James C. Paulson, PhD, at the Scripps Research Institute (TSRI). Co-first authors of the paper are Sean Stowell, MD/PhD (a resident in in laboratory and transfusion medicine at Emory), Connie Arthur, PhD (postdoctoral fellow at Emory with Stowell), and research assistant Ryan McBride at TSRI.
In contrast to antibodies, the galectins kill the bacteria directly, without needing other parts of the immune system to pile on. The researchers identified several varieties of bacteria (Pseudomonas aeruginosa, Providencia alcalifaciens, Klebsiella pneumoniae, and Serratia marcescens, for example) targeted for killing by galectins. In some cases, only certain strains of a given bacteria were vulnerable, because only those strains carried the target glycan.
“These studies have opened the way to understanding the ways in which adaptive or antibody-based factors work together with innate or galectin-based factors to give us immunity against a broad range of microbes,” Cummings says.
In addition, the microarray technology provides tools to study glycan-binding antibodies and galectins in populations, he says.
“These studies use tiny amounts of blood – just a few drops – and show how glycan microarrays could supersede previous technology,” he says. “Using these tools, investigators could identify developmental- and age-specific differences in anti-microbial glycan antibodies in humans, which may predict susceptibility to disease.”
The breakthrough, published in the journal Nature Materials, could offer an easier way of detecting pathogenic bacteria outside of a clinical setting and could be particularly important for the developing world, where access to more sophisticated laboratory techniques is often limited.
The research was led by Professor Cameron Alexander, Head of the Division of Drug Delivery and Tissue Engineering and EPSRC Leadership Fellow in the University’s School of Pharmacy, building on work by PhD student Peter Magennis. Professor Alexander said: “Essentially, we have hijacked some of the metabolic machinery which bacteria use to control their environment, and used it instead to grow polymers which bind strongly to the specific bacteria that produce them.
“The neat thing about this is that the functionality of the polymers grown on the surface of the bacteria is programmed by the cells so that they can recognise their own ‘kind’. We used fluorescent labels to light up the polymers and were able to capture this labelling using a mobile phone camera, so in principle it could be possible to use these materials as point-of-care diagnostics for pathogenic bacteria.”
The study has shown that the bacteria helped to synthesise polymers on their own surfaces which not only were different from those made by conventional methods, but which retained a form of ‘structural memory’ of that surface. This means in future it should be possible to make specific detection agents or additives for topical anti-infectives that target a number of harmful bacteria all by a common route.
“The initial focus of the research was to explore ways to use synthetic polymers to selectively target and bind the bacteria that cause dental cavities and periodontal diseases in order to facilitate their removal from the oral cavity,” said Dr David Churchley, Principal Scientist, Oral Health Category Research and Development, GSK Consumer Healthcare. “As we continued our work, we saw that our research had broader implications and potential for a wider range of uses.”
Rapidly identifying harmful bacteria at the heart of a serious medical or dental condition can be a difficult and costly task. The group’s findings may even lead to new ways of treating bacterial infections. “These types of polymers may be designed to contain antibacterial functionalities so that they specifically bind to and kill bacterial pathogens,” said Dr Klaus Winzer, a microbiologist at The University of Nottingham involved in the study. The selective binding of specific bacterial species and/or strains in current practice requires expensive ‘cold-chain’ reagents such as antibodies which often preclude using these processes outside of a hospital setting or in developing nations.
The new approach, termed ‘bacterial-instructed synthesis’, has the potential for use in the developing world, in the field or in less specialised laboratory settings.
Dr David Bradshaw, Principal Scientist, Oral Health Category Research and Development, GSK Consumer Healthcare, said: “The ingredients used to form the polymers are all easy to obtain, inexpensive and widely available. With the simplicity and accessibility of the chemistry, a number of diagnostic and other applications may be possible.”
Researchers at the University of California, San Diego School of Medicine have identified a mechanism that explains why people with the hepatitis C virus get liver disease and why the virus is able to persist in the body for so long.
The hard-to-kill pathogen, which infects an estimated 200 million people worldwide, attacks the liver cells’ energy centers – the mitochondria – dismantling the cell’s innate ability to fight infection. It does this by altering cells mitochondrial dynamics.
The study, published in today’s issue of the Proceedings of the National Academy of Sciences, suggests that mitochondrial operations could be a therapeutic target against hepatitis C, the leading cause of liver transplants and a major cause of liver cancer in the U.S.
“Our study tells us the story of how the hepatitis C virus causes liver disease,” said Aleem Siddiqui, PhD, professor of medicine and senior author. “The virus damages mitochondria in liver cells. Cells recognize the damage and respond to it by recruiting proteins that tell the mitochondria to eliminate the damaged area, but the repair process ends up helping the virus.”
Mitochondria are organelles in a cell that convert energy from food (glucose) into a form of energy that can be used by cells called adenosine triphosphate.
Specifically, the researchers discovered that the virus stimulates the production of a protein (Drp 1) that induces viral-damaged mitochondria to undergo asymmetric fragmentation. This fragmentation (fission) results in the formation of one healthy mitochondrion and one damaged or bad mitochondrion, the latter of which is quickly broken down (catabolized) and dissolved in the cell’s cytoplasm.
Although the fragmentation serves to excise the damaged area from the mitochondrion, the formation of a healthy mitochondrion also helps keep the virus-infected cell alive. Moreover, the virus is able to use the mitochondrial remains (all the amino acids and lipids from the catabolized mitochondrion) to help fuel its continued replication and virulence.
“It’s like the bad part of the house is demolished to the benefit of the virus,” Siddiqui said.
In their experiments, the researchers showed that hepatitis C-infected cells with higher Drp 1 protein levels also produced less interferon, the body’s natural immune booster. These cells were also less likely to undergo apoptosis, a process that would encourage damaged cells to essentially kill themselves.
The reverse was also observed: When the Drp 1 protein was “silenced,” interferon production and apoptotic activity increased.
“Mitochondrial processes are at the center of understanding the persistence of the virus and how it flies under the radar of the body’s natural immune response,” he said. “The trick is to find a way to deliver a drug that could target the Drp 1 protein specifically in hepatitis C-infected liver cells, maybe through nanotechnology.
Scientists at Chicago’s Field Museum and international collaborators have reconstructed the phylogeny and biological history for the Yellow-shouldered bats in the New World tropics, the region of the Earth surrounding the equator. In-depth analysis of mitochondrial and nuclear DNA sequences uncovered three species new to science, each having previously been confused with another species. Since 1960, when modern studies on this group began, Sturnira has grown from eight species to 22. The newest additions were described in a new study, published online in ZooKeys.
The New World tropics have long been recognized as a region teeming with some of the richest biodiversity on Earth. It is home to a group of small, fruit-eating bats ranging from half-an-ounce to three ounces in size. The bats belong to the genus Sturnira, commonly named yellow-shouldered bats, which are found from northern Mexico to northern Argentina. One species in particular, Sturnira lilium, has figured among the most widespread and locally abundant bats of the New World topics.
“A curator’s job is to bring order out of chaos,” said Bruce Patterson, PhD, MacArthur Curator of Mammals at The Field Museum. “This group of bats offered an excellent opportunity study the process of species formation across the entire New World tropics.”
Paúl Velazco, PhD, who formerly worked at The Field Museum and now is with the American Museum of Natural History in New York, is the lead author on the new study. Velazco and Patterson began their endeavor by collecting 38 samples of six species from three countries. They also borrowed 94 samples from 24 countries from museums around the world in order to complete the project, highlighting the importance of museum collections for the growing body of scientific knowledge.
The researchers isolated DNA from a small portion of liver or muscle samples that had been frozen or preserved from each specimen. They then amplified and sequenced two nuclear and three mitochondrial genes from each tissue, amounting to nearly 5,000 base pairs of DNA, from over 120 individuals.
“We chose these genes because they have proven useful for classification of related groups of bats,” said Velazco. “Mitochondrial sequences tend to be fast-evolving and informative about very recent evolutionary splits, while nuclear genes tend to be slow-evolving and shed light on more ancient divergence events.”
By sequencing both classes of DNA, the researchers could recover the group’s entire history, which stretches back about 8 million years.
Every museum specimen that was sequenced already had both a name and a geographic distribution. However, the sequence analysis led the investigators to believe that some of the branch labels were incorrect. Indeed, after re-examining the museum specimens associated with each sample, they found that nearly 20 percent of the specimens had been incorrectly labeled!
How could so many individual animals have been misidentified? The answer lies within technology.
“The differences between species are often subtle, and difficult to describe in writing. The historic literature lacked access to the visual documentation that we rely on today, such as color photography and digital libraries,” said Patterson. “For this reason, small and imprecisely described morphological differences were often overlooked during the original identification of the specimens. This type of error pervades all biological collections.”
Their results identified three species entirely new to science, and provided evidence for the elevation of three subspecies to the species level. Two of the new species are described in the ZooKeys article.
In the process, Velazco and Patterson were able to revise the supposed geographic range of Sturnira lilium. Instead of extending from Mexico to Argentina, the real Sturnira lilium is limited to Bolivia, Brazil, Paraguay, Uruguay, and northern Argentina. The rest of its presumed range is occupied by six other close relatives that replace one another in jigsaw-like fashion across the Neotropics.
The distribution of Sturnira species across most of the New World tropics and its diversification throughout its eight-million-year existence make it informative for other sorts of biological reconstructions, such as the seed plants upon which it feeds.
In addition to its scientific usefulness, this study demonstrates the need for the ongoing revision of the Earth’s biological history, and highlights the immense value of museum collections in uncovering new knowledge.
“For this particular group of mammals, we are much closer that we were in framing their diversity, although there may be additional Sturnira out there,” said Patterson. “Over the years, I’ve learned that no one has the last word in science.”
By tracking brain activity when an animal stops to look around its environment, neuroscientists at the Johns Hopkins University believe they can mark the birth of a memory.
Using lab rats on a circular track, James Knierim, professor of neuroscience in the Zanvyl Krieger Mind/Brain Institute at Johns Hopkins, and a team of brain scientists noticed that the rats frequently paused to inspect their environment with head movements as they ran. The scientists found that this behavior activated a place cell in their brain, which helps the animal construct a cognitive map, a pattern of activity in the brain that reflects the animal’s internal representation of its environment.
In a paper recently published in the journal Nature Neuroscience, the researchers state that when the rodents passed that same area of the track seconds later, place cells fired again, a neural acknowledgement that the moment has imprinted itself in the brain’s cognitive map in the hippocampus.
The hippocampus is the brain’s warehouse for long- and short-term processing of episodic memories, such as memories of a specific experience like a trip to Maine or a recent dinner. What no one knew was what happens in the hippocampus the moment an experience imprints itself as a memory.
“This is like seeing the brain form memory traces in real time,” said Knierim, senior author of the research. “Seeing for the first time the brain creating a spatial firing field tied to a specific behavioral experience suggests that the map can be updated rapidly and robustly to lay down a memory of that experience.”
A place cell is a type of neuron within the hippocampus that becomes active when an animal or human enters a particular place in its environment. The activation of the cells helps create a spatial framework much like a map, that allows humans and animals to know where they are in any given location. Place cells can also act like neural flags that “mark” an experience on the map, like a pin that you drop on Google maps to mark the location of a restaurant.
“We believe that the spatial coordinates of the map are delivered to the hippocampus by one brain pathway, and the information about the things that populate the map, like the restaurant, are delivered by a separate pathway,” Knierim said. “When you experience a new item in the environment, the hippocampus combines these inputs to create a new spatial marker of that experience.”
In the experiments, researchers placed tiny wires in the brains of the rats to monitor when and where brain activity increased as they moved along the track in search of chocolate rewards. About every seven seconds, the rats stopped moving forward and turned their heads to the perimeter of the room as they investigated the different landmarks, behavior called “head-scanning.”
“We found that many cells that were previously silent would suddenly start firing during a specific head-scanning event,” Knierim said. “On the very next lap around the track, many of these cells had a brand new place field at that exact same location and this place field remained usually for the rest of the laps. We believe that this new place field marks the site of the head scan and allows the brain to form a memory of what it was that the rat experienced during the head scan.”
Knierim said the formation and stability of place fields and the newly activated place cells requires further study. The research is primarily intended to understand how memories are formed and retrieved under normal circumstances, but it could be applicable to learning more about people with brain trauma or hippocampal damage due to aging or Alzheimer’s.
“There are strong indications that humans and rats share the same spatial mapping functions of the hippocampus, and that these maps are intimately related to how we organize and store our memories of prior life events,” Knierim said. “Since the hippocampus and surrounding brain areas are the first parts of the brain affected in Alzheimer’s, we think that these studies may lend some insight into the severe memory loss that characterizes the early stages of this disease.”
Exposing leafy vegetables grown during spaceflight to a few bright pulses of light daily could increase the amount of eye-protecting nutrients produced by the plants, according to a new study by researchers at the University of Colorado Boulder.
One of the concerns for astronauts during future extended spaceflights will be the onslaught of eye-damaging radiation they’ll be exposed to. But astronauts should be able to mitigate radiation-induced harm to their eyes by eating plants that contain carotenoids, especially zeaxanthin, which is known to promote eye health.
Zeaxanthin could be ingested as a supplement, but there is evidence that human bodies are better at absorbing carotenoids from whole foods, such as green leafy vegetables.
Already, NASA has been studying ways to grow fresh produce during deep space missions to maintain crew morale and improve overall nutrition. Current research into space gardening tends to focus on getting the plants to grow as large as possible as quickly as possible by providing optimal light, water and fertilizer. But the conditions that are ideal for producing biomass are not necessarily ideal for the production of many nutrients, including zeaxanthin.
“There is a trade-off,” said Barbara Demmig-Adams, professor of distinction in the Department of Ecology and Evolutionary Biology and a co-author of the study published in the journal Acta Astronautica. “When we pamper plants in the field, they produce a lot of biomass but they aren’t very nutritious. If they have to fend for themselves—if they have to defend themselves against pathogens or if there’s a little bit of physical stress in the environment—plants make defense compounds that help them survive. And those are the antioxidants that we need.”
Plants produce zeaxanthin when their leaves are absorbing more sunlight than they can use, which tends to happen when the plants are stressed. For example, a lack of water might limit the plant’s ability to use all the sunlight it’s getting for photosynthesis. To keep the excess sunlight from damaging the plant’s biochemical pathways, it produces zeaxanthin, a compound that helps safely remove excess light.
Zeaxanthin, which the human body cannot produce on its own, plays a similar protective role in our eyes.
“Our eyes are like a leaf—they are both about collecting light,” Demmig-Adams said. “We need the same protection to keep us safe from intense light.”
The CU-Boulder research team—which also included undergraduate researcher Elizabeth Lombardi, postdoctoral researcher Christopher Cohu and ecology and evolutionary biology Professor William Adams—set out to determine if they could find a way to “have the cake and eat it too” by simultaneously maximizing plant growth and zeaxanthin production.
Using the model plant species Arabidopsis, the team demonstrated that a few pulses of bright light on a daily basis spurred the plants to begin making zeaxanthin in preparation for an expected excess of sunlight. The pulses were short enough that they didn’t interfere with the otherwise optimal growing conditions, but long enough to cause accumulation of zeaxanthin.
“When they get poked a little bit with light that’s really not a problem, they get the biomechanical machine ready, and I imagine them saying, ‘Tomorrow there may be a huge blast and we don’t want to be unprepared,’ ” Demmig-Adams said.
Arabidopsis is not a crop, but past research has shown that its behavior is a good indicator of what many edible plant species will do under similar circumstances.
The idea for the study came from Lombardi, who began thinking about the challenges of growing plants during long spaceflights while working with CU-Boulder’s Exploration Habitat graduate projects team in the Department of Aerospace Engineering Sciences, which built a robotic gardening system that could be used in space.
While the study is published in an astronautics journal, Lombardi says the findings are applicable on Earth as well and could be especially relevant for future research into plant-based human nutrition and urban food production, which must maximize plant growth in small areas. The findings also highlight the potential for investigating how to prod plants to express traits that are already written in their genetic codes either more fully or less fully.
“Learning more about what plants already ‘know’ how to do and trying to manipulate them through changing their environment rather than their genes could possibly be a really fruitful area of research,” Lombardi said.
Johns Hopkins researchers identify set of genes that can be turned back on and potentially allow for more effective treatment
Johns Hopkins researchers say they have identified a set of genes that appear to predict which tumors can evade detection by the body’s immune system, a step that may enable them to eventually target only the patients most likely to respond best to a new class of treatment.
Immune therapy for ovarian, breast and colorectal cancer — treatments that encourage the immune system to attack cancer cells as the foreign invaders they are — has so far had limited success, primarily because the immune system often can’t destroy the cancer cells. In a report published online Feb. 16 in the journal Oncotarget, the Johns Hopkins team says it has identified genes that have been repressed through so-called epigenetic changes — modifications that alter the way genes function without changing their DNA sequence — which help the cells to evade the immune system. The researchers were able to reverse these epigenetic changes with the use of an FDA-approved drug, forcing the cancer cells out of hiding and potentially making them better targets for the same immune therapy that in the past may have failed.
“Chemotherapy often works, but in most cases, it eventually stops working,” says one of the study leaders, Nita Ahuja, M.D., an associate professor of surgery, oncology and urology at the Johns Hopkins University School of Medicine. “What if we could get the immune system itself to fight the tumors and keep the cancer in check forever? That is the ultimate goal, and this gene panel may get us closer.” The other study leader is Cynthia Zahnow, Ph.D., an associate professor of oncology at Johns Hopkins.
The researchers treated 63 cancer cell lines (26 breast, 14 colorectal and 23 ovarian) with low-dose 5-azacitidine (AZA), an FDA-approved drug for myelodysplastic syndrome, that reverses epigenetic changes by stripping off the methyl group that silences the gene. They identified a panel of 80 biological pathways commonly increased in expression by AZA in all three cancers, finding that 16 of them (20 percent) are related to the immune system. These pathways appeared to be dialed down in the cancer cells, allowing for evasion. After treatment with AZA, the epigenetic changes were reversed, rendering the cancer cells unable to evade the immune system any longer.
The researchers found that these immune system pathways were suppressed in a large number of primary tumors — roughly 50 percent of ovarian cancers studied, 40 percent of colorectal cancers and 30 percent of breast cancers. The findings may be applicable to other cancer types such as lung cancer or melanoma, they say.
After looking in cell lines, the Johns Hopkins team extended their work to human tumor samples. Again they found evidence that these immune system pathways are turned down in some patients and, that these immune genes can be turned back up in a small number of patients with breast and colorectal cancer who had been treated with epigenetic therapies.
“Most of us haven’t thought of these common cancers as being immune-driven,” Ahuja says. “We haven’t held out much hope for immune therapy to work in them because before you can enter cancer cells to knock them down, you have to be able to get inside. They were locked and now we may have identified a key.”
The hope is that clinicians could eventually pinpoint which patients with these common cancers would benefit from a dose of AZA followed by an immune therapy that stimulates the immune system to attack cancer cells.
“This would tell us which patients’ tumors are hiding from the immune system and will allow us to use all of our tools to flush that cancer out,” she says.
While most of the work was done in the lab, Ahuja says her colleagues have already started to put the panel into use in a lung cancer trial. Six patients were treated first with epigenetic therapy followed by immune therapy. Though the sample is small and time has been short, four of the patients have had their cancer suppressed for many months.
“If this works — and we don’t know yet if it will — this could have the potential to control someone’s cancer for good,” she says.
A new publication from researchers at the University of Southampton and the National Oceanography Centre, Southampton highlights the importance of nutrients for coral reef survival.
Despite the comparably small footprint they take on the ocean floor, tropical coral reefs are home to a substantial part of all marine life forms. Coral reefs also provide numerous benefits for human populations, providing food for millions and protecting coastal areas from erosion. Moreover, they are a treasure chest of potential pharmaceuticals and coral reef tourism provides recreation and income for many.
Unfortunately, coral reefs are declining at an alarming rate. To promote management activities that can help coral reef survival, an international group of world renowned scientists have summarised the present knowledge about the challenges that coral reefs are facing now and in the future in a special issue of the journal Current Opinion in Environmental Sustainability.
The contribution of scientists from the University of Southampton to this special issue, which highlights the crucial role of nutrients for the functioning of coral reefs, can be freely downloaded from;
The University of Southampton researchers who are based at the Coral Reef Laboratory in the National Oceanography Centre, Southampton, explain that “too many” nutrients can be as bad for corals as “not enough”.
Professor Jörg Wiedenmann, Professor of Biological Oceanography at the University of Southampton and Head of the Coral Reef Laboratory, says: “The nutrient biology of coral reefs is immensely complex. It is important to distinguish between the different direct and indirect effects that a disturbance of the natural nutrient environment can have on a coral reef ecosystem.”
Since corals live in a symbiotic relationship with microscopically small plant cells, they require certain amounts of nutrients as “fertiliser”. In fact, the experimental addition of nutrients can promote coral growth. “One should not conclude from such findings, however, that nutrient enrichment is beneficial for coral reefs – usually the opposite is true,” explains Dr Cecilia D’Angelo, Senior Research Fellow in the Coral Reef Laboratory and co-author on the article.
Professor Wiedenmann, whose research on coral reef nutrient biology is supported by one of the prestigious Starting Grants from the European Research Commission, adds: “Too many nutrients harm corals in many different ways, easily outweighing the positive effects that they can undoubtedly have for the coral–alga association. Paradoxically, the initial addition of nutrients to the water column might result in nutrient starvation of the corals at a later stage. In this publication, we conceptualise the important role that the competition for nutrients by phytoplankton, the free-living relatives of the corals’ symbiotic algae, may have in this context.”
“Nutrient pollution will continue to increase in many coral reefs. Therefore, an important prerequisite to develop efficient management strategies is a profound understanding of the different mechanisms by which corals suffer from nutrient stress.”
Scoffing at or cutting funds for basic biological research on unusual animal adaptations from Gila monster venom to snail sex, though politically appealing to some, is short-sighted and only makes it more likely that important economic and social benefits will be missed in the long run, say a group of evolutionary biologists at the University of Massachusetts Amherst.
Writing in a recent issue of BioScience, researchers Patricia Brennan, Duncan Irschick, Norman Johnson and Craig Albertson argue that “innovations often arise from unlikely sources” and “reducing our ability to creatively examine unique biological phenomena will ultimately harm not only education and health but also the ability to innovate, a major driver of the global economy.”
First author Patricia Brennan, known for her duck genitalia studies that could eventually aid human medical science points out, “Basic science has increasingly come under attack, and there is a growing perception that studying ‘odd’ science ideas with no clear societal benefits should be stopped. But we feel that these are the precise sorts of investigations that may lead to major innovations in biomedicine, technology and military applications.”
She and colleagues point to several specific examples where advances in understanding basic biological evolutionary adaptations led to successful technological applications, sometimes decades after the original work. Without basic work first published in 1967 on the enzyme Taq polymerase, for example, science wouldn’t have the immensely powerful DNA replication technique known as polymerase chain reaction, PCR, now providing “vast benefits” in medicine, agriculture and criminal justice.
A recent invention from UMass Amherst underscores the value of basic science, the authors add. After more than 50 years of basic research on gecko ecology and the remarkable anatomy that allows these lizards to walk up smooth walls and across the ceiling, a UMass Amherst research team invented Geckskin, an adhesive that can attach a 700-lb. weight to a smooth surface on an index-card-sized pad.
Functional morphologist Duncan Irschick, a member of that team, says, “Gecko adhesion stands as a classic example where long-term research on a seemingly frivolous topic has led to a major innovation with enormous potential for making an economic contribution.” He and colleagues say experts have identified more than 2,000 instances of technology inspired by evolutionary innovations, including highly efficient solar panels, insulated glass and body armor inspired by mantis shrimp appendages.
The public is already interested in “oddball science” and related success stories, the authors add, and “the abundance of organismal biology science stories in the news shows that [such] studies have mass appeal. This suggests they can play a role in education,” particularly in a nation where only 40 percent of the public acknowledges evolution.
Evolutionary developmental biologist Craig Albertson notes, “It’s easy to assume that innovation happens from well-planned research, but the history of innovation does not tell that story.” Norman Johnson adds, “We are not suggesting that applied science is unimportant, far from it. We are merely pointing out the long-term value and innovations that arise from what is commonly viewed as wasteful spending.”