A study at Macquarie University in Sydney found that sharks could recognise jazz – if there was food on offer
Researchers at Sydney’s Macquarie University have discovered that sharks can recognise jazz music.
In a paper published in Animal Cognition, the researchers, led by Catarina Vila Pouca, trained juvenile Port Jackson sharks to swim over to where jazz was playing, to receive food. It has been thought that sharks have learned to associate the sound of a boat engine with food, because food is often thrown from tourist boats to attract sharks to cage-diving expeditions – the study shows that they can learn these associations quickly.
The test was made more complex with the addition of classical music – this confused the sharks, who couldn’t differentiate between jazz and classical. “It was obvious that the sharks knew that they had to do something when the classical music was played, but they couldn’t figure out that they had to go to a different location,” said researcher Culum Brown. “The task is harder than it sounds, because the sharks had to learn that different locations were associated with a particular genre of music, which was then paired with a food reward. Perhaps with more training, they would have figured it out.”
Vila Pouca added: “Sharks are generally underestimated when it comes to learning abilities – most people see them as mindless, instinctive animals. However, they have really big brains and are obviously much smarter than we give them credit for.” She said that the evidence would hopefully prompt more conservation work.
The mystery behind how birds navigate might finally be solved: it’s not the iron in their beaks providing a magnetic compass, but a newly discovered protein in their eyes that lets them “see” Earth’s magnetic fields.
These findings come courtesy of two new papers – one studying robins, the other zebra finches.
The fancy eye protein is called Cry4, and it’s part of a class of proteins called cryptochromes – photoreceptors sensitive to blue light, found in both plants and animals. These proteins play a role in regulating circadian rhythms.
There’s also been evidence in recent years that, in birds, the cryptochromes in their eyes are responsible for their ability to orient themselves by detecting magnetic fields, a sense called magnetoreception.
This seems to confirm that the mechanism is a visual one, based in the cryptochromes, which may be able to detect the fields because of quantum coherence.
To find more clues on these cryptochromes, two teams of biologists set to work. Researchers from Lund University in Sweden studied zebra finches, and researchers from the Carl von Ossietzky University Oldenburg in Germany studied European robins.
The Lund team measured gene expression of three cryptochromes, Cry1, Cry2 and Cry4, in the brains, muscles and eyes of zebra finches. Their hypothesis was that the cryptochromes associated with magnetoreception should maintain constant reception over the circadian day.
They found that, as expected for circadian clock genes, Cry1 and Cry2 fluctuated daily – but Cry4 expressed at constant levels, making it the most likely candidate for magnetoreception.
This finding was supported by the robin study, which found the same thing.
“We also found that Cry1a, Cry1b, and Cry2 mRNA display robust circadian oscillation patterns, whereas Cry4 shows only a weak circadian oscillation,” the researchers wrote.
But they made a couple of other interesting findings, too. The first is that Cry4 is clustered in a region of the retina that receives a lot of light – which makes sense for light-dependent magnetoreception.
The other is that European robins have increased Cry4 expression during the migratory season, compared to non-migratory chickens.
Both sets of researchers caution that more research is needed before Cry4 can be declared the protein responsible for magnetoreception.
The evidence is strong, but it’s not definitive, and both Cry1 and Cry2 have also been implicated in magnetoreception, the former in garden warblers and the latter in fruit flies.
Observing birds with non-functioning Cry4 could help confirm the role it seems to play, while other studies will be needed to figure Cry1’s role.
New study sheds light on the developmental origins of interneurons
Drawing of the cells of the chick cerebellum by Santiago Ramón y Cajal, from “Estructura de los centros nerviosos de las aves,” Madrid, circa 1905.
Modern neuroscience, for all its complexity, can trace its roots directly to a series of pen-and-paper sketches rendered by Nobel laureate Santiago Ramón y Cajal in the late 19th and early 20th centuries.
His observations and drawings exposed the previously hidden composition of the brain, revealing neuronal cell bodies and delicate projections that connect individual neurons together into intricate networks.
As he explored the nervous systems of various organisms under his microscope, a natural question arose: What makes a human brain different from the brain of any other species?
At least part of the answer, Ramón y Cajal hypothesized, lay in a specific class of neuron—one found in a dazzling variety of shapes and patterns of connectivity, and present in higher proportions in the human brain than in the brains of other species. He dubbed them the “butterflies of the soul.”
Known as interneurons, these cells play critical roles in transmitting information between sensory and motor neurons, and, when defective, have been linked to diseases such as schizophrenia, autism and intellectual disability.
Despite more than a century of study, however, it remains unclear why interneurons are so diverse and what specific functions the different subtypes carry out.
Now, in a study published in the March 22 issue of Nature, researchers from Harvard Medical School, New York Genome Center, New York University and the Broad Institute of MIT and Harvard have detailed for the first time how interneurons emerge and diversify in the brain.
Using single-cell analysis—a technology that allows scientists to track cellular behavior one cell at a time—the team traced the lineage of interneurons from their earliest precursor states to their mature forms in mice. The researchers identified key genetic programs that determine the fate of developing interneurons, as well as when these programs are switched on or off.
The findings serve as a guide for efforts to shed light on interneuron function and may help inform new treatment strategies for disorders involving their dysfunction, the authors said.
“We knew more than 100 years ago that this huge diversity of morphologically interesting cells existed in the brain, but their specific individual roles in brain function are still largely unclear,” said co-senior author Gordon Fishell, HMS professor of neurobiology and a faculty member at the Stanley Center for Psychiatric Research at the Broad.
“Our study provides a road map for understanding how and when distinct interneuron subtypes develop, giving us unprecedented insight into the biology of these cells,” he said. “We can now investigate interneuron properties as they emerge, unlock how these important cells function and perhaps even intervene when they fail to develop correctly in neuropsychiatric disease.”
A hippocampal interneuron. Image: Biosciences Imaging Gp, Soton, Wellcome Trust via Creative Commons
Origins and Fates
In collaboration with co-senior author Rahul Satija, core faculty member of the New York Genome Center, Fishell and colleagues analyzed brain regions in developing mice known to contain precursor cells that give rise to interneurons.
Using Drop-seq, a single-cell sequencing technique created by researchers at HMS and the Broad, the team profiled gene expression in thousands of individual cells at multiple time points.
This approach overcomes a major limitation in past research, which could analyze only the average activity of mixtures of many different cells.
In the current study, the team found that the precursor state of all interneurons had similar gene expression patterns despite originating in three separate brain regions and giving rise to 14 or more interneuron subtypes alone—a number still under debate as researchers learn more about these cells.
“Mature interneuron subtypes exhibit incredible diversity. Their morphology and patterns of connectivity and activity are so different from each other, but our results show that the first steps in their maturation are remarkably similar,” said Satija, who is also an assistant professor of biology at New York University.
“They share a common developmental trajectory at the earliest stages, but the seeds of what will cause them to diverge later—a handful of genes—are present from the beginning,” Satija said.
As they profiled cells at later stages in development, the team observed the initial emergence of four interneuron “cardinal” classes, which give rise to distinct fates. Cells were committed to these fates even in the early embryo. By developing a novel computational strategy to link precursors with adult subtypes, the researchers identified individual genes that were switched on and off when cells began to diversify.
For example, they found that the gene Mef2c—mutations of which are linked to Alzheimer’s disease, schizophrenia and neurodevelopmental disorders in humans—is an early embryonic marker for a specific interneuron subtype known as Pvalb neurons. When they deleted Mef2c in animal models, Pvalb neurons failed to develop.
These early genes likely orchestrate the execution of subsequent genetic subroutines, such as ones that guide interneuron subtypes as they migrate to different locations in the brain and ones that help form unique connection patterns with other neural cell types, the authors said.
The identification of these genes and their temporal activity now provide researchers with specific targets to investigate the precise functions of interneurons, as well as how neurons diversify in general, according to the authors.
“One of the goals of this project was to address an incredibly fascinating developmental biology question, which is how individual progenitor cells decide between different neuronal fates,” Satija said. “In addition to these early markers of interneuron divergence, we found numerous additional genes that increase in expression, many dramatically, at later time points.”
The association of some of these genes with neuropsychiatric diseases promises to provide a better understanding of these disorders and the development of therapeutic strategies to treat them, a particularly important notion given the paucity of new treatments, the authors said.
Over the past 50 years, there have been no fundamentally new classes of neuropsychiatric drugs, only newer versions of old drugs, the researchers pointed out.
“Our repertoire is no better than it was in the 1970s,” Fishell said.
“Neuropsychiatric diseases likely reflect the dysfunction of very specific cell types. Our study puts forward a clear picture of what cells to look at as we work to shed light on the mechanisms that underlie these disorders,” Fishell said. “What we will find remains to be seen, but we have new, strong hypotheses that we can now test.”
Building the bacterial wall: The blue balls are wall-making proteins. The yellow represents a newly synthesized bacterial cell wall. The green color represents “scaffolding” proteins. Video: Janet Iwasa for Harvard Medical School
The wall that surrounds bacteria to shield them from external assaults has long been a tantalizing target for drug therapies. Indeed, some of modern medicine’s most reliable antibiotics disarm harmful bacteria by disrupting the proteins that build their protective armor.
For decades, scientists knew of only one wall-making protein family. Then, in 2016, a team of Harvard Medical School scientists discovered that a previously unsuspected family of proteins that regulate cell division and cell shape had a secret skill: building bacterial walls.
Now, in another scientific first described March 28 in Nature, members of the same research team have revealed the molecular building blocks—and a structural weak spot—of a key member of that family.
“Our latest findings reveal the molecular structure of RodA and identify targetable spots where new antibacterial drugs could bind and subvert its work,” said study senior investigator Andrew Kruse, associate professor of biological chemistry and molecular pharmacology at Harvard Medical School.
The newly profiled protein, RodA, belongs to a family collectively known as SEDS proteins, present in nearly all bacteria. SEDS” near-ubiquity renders these proteins ideal targets for the development of broad-spectrum antibiotics to disrupt their structure and function, effectively neutralizing a range of harmful bacteria.
A weak link
In their earlier work, the scientists showed that RodA builds the cellular wall by knitting together large sugar molecules with clusters of amino acids. Once constructed, the wall encircles the bacterium, keeping it structurally intact, while repelling toxins, drugs and viruses.
The latest findings, however, go a step further and pinpoint a potential weak link in the protein’s makeup.
Specifically, the protein’s molecular profile reveals structural features reminiscent of other proteins whose architecture Kruse has disassembled. Among them, the cell receptors for the neurotransmitters acetylcholine and adrenaline, which are successfully targeted by medications that boost or stem the levels of these nerve-signaling chemicals to treat a range of conditions, including cardiac and respiratory diseases.
One particular feature caught the scientists’ attention—a pocket-like cavity facing the outer surface of the protein. The size and shape of the cavity, along with the fact that it is accessible from the outside, make it a particularly appealing drug target, the researchers said.
“What makes us excited is that this protein has a fairly discrete pocket that looks like it could be easily and effectively targeted with a drug that binds to it and interferes with the protein’s ability to do its job,” said study co-senior author David Rudner, professor of microbiology and immunobiology at Harvard Medical School.
In a set of experiments, researchers altered the structure of RodA in two bacterial species—the textbook representatives of the two broad classes that make up most of disease-causing bacteria. One of them was Escherichia coli, which belongs to a class of organisms with a double-cell membrane known as gram-negative bacteria, so named due to a reaction to staining test used in microbiology. The other bacterium was Bacillus subtilis, a single-membrane organism that belongs to so-called gram-positive bacteria.
When researchers induced even mild alterations to the structure of RodA’s cavity, the protein lost its ability to perform its work. E. coli and B. subtilis cells with disrupted RodA structure rapidly enlarged and became misshapen, eventually bursting and leaking their contents.
“A chemical compound—an inhibitor—that binds to this pocket would interfere with the protein’s ability to synthesize and maintain the bacterial wall,” Rudner said. “That would, in essence, crack the wall, weaken the cell and set off a cascade that eventually causes it to die.”
Additionally, because the protein is highly conserved across all bacterial species, the discovery of an inhibiting compound means that, at least in theory, a drug could work against many kinds of harmful bacteria.
“This highlights the beauty of super-basic scientific discovery,” said co-investigator Thomas Bernhardt, professor of microbiology and immunobiology at Harvard Medical School. “You get to the most fundamental level of things that are found across all species, and when something works in one of them, chances are it will work across the board.”
Solving for X
To determine RodA’s structure, scientists used a visualization technique known as X-ray crystallography, which reveals the molecular architecture of protein crystals based on a pattern of scattered X-ray beams. The technique requires two variables—the intensity of scattered X-rays and a so-called “phase angle,” a property related to the configuration of the atoms in a protein. The latter is measured indirectly, typically by using a closely related protein as a substitute to calculate the variable.
In this case, however, the team had on its hands a never-before-described protein with no known molecular siblings.
“In most cases you can use a related structure and bootstrap to a solution,” Kruse said. “In this case, we couldn’t do that. We had to predict what RodA looked like without any prior information about it.”
They needed a new way to solve for X.
In a creative twist, researchers turned to evolution and predictive analytics. Working with Debora Marks, assistant professor of systems biology at Harvard Medical School, they constructed a virtual model of the RodA’s folding pattern by analyzing the sequences of its closest evolutionary cousins.
The success of this “roundabout” approach, researchers said, circumvents a significant hurdle in field of structural biology and can open the doors toward defining the structures of many more newly discovered proteins.
“These insights underscore the importance of creative crosspollination among scientists from multiple disciplines and departments,” said study first author Megan Sjodt, a research fellow in biological chemistry and molecular pharmacology at Harvard Medical School. “We believe our results set the stage for subsequent work toward the discovery and optimization of new classes of antibiotics.”
When artificial sperm and eggs become a reality, the sex of your baby-making partner won’t matter.
Renata Moreira’s 1-year-old daughter is just beginning to talk. She calls Renata “Mommy,” her other mother, Lori, Renata’s ex-wife and co-parent, “Mama,” and the man who donated the sperm that gave her life, “Duncle,” short for donor uncle. The couple’s sperm donor is Renata’s younger brother.
“I frankly never contemplated having kids because I didn’t have any role models,” Moreira begins as she tells her daughter’s origin story. But when she met Lori at a bar in New York in 2013, the gay marriage movement was in full swing. When the couple decided to marry, they saw many of their friends starting families because of the new legal protections that marriage offered LGBTQ families, and they too began thinking about their options.
After months of research and thinking about the values that were most important to their family, they decided that a genetic connection to their kid was a high priority. “It wasn’t that we didn’t believe in adoption,” says Moreira, who is executive director of Our Family Coalition, a nonprofit that works to advance equity for LGBTQ families. “But the idea was that we wanted a child that was related to our ancestors and the genetic code that carries.”
Moreira is Brazilian, of indigenous and Portuguese ancestry, and Lori is Italian. Given that they both wanted to carry on their genetic heritage, they asked Renata’s brother to donate his sperm, to be matched with Lori’s eggs. The family’s fertility doctor used in-vitro fertilization to conceive an embryo in a dish and implanted it into Moreira’s uterus, making her into her daughter’s “gestational carrier.”
Even as the social stigma around gay parenting lessens — the Williams Institute at UCLA estimates that as many as six million Americans have a lesbian, gay, bisexual or transgender parent — LGBTQ families that want a biological connection to their children have a lot to think about. A same-sex couple who make a baby must work through an arduous puzzle of personal values, technologies, and intermediary fertility doctors, egg and sperm donors, or surrogates.
But that could change dramatically before long. A developing technology known as IVG, short for in-vitro gametogenesis, could make it possible for same-sex couples to conceive a baby out of their own genetic material and no one else’s. They’d do this by having cells in their own bodies turned into sperm or egg cells.
The science of IVG has been underway for the last 20 years. But it really took off with research that would later win a Nobel Prize for a Japanese scientist named Shinya Yamanaka. In 2006, he found a way to turn any cell in the human body, even easy-to-harvest ones like skin and blood cells, into cells known as induced pluripotent stem cells (iPS cells), which can be reprogrammed to become any cell in the body. Until that breakthrough, scientists working in regenerative medicine had to use more limited — and controversial — stem cells derived from frozen human embryos.
There is a small international group of scientists racing to reprogram human iPS cells into sperm and egg cells.
In 2016, researchers at Kyoto University in Japan announced that they had turned cells from a mouse’s tail into iPS cells and then made those into eggs that went on to gestate into pups. There are a lot of steps that still need to be perfected before this process of creating sex cells, also known as gametes, could work in humans.
If it does work, the first application likely would be in reversing infertility: men would have new sperm made and women would have new eggs made from other cells in their bodies. But a more mind-bending trick is also possible: that cells from a man could be turned into egg cells and cells from a woman could be turned into sperm cells. And that would be an even bigger leap in reproductive medicine than in-vitro fertilization. It would alter our concept of family in ways we are only beginning to imagine.
There is now a small international group of scientists racing to recreate the mouse formula and reprogram human iPS cells into sperm and egg cells.
One of the key players is Amander Clark, a stem cell biologist at UCLA. On a Friday afternoon, she walks me through her open lab area and introduces Di Chen, a postdoctoral fellow from China who’s working on creating artificial gametes. We enter a small room with a microscope, a refrigerator incubator, and a biosafety cabinet where students work with iPS cells. Chen invites me to peer down the microscope and shows off a colony of fresh iPS cells. They look like a large amoeba.
Getting cells like these to become viable eggs or sperm requires six major steps, Clark says. All of them have been accomplished in a mouse, but doing it in a human will be no easy feat. (In 2016, scientists reported that they had turned human skin cells into sperm cells, a development that Clark calls “interesting — but no one has repeated it yet.”) And no one has yet made an artificial human egg.
Clark’s group and other labs are essentially stuck on step three. After the steps in which a cell from the body is turned into an iPS cell, the third step is to coax it into an early precursor of a germ cell. For the work in mice, one Japanese researcher, Katsuhiko Hayashi, combined a precursor cell with cells from embryonic ovaries — ovaries at the very beginning of development — which were taken from a different mouse at day 12 in its gestation. This eventually formed an artificial ovary that produced a cell that underwent sex-specific differentiation (step four) and meiosis (step five), and became a gamete (step six).
Other researchers, Azim Surani at Cambridge and Jacob Hanna at the Weizmann Institute of Science in Israel, have gotten to step three with both human embryonic stem cells and iPS cells, turning them into precursors that can give rise to either eggs or sperm. Surani’s former student Mitinori Saitou, now at Kyoto University, also accomplished this feat.
It’s an impressive achievement: they’ve made something that normally begins to develop around day 17 of gestation in a human embryo. But the next step, growing these precursor cells into mature eggs and sperm, is “a very, very huge challenge,” Surani says. It will require scientists to recreate a process that takes almost a year in natural human development. And in humans they can’t take the shortcut used in mice, taking embryonic ovary cells from a different mouse.
At UCLA, Clark refers to the next three steps needed to get to a human artificial gamete as “the maturation bottleneck.”
Those amoeba-like iPS cells that Chen showed me are sitting in a dish that he lifts off the microscope and carries to the biosafety cabinet. There he separates the cells into a new dish, and adds a liquid with proteins and other ingredients to help the cells grow. He puts the cells into an incubator for one day; then he’ll collect the cells again and add more ingredients. After around four days, the cells ideally will have grown into a ball that is around the size of a grain of sand, visible to the naked eye. This ball contains the precursors to a gamete. Clark’s lab and other international teams are studying it to understand its properties, with the hope that it will offer clues to getting all the way to step six — an artificial human gamete.
“I do think we’re less than 10 years away from making research-grade gametes,” she says. Commercializing the technology would take longer, and no one can really predict how much so — or what it would possibly cost.
Even then, same-sex reproduction will face one more biological hurdle: scientists would need to somehow make a cell derived from a woman, who has two X chromosomes, into a sperm cell with one X and one Y chromosome, and do the reverse, turning an XY male cell into an XX female egg cell. Whether both steps are feasible has been debated for at least a decade. Ten years ago, the Hinxton Group, an international consortium on stem cells, ethics, and law, predicted that making sperm from female cells would be “difficult, or even impossible.” But gene editing and various cellular-engineering technologies might be increasing the likelihood of a workaround. In 2015, two British researchers reported that women could “in theory have offspring together” by injecting genetic material from one partner into an egg from the other. With this method, the children would all be girls, “as there would be no Y chromosomes involved.”
Yet another possibility: a single woman might even be able to reproduce by herself in a human version of parthenogenesis, which means “virgin birth.” It could be the feminist version of the goddess Athena springing from Zeus’s head.
The genderqueer nuclear family
The question remains whether society will want this technology — and how often LGBTQ families will choose to use it. Current advanced reproductive technologies are already diversifying the ways we reproduce and opening reproduction to groups who previously may not have had access to it. This is expanding the concept of family beyond the traditional Ozzie and Harriet hetero-nuclear family. Many people who are single parents by choice now include their gamete donors as members. Many LGBTQ families are collaborations of friends and relatives who become egg and sperm donors and help raise the kids.
So it’s understandable that social and legal observers are already thinking about the potential consequences of artificial gametes for the shape of families. If the technology means that lesbian couples wouldn’t need a sperm donor, and gay male couples wouldn’t need a donor egg, it could, among other things, make it “easier for the intended parents to preserve the integrity and privacy of the family unit,” Sonia Suter, a law professor at George Washington University, wrote in the Journal of Law and Biosciences.
A single woman might be able to reproduce by herself, the feminist version of Athena springing from Zeus’s head.
Ironically, however, the technology also could create something rather conventional — a biological nuclear family, albeit one that looks more like Ozzie and Ozzie. “Collaborative reproduction has paved the way for radical new definitions of family, which really helped to lead the movement for marriage equality,” says Radhika Rao, a law professor at UC Hastings law school. “Instead of challenging hetero-normative values, IVG could end up perpetuating them.”
That’s why Renata Moreira isn’t sure she would have chosen it. “It might take away from this great opportunity to challenge and expand the notion of what family looks like,” she says.
But new reproductive technologies are invented to expand our choices more than to limit them, as egg freezing and IVF allow women to pause and even extend their biological clocks. In the coming decades, IVG could let us bend biology to bring together the genetic codes, as Moreira puts it, of people who otherwise can’t. This would increase the freedom to shape our families to meet our personal values and desires, and push human evolution in an altogether new direction.
Light pollution can be problematic for animals like the Cory’s shearwater. Image credit – Airam Rodríguez (Estación Biológica de Doñana CSIC), licensed under CC BY 4.0
You could call it fatal attraction. Drawn by artificial lights in our brightening night-time world, animals find their lives in peril.
Fledgling birds disorientated by lights can collide with human structures on the ground and then get hit by cars, or become more vulnerable to predation, starvation or dehydration. Or newly hatched turtles may set out in the opposite direction to the sea, exposing themselves to similar dangers.
And our skies are getting brighter. A recent study found that our planet’s artificially lit outdoor area grew by about 2% each year between 2012 and 2016, while already lit areas brightened at the same rate.
‘Global growth in lighting at that kind of level is quite profound,’ said Kevin Gaston, a professor of biodiversity and conservation at the University of Exeter, UK. ‘We know that lighting is getting steadily worse.’
Researchers say one big problem has been a lack of awareness about light pollution. That is growing, but in the meantime, certain factors are potentially heightening its impact.
For example, white light-emitting diodes (LEDs) have been swiftly replacing traditional outdoor lighting such as yellow sodium street lights because of their higher energy efficiency. But because they emit light across a broad part of the visible spectrum, LEDs can affect a wider range of photosensitive cells in different organisms.
‘The negative consequences of light pollution are as unknown by the population as those of smoking in the 80s.’
Professor Oscar Corcho, Universidad Politécnica de Madrid, Spain
In a project called ECOLIGHTS FOR SEABIRDS, which ran from 2014 to the end of 2016, researchers found that the threat to fledgling shearwaters of being grounded on Phillip Island in south-eastern Australia was higher from broader-spectra metal halide and LED lights than from sodium lights. This suggests that using certain types of lights in different areas could be used to limit the effects on these birds.
Separate studies on the Spanish island of Tenerife found that half of the Cory’s shearwater fledglings grounded around lights were within 3 kilometres of their nest sites and tended to be from inland colonies.
Dr Airam Rodríguez, a postdoctoral researcher at Doñana Biological Station in Seville, Spain, who worked on the project, said that knowing such information makes it easier to do things such as arrange safe corridors between breeding colonies and the ocean.
Many effects of light pollution on such seabirds have been poorly understood before, because of factors such as their breeding in remote locations and the fact they need to be tracked at night. Advances in technology are helping though, with the team using miniature GPS trackers and nocturnal high-resolution satellite imagery to follow the birds’ routes.
Dr Rodríguez said his team is now using GPS to look in more detail at what happens to birds rescued after being grounded by lights during their first days out on the ocean. He would also like to look more into the physiology of their eyes to find out which wavelengths the birds are more sensitive to.
Another little-known facet has been how much artificial lighting affects whole communities of organisms rather than just individual species, but recent research shows the effects can be significant.
As part of a project called ECOLIGHT, which finished last year, researchers set up 54 outdoor experimental environments, known as mesocosms, at the University of Exeter. These took the form of mesh-covered containers that held different combinations of plants, invertebrates and types of lighting, or were unlit. From this, they discovered that lighting seemed to suppress the flowering of the trefoil Lotus pedunculatus, and, in turn, the pea aphid population that feeds on them.
The team found similar effects in an experiment with bean plants and aphids.
Container-based experiments at the University of Exeter showed that lighting seemed to suppress the flowering of pea and bean plants and affected the aphid population that feeds on them. Image credit – James Duffy
Prof. Gaston, who was principal investigator on ECOLIGHT and also used field experiments to investigate the impact of light pollution, said: ‘This leads to the conclusion that lighting is having pretty pervasive ecological impacts. The effects are exceedingly widespread and are shaping the way that communities are structured – which was something that people hadn’t observed before.’
He also pointed to other research showing that bud burst in trees can happen a week earlier in the brightest compared with the darkest areas. ‘When we’ve discovered these kinds of things for climate change and they’ve shifted by about a week, we’ve said that’s profoundly worrying,’ he said.
His team is now looking more into the impacts of different intensities and colours of lights to build a more detailed picture.
In addition, they are scouring through images of Earth photographed by astronauts on the International Space Station so they can map how the colours of lights are changing as cities introduce more white LEDs.
Prof. Gaston explained that satellites are effectively colour-blind to the shift to white light, so using the pictures that astronauts take is a good way to track this, with about half a million pictures taken at night between 2003 and 2015.
This work complements the Cities at Night project, a citizen science initiative that gets help from volunteers to classify, locate and georeference these pictures.
A composite image of the Earth at night shows changes in light intensity between 2012 and 2016 including, for example, rapid electrification in India. Image credit – NASA’s Goddard Space Flight Center
Also involved in Cities at Night is the STARS4ALL project, coordinated by Oscar Corcho, a professor at the Universidad Politécnica de Madrid in Spain, which acts as a platform to raise awareness of the issues involved in light pollution and inspire further research and better planning in lighting programmes. It seeks to engage people through methods such as games, broadcasting of astronomical events and a citizen-sensor network of low-cost photometers for people to measure light pollution in their area.
‘The negative consequences of light pollution are as unknown by the population as those of smoking in the (19)80s,’ said Prof. Corcho. ‘It’s still a very difficult problem to understand. Light pollution does not have the same immediate effects over animals as other forms of pollution.’
Prof. Corcho said that one of STARS4ALL’s main aims this year is to run a petition on its website to ask for more overarching regulation to avoid light pollution at an EU level. STARS4ALL will collect signatures from citizens and hopes to present the petition in Brussels by the end of the year.
He says the good news is that there are easy fixes. ‘There are good technology options. For instance, there are types of lamps that could be used that are both respectful to the environment in terms of light pollution and at the same time as energy-efficient as white LEDs.’ He cites PC amber LEDs, for example.
If we move to solve these issues, there might well be an added bonus for us all. ‘As an indirect result… our recommendations for public lighting may result in having more populated places where we can see more and more stars in our sky,’ said Prof. Corcho.
The two ‘super-organisms’ seem to follow the same rules.
The human brain follows certain laws, which govern how the complex organ reacts to stimuli and makes decisions. In a new study, scientists argue that super-organisms like honeybees follow the same laws: Like neurons in the brain, they argue, the different bees in a colony coordinate their responses to external stimuli according to strict rules. This discovery suggests, for the first time, that psychological and physical laws don’t just operate in human brains but drive other natural behaviors as well.
In the study, released Tuesday in Scientific Reports, researchers from the University of Sheffield and the Italian National Research Council observe bees to better understand the basic principles that guide these laws. If bees follow the same laws as neurons, then observing them can lead to a better understanding of the human brain. Studying bee colonies, they figure, is simpler than watching the neurons of a brain while a human makes a decision.
“This study is exciting because it suggests that honeybee colonies adhere to the same laws as the brain when making collective decisions,” co-author Andreagiovannia Reina, Ph.D. explained in a statement released Tuesday. “This study also supports the view of bee colonies as being similar to complete organisms or better still, super-organisms, composed of a large number of fully developed and autonomous individuals that interact with each other to bring forth a collective response.”
Most biologists refer to honeybees as super-organisms, wherein the individuals comprising a hive are comparable to the cells that make up a single organism. Working together through structured, cooperative behavior bolsters the hive’s chance for survival. The ability to make decisions collectively has previously been compared to the way a brain’s different parts are involved in cognitive deliberation, but here, the scientists take the analysis a step further by observing how bees make the difficult decision of choosing a nest location for the entire group.
In the spring, colonies of European bees go through a mix-up: Part of the swarm leaves to find the best possible nesting location, while the other half stays behind to protect the queen. After exploring, scout bees return to the hive to recruit other scouts to check out the site, delivering “stop signals.” When the honeybees reach a collective agreement for the same option, the colony moves.
This process became the basis of the researchers’ theoretical model, which led the researchers to determine that the bee colony acts as a single super-organism that then coordinates a response to an external stimulus. They conclude, in the statement accompanying the paper, that “the way in which bees ‘speak’ with each other and make decisions is comparable to the way the many individual neurons in the human brain interact with each other.”
Just as individual neurons in the brain don’t obey psychophysical laws themselves but do so as part of the whole brain, single bees sometimes fire off different signals than the other bees. But regardless, the super-organism still obeys the rules — just like the brain.
And, just like bees, the human brain is known to follow certain rules. Pieron’s Law, for example, states that the brain makes decisions more quickly when the options to choose from are all of high quality. Hick’s Law, meanwhile, shows that the brain makes decisions more slowly when the number of options increases; with their model, the scientists determined that decision-making among bees follows similar guidelines. The colony chooses the location of their new hive more quickly when it has high-quality nest-site options and does so more slowly when the site options are limited.
Then, there’s Weber’s Law, which states that the brain selects the best option when there is a “minimum difference between the qualities of the options.” Like the brain, bee colonies were shown to do the same.
“With this view in mind, parallels between bees in a colony and neurons n a brain can be traced,” says Reina, “helping us to understand and identify the general mechanisms underlying psychophysics laws, which may ultimately lead to a better understanding of the human brain.”
“It’s not that water allows you to be a big mammal.”
Fifty million years ago, whales were four-footed, tailed land mammals about the size of wolves. Over the next 12 million years, these terrestrial whales evolved into fully aquatic animals, complete with oceanic adaptations like flippers and flukes. Today, all of the Earth’s largest mammals live in the sea, including blue whales, considered the biggest animal to have ever existed. For a long time, scientists believed these ocean mammals grew to their modern sizes because the ocean provided them with immense space and the ability to float, but a new study presents an entirely different line of reasoning.
According to a study published Monday in the Proceedings of the National Academy of Sciences, mammal growth is actually more constrained in water than on land. Size in the ocean is bound by hard limits, the scientists from Stanford and Louisiana Universities Marine Consortium explain: Mammals that are too small struggle to retain heat in the cold water, and those that are too large must capture enough food to live.
“Many people have viewed going into the water as more freeing for mammals, but what we’re seeing is that it’s actually more constraining,” co-author and Stanford geological sciences professor Jonathan Payne, Ph.D., explained in a statement released Monday. “It’s not that water allows you to be a big mammal, it’s that you have to be a big mammal in water — you don’t have any other options.”
Payne and his team compiled data sets of the body masses for 3,859 living species and 2,999 fossil mammal species, paying attention to when the mammals turned aquatic and when they became their modern size. They determined a pattern: Once the land mammals became aquatic, they evolved very quickly to their new size until they reached a plateau and stalled growth.
The researchers’ reason that being large means being in charge is because larger mammals are better at retaining heat in water that’s lower than their body temperature. Metabolism, however, increases with size more than the animal’s actual ability to gather food, which puts a limit on how big they can get.
Baleen whales, for example, can be so huge because they spend less energy on feeding. Their mouth contains a filter-feeder system, which means that when a baleen whale opens its mouth, it scoops up water, then pushes it out through its bristle-like baleen. While the water is filtered away, the krill captured in the water remains as a meal. This method allows them to grow larger than mammals that use teeth to munch and capture prey, like orcas.
“The sperm whale seems to be the largest you can get without a new adaptation,” lead author and Stanford Ph.D. candidate Will Gearty explained in a statement. “The only way to get as big as a baleen whale is to completely change how you’re eating.”
What sizes comes down to, the researchers contend, are the basic principles of physics and chemistry. Living in water imposes selective pressures on metabolic rates and size — to be a big boy of the sea you need to live a pretty chill existence so that you don’t waste any precious energy not maintaining your largeness.
There’s one exception, though. The only aquatic mammals that didn’t rapidly evolve to be huge once they entered the sea are the much more manageable-sized sea otters. The scientists theorize that’s because these water-loving mammals took to the ocean relatively recently and, per the study’s accompanying statement, “many otter species still live much of their lives on land.”
Just when we thought octopuses couldn’t be any weirder, it turns out that they and their cephalopod brethren evolve differently from nearly every other organism on the planet.
In a surprising twist, in April last year scientists discovered that octopuses, along with some squid and cuttlefish species, routinely edit their RNA (ribonucleic acid) sequences to adapt to their environment.
This is weird because that’s really not how adaptations usually happen in multicellular animals. When an organism changes in some fundamental way, it typically starts with a genetic mutation – a change to the DNA.
Those genetic changes are then translated into action by DNA’s molecular sidekick, RNA. You can think of DNA instructions as a recipe, while RNA is the chef that orchestrates the cooking in the kitchen of each cell, producing necessary proteins that keep the whole organism going.
But RNA doesn’t just blindly execute instructions – occasionally it improvises with some of the ingredients, changing which proteins are produced in the cell in a rare process called RNA editing.
When such an edit happens, it can change how the proteins work, allowing the organism to fine-tune its genetic information without actually undergoing any genetic mutations. But most organisms don’t really bother with this method, as it’s messy and causes problems more often that solving them.
“The consensus among folks who study such things is Mother Nature gave RNA editing a try, found it wanting, and largely abandoned it,” Anna Vlasits reported for Wired.
But it looks like cephalopods didn’t get the memo.
In 2015, researchers discovered that the common squid has edited more than 60 percent of RNA in its nervous system. Those edits essentially changed its brain physiology, presumably to adapt to various temperature conditions in the ocean.
The team returned in 2017 with an even more startling finding – at least two species of octopus and one cuttlefish do the same thing on a regular basis. To draw evolutionary comparisons, they also looked at a nautilus and a gastropod slug, and found their RNA-editing prowess to be lacking.
“This shows that high levels of RNA editing is not generally a molluscan thing; it’s an invention of the coleoid cephalopods,” said co-lead researcher, Joshua Rosenthal of the US Marine Biological Laboratory.
The researchers analysed hundreds of thousands of RNA recording sites in these animals, who belong to the coleoid subclass of cephalopods. They found that clever RNA editing was especially common in the coleoid nervous system.
“I wonder if it has to do with their extremely developed brains,” geneticist Kazuko Nishikura from the US Wistar Institute, who wasn’t involved in the study, told Ed Yong at The Atlantic.
So it’s certainly a compelling hypothesis that octopus smarts might come from their unconventionally high reliance on RNA edits to keep the brain going.
“There is something fundamentally different going on in these cephalopods,” said Rosenthal.
But it’s not just that these animals are adept at fixing up their RNA as needed – the team found that this ability came with a distinct evolutionary tradeoff, which sets them apart from the rest of the animal world.
In terms of run-of-the-mill genomic evolution (the one that uses genetic mutations, as mentioned above), coleoids have been evolving really, really slowly. The researchers claimed that this has been a necessary sacrifice – if you find a mechanism that helps you survive, just keep using it.
“The conclusion here is that in order to maintain this flexibility to edit RNA, the coleoids have had to give up the ability to evolve in the surrounding regions – a lot,” said Rosenthal.
As the next step, the team will be developing genetic models of cephalopods so they can trace how and when this RNA editing kicks in.
“It could be something as simple as temperature changes or as complicated as experience, a form of memory,” said Rosenthal.
With electrical signals, cells can organize themselves into complex societies and negotiate with other colonies.
Bacteria have an unfortunate — and inaccurate — public image as isolated cells twiddling about on microscope slides. The more that scientists learn about bacteria, however, the more they see that this hermitlike reputation is deeply misleading, like trying to understand human behavior without referring to cities, laws or speech. “People were treating bacteria as … solitary organisms that live by themselves,” said Gürol Süel, a biophysicist at the University of California, San Diego. “In fact, most bacteria in nature appear to reside in very dense communities.”
The preferred form of community for bacteria seems to be the biofilm. On teeth, on pipes, on rocks and in the ocean, microbes glom together by the billions and build sticky organic superstructures around themselves. In these films, bacteria can divide labor: Exterior cells may fend off threats, while interior cells produce food. And like humans, who have succeeded in large part by cooperating with each other, bacteria thrive in communities. Antibiotics that easily dispatch free-swimming cells often prove useless against the same types of cells when they’ve hunkered down in a film.
As in all communities, cohabiting bacteria need ways to exchange messages. Biologists have known for decades that bacteria can use chemical cues to coordinate their behavior. The best-known example, elucidated by Bonnie Bassler of Princeton University and others, is quorum sensing, a process by which bacteria extrude signaling molecules until a high enough concentration triggers cells to form a biofilm or initiate some other collective behavior.
But Süel and other scientists are now finding that bacteria in biofilms can also talk to one another electrically. Biofilms appear to use electrically charged particles to organize and synchronize activities across large expanses. This electrical exchange has proved so powerful that biofilms even use it to recruit new bacteria from their surroundings, and to negotiate with neighboring biofilms for their mutual well-being.
“I think these are arguably the most important developments in microbiology in the last couple years,” said Ned Wingreen, a biophysicist who researches quorum sensing at Princeton. “We’re learning about an entirely new mode of communication.”
Biofilms were already a hot topic when Süel started focusing on them as a young professor recruited to San Diego in 2012. But much about them was still mysterious, including how individual bacteria give up their freedom and settle into large, stationary societies. To gain insight, Süel and his colleagues grew biofilms of Bacillus subtilis, a commonly studied rod-shaped bacterium, and observed them for hours with sophisticated microscopes. In time-lapse movies, they saw biofilms expand outward until cells in the interior consumed the available reserves of the amino acid glutamate, which the bacteria use as a nitrogen source. Then the biofilms would stop expanding until the glutamate was replenished. Süel and his colleagues became curious about how the inner bacteria were telling the outer cells when to divide and when to chill.
Quorum sensing was the obvious suspect. But Süel, who was trained in physics, suspected that something more than the diffusion of chemical messengers was at work in his Bacillus colonies. He focused on ion channels — specialized molecules that nestle into cells’ outer membranes and ferry electrically charged particles in and out. Ion channels are probably most famous for their role in nerve cells, or neurons. Most of the time, neurons pump out sodium ions, which carry a single positive charge, and let in a different number of potassium ions, also with single positive charges. The resulting charge imbalance acts like water piling up behind a dam. When an electrical impulse jolts a neuron’s membrane, specialized channels open to allow the concentrated ions to flood in and out, essentially opening the dam’s floodgates. This exchange propagates along the neuron, creating the electrical “action potentials” that carry information in the brain.
Süel knew that bacteria also pump ions across their membranes, and several recent papers had reported spikes of electrical activity in bacteria that at least loosely resembled those found in the brain. Could bacteria also be using the action-potential mechanism to transmit electrical signals? he wondered.
He and his colleagues treated biofilms in their lab with fluorescent markers that are activated by potassium and sodium ions, and the potassium marker lit up as ions flowed out of starved cells. When the ions reached nearby cells, those cells also released potassium, refreshing the signal. The signal flowed outward in this way until it reached the biofilm’s edge. And in response to the signal, edge cells stopped dividing until the interior cells could get a meal, after which they stopped releasing potassium.
Süel’s team then created mutant bacteria without potassium channels, and they found that the cells did not grow in the same stop-start manner. (The researchers also saw no movement of labeled sodium ions in their experiments.) Like neurons, bacteria apparently use potassium ions to propagate electrical signals, Süel and his colleagues reported in Nature in 2015.
Despite the parallels to neural activity, Süel emphasizes that biofilms are not just like brains. Neural signals, which rely on fast-acting sodium channels in addition to the potassium channels, can zip along at more than 100 meters per second — a speed that is critical for enabling animals to engage in sophisticated, rapid-motion behaviors such as hunting. The potassium waves in Bacillus spread at the comparatively tortoise-like rate of a few millimeters per hour. “Basically, we’re observing a primitive form of action potential in these biofilms,” Süel said. “From a mathematical perspective they’re both exactly the same. It’s just that one is much faster.”
Süel and his colleagues had more questions about that electric signal, however. When the wave of potassium-driven electrical activity reaches the edge of a biofilm, the electrical activity might stop, but the cloud of potassium ions released into the environment keeps going. The researchers therefore decided to look at what happens once the potassium wave leaves a biofilm.
The first answer came earlier this year in a Cell paper, in which they showed that Bacillus bacteria seem to use potassium ions to recruit free-swimming cells to the community. Amazingly, the bacteria attracted not only other Bacillus, but also unrelated species. Bacteria, it seems, may have evolved to live not just in monocultures but in diverse communities.
A few months later, in Science, Süel’s team showed that by exchanging potassium signals, two Bacillus biofilms can “time-share” nutrients. In these experiments, two bacterial communities took turns eating glutamate, enabling the biofilms to consume the limited nutrients more efficiently. As a result of this sharing, the biofilms grew more quickly than they could have if the bacteria had eaten as much as they could without interruption. When the researchers used bacteria with ion channels that had been modified to give weaker signals, the biofilms, no longer able to coordinate their feeding, grew more slowly.
Süel’s discoveries about how bacteria communicate electrically have exhilarated bacteria researchers.
“I think it’s some of the most interesting work going on in all of biology right now,” said Moh El-Naggar, a biophysicist at the University of Southern California. El-Naggar studies how bacteria transfer electrons using specialized thin tubes, which he calls nanowires. Even though this transfer could also be considered a form of electrical communication, El-Naggar says that in the past, he would “put the brakes on” if someone suggested that bacteria behave similarly to neurons. Since reading Süel’s 2015 paper, he’s changed his thinking. “A lot of us can’t wait to see what comes out of this,” he said.
For Gemma Reguera, a microbiologist at Michigan State University, the recent revelations bolster an argument she has long been making to her biologist peers: that physical signals such as light, sound and electricity are as important to bacteria as chemical signals. “Perhaps [Süel’s finding] will help the scientific community and [people] outside the scientific community feel more open about other forms of physical communication” among bacteria, Reguera said.
Part of what excites researchers is that electrical signaling among bacteria shows signs of being more powerful than chemically mediated quorum sensing. Chemical signals have proved critical for coordinating certain collective behaviors, but they quickly get diluted and fade out once they’re beyond the immediate vicinity of the bacteria emitting the signal. In contrast, as Süel’s team has found, the potassium signals released from biofilms can travel with constant strength for more than 1,000 times the width of a typical bacterial cell — and even that limit is an artificial upper bound imposed by the microfluidic devices used in the experiments. The difference between quorum sensing and potassium signaling is like the difference between shouting from a mountaintop and making an international phone call.
Moreover, chemicals enable communication only with cells that have specific receptors attuned to them, Wingreen noted. Potassium, however, seems to be part of a universal language shared by animal neurons, plant cells and — scientists are increasingly finding — bacteria.
A Universal Chemical Language
“I personally have found [positively charged ion channels] in every single-celled organism I’ve ever looked at,” said Steve Lockless, a biologist at Texas A&M University who was Süel’s lab mate in graduate school. Bacteria could thus use potassium to speak not just with one another but with other life-forms, including perhaps humans, as Lockless speculated in a commentary to Süel’s 2015 paper. Research has suggested that bacteria can affect their hosts’ appetite or mood; perhaps potassium channels help provide that inter-kingdom communication channel.The fact that microbes use potassium suggests that this is an ancient adaptation that developed before the eukaryotic cells that make up plants, animals and other life-forms diverged from bacteria, according to Jordi Garcia-Ojalvo, a professor of systems biology at Pompeu Fabra University in Barcelona who provided theoretical modeling to support Süel’s experiments. For the phenomenon of intercellular communications, he said, the bacterial channel “might be a good candidate for the evolutionary ancestor of the whole behavior.”
The findings form “a very interesting piece of work,” said James Shapiro, a bacterial geneticist at the University of Chicago. Shapiro is not afraid of bold hypotheses: He has argued that bacterial colonies might be capable of a form of cognition. But he approaches analogies between neurons and bacteria with caution. The potassium-mediated behaviors Süel has demonstrated so far are simple enough that they don’t require the type of sophisticated circuitry brains have evolved, Shapiro said. “It’s not clear exactly how much information processing is going on.”
Süel agrees. But he’s currently less interested in quantifying the information content of biofilms than in revealing what other feats bacteria are capable of. He’s now trying to see if biofilms of diverse bacterial species time-share the way biofilms of pure Bacillus do.
He also wants to develop what he calls “bacterial biofilm electrophysiology”: techniques for studying electrical activity in bacteria directly, the way neuroscientists have probed the brain for decades. Tools designed for bacteria would be a major boon, said Elisa Masi, a researcher at the University of Florence in Italy who has used electrodes designed for neurons to detect electrical activity in bacteria. “We are talking about cells that are really, really small,” she said. “It’s difficult to observe their metabolic activity, and there is no specific method” for measuring their electrical signals.
Süel and his colleagues are now developing such tools as part of a $1.5 million grant from the Howard Hughes Medical Institute, the Bill and Melinda Gates Foundation, and the Simons Foundation (which publishes Quanta).
The findings could also lead to new kinds of antibiotics or bacteria-inspired technologies, Süel said, but such applications are years away. The more immediate payoff is the excitement of once again revolutionizing our conceptions about bacteria. “It’s amazing how our understanding of bacteria has evolved over the last couple decades,” El-Naggar said. He is curious about how well potassium signaling works in complex, ion-filled natural settings such as the ocean. “Now we’re thinking of [bacteria] as masters of manipulating electrons and ions in their environment. It’s a very, very far cry from the way we thought of them as very simplistic organisms.”
“Step by step we find that all the things we think bacteria don’t do, they actually do,” Wingreen said. “It’s displacing us from our pedestal.”