Cholesterol is a fatty substance that our body produces and acquires through food. Despite its negative image, this molecule is an integral part of most animal bodies. It is an essential component of the membranous packaging of our cells. Cholesterol is also needed to synthesize various vitamins and hormones crucial for the smooth functioning of our body and for the bile necessary for digesting fats. The problem arises when too much of it starts floating around in the blood, clumping together to form plaque on vessel walls and blocking the flow of blood to organs.

Just like oil and water don’t mix, cholesterol also remains insoluble in blood due to its waxy, lipid-like properties. Most vertebrate animals have a system wherein cholesterol is packaged with lipids and proteins called "apolipoproteins" to form small ‘lipoprotein’ droplets that can be easily moved around in blood. Depending on the amount of lipid and the type of protein, these droplets can be ‘low density lipoproteins’ (LDL) or ‘high density lipoproteins’ (HDL). LDL carries cholesterol to the cells which need it, where it attaches with a protein on the cell surface called LDL-receptor (LDLR) and gets engulfed by the cell. Inside, the cholesterol is taken out of the packaging and LDLR is returned to the cell surface. On the other hand, HDL picks up excess cholesterol from all around and takes it to the liver to be excreted out of the body. 

Sometimes, cells do not gulp LDL very efficiently. This could either be because they already have enough of it for cellular function, so they stop decorating their surface with LDLRs. This can lead to high levels in the blood, causing a build-up of plaque on artery walls. If not checked in time, the plaque can grow and plug up the artery. It’s like a really slow pile up of cars on the highway.

Genetic causes like a mutation in the LDLR gene can also cause the transport and uptake of these lipoproteins to malfunction, resulting in a genetic disorder called "familial hypercholesterolemia." Approximately 1 in 250 people suffer from this condition, in which levels of LDL cholesterol in the blood can shoot up to very high values and lead to heart attacks at young ages. Until recently, scientists believed this was true for all vertebrate animals. In a rather serendipitous turn of events, a group of researchers from Brazil and the U.S. discovered an exception that left them astonished. They found that zebra finches, as well as other songbirds, lacked three major regions of the LDLR gene, which possibly made the receptor non-functional, yet did not develop high levels of LDL cholesterol or have any heart related issues.

This is not something the team could have hypothesized out of the blue. The story begins somewhere else entirely. Many animal experiments involve introducing foreign genes into embryos to see the effect on things like animal growth, development, or behavior. This is regularly done using viruses engineered with the gene one wants to insert. Engineered viruses decorated with a protein called Vesicular Stomatitis Virus G-protein (VSV-G) are a common tool used to manipulate avian embryos. Zebra finch eggs are notoriously resistant to such virus-aided gene expression. The authors were interested in finding out why. “I’ve had to inject probably 6000 eggs, if not more, [in the course of my research]," said Tarciso Velho, a neurobiologist at Federal University of Rio Grande do Norte in Brazil and the lead author of the study. "I've been trying for several years to make transgenic zebra finches, but it has been difficult. We never quite understood why.”

In 2014, a study described how the VSV-G protein attaches to LDLRs and enters the cells. All cells which did not have any low density lipoprotein receptors showed resistance to the entry of the virus. This was the perfect starting point for understanding the poor infection rates in zebra finch embryos. The authors combed the finch genome to see if the LDLR gene was present. They found it, but saw that it was missing big chunks important for placing the receptor on the surface of the cell an interaction with G-protein. Essentially, they’d hit the jackpot in their quest. To make sure that this divergent receptor was the reason for the poor infection rates, they introduced the full human low-density lipoprotein receptor, or LDLR, into the finch eggs and then tried introducing the virus with the G protein. These engineered eggs showed a remarkable improvement in expression of the virus-aided genes, proving that the variant LDLR was responsible for the resistance.

But what perplexed the authors was how these birds remained alive and healthy without receptors to clear low-density cholesterol from their blood. They examined the lipoprotein levels of the birds and found that they had no low-density lipoproteins at all. All of their cholesterol was bound to high-density lipoproteins.

No LDLR, no LDL, no plaque build-up, no problem, right? Not quite. Zebra finch cells have the same need for cholesterol as other animals, or at least that’s the assumption for now. What transports it for them? “We still have no idea," Tarciso told me. "This is something we're super curious about. The cholesterol must be (transported) to the peripheral tissue somehow via HDL.” So, then what is this variant LDL receptor even doing? “We don't quite know if this receptor is capable of actually taking up cholesterol or not. This is something that we're pursuing, by putting the receptor into a cell and seeing how it behaves and what it's capable of.”

These surprising findings tell us that even the most conserved and canonical biological processes can be altered, given the right mix of evolutionary pressures. It’s quite possible that songbirds or their common ancestors lost these receptors as a way to develop resistance against VSV infections, and in doing so, developed a unique system of cholesterol transport. This opens up a host of new avenues to pursue in the attempts to treat the genetic causes of high cholesterol in humans. “Now we know there are different ways to transport cholesterol," Tarciso said. "If we could precisely identify the mechanism and a common receptor that is performing this role, [we] could direct cholesterol transport to that, instead of LDLR.” Though controversial, using genetic approaches such as CRISPR to re-route the movement of cholesterol in patients lacking the necessary receptor could make medication for this condition obsolete.

There’s a ton of work to be done before we fully understand the mysteries of songbird cholesterol. But there’s also much to look forward to during the journey. Unexpected changes in direction, like this one, are the basis on which many serendipitous discoveries stand. As Tarciso puts it, “the unexpected things, how science takes you on turns that you're completely unprepared for,” those are what push you to ask questions like, ‘What can I learn about my body from studying this tiny bird?’

Every morning, I would rush to the lab to see if my fish had laid eggs. I watched the brain cells of these completely transparent organisms multiply under the lens. I still remember the first time I saw a live neuron grow in front of my eyes, in the brain of a young fish larva. This striped tropical fish could fit in the palm of my hands, and yet is one of the most important organisms in biology, allowing researchers to answer fundamental questions in neuroscience, developmental, cancer, disease and regenerative biology.

The beginnings of zebrafish research can be traced back to early 1930s when Charles Creaser at Wayne State University in Detroit began using zebrafish (Danio rerio) eggs to show students the development of a live embryo and the movement of blood inside its arteries. Creaser was able to do this because zebrafish females release eggs from their body which are fertilized by the sperm released from the male. The freshly formed embryo is accessible to the observer from the moment it is fertilized. The fact that zebrafish embryos and larvae are transparent means studying the internal parts of the animal is a breeze. Creaser established methods for rearing, feeding and breeding zebrafish in the lab, but widespread use of the animal did not take off for another three decades.

Like Mendelian genetics, zebrafish had to be rediscovered. In the late 1930s, George Streisinger and his family moved across the Atlantic in an attempt to escape the anti-Semitic living conditions of 20th century Hungary. Streisinger's passion for science got him a job under Myron Gordon, one of the fish researchers at the New York Zoological Society.

Streisinger dedicated almost two decades of his career to studying the genetic code of viruses that infect bacteria, called bacteriophages. He used these viruses to decipher the way genetic material is coded in living beings. Despite having made such fundamental contributions to science using phages, Streisinger wished to switch to a different system. He aspired to understand the developmental of the nervous system in vertebrates, especially how neurons find their partners and make connections. At this time, in early 20th century, animals such as medaka fish and goldfish were the go-to choices for researchers interested in understanding development. But Streisinger went another way. “The story goes that he walked into a pet store in Oregon, and asked the owner, ‘what’s a good simple vertebrate that I could study?’ and the owner pointed at zebrafish. At least that’s what fishlore says," recounts Karuna Sampath, a professor studying control of embryo development at Warwick Medical School.

Having already worked with zebrafish at the Zoological Society in New York, he was aware of the immense potential the fish held for biology experiments. When he joined the University of Oregon in 1960, Streisinger jumped headfirst into generating mutant fish strains. His initial lab was a converted army barrack, inside which he and his colleague Charlene Walker reared zebrafish in tanks. Zebrafish are naturally found in tropical climates of South Asia and can only survive in temperatures from 24°C-38°C, which meant that Streisinger and Walker had to get creative in maintaining the temperature of the hut at a sweet spot. In summer, water was poured on the roof to keep things cool, while in winter, electric heaters kept the hut toasty. Things soon started to pick up. In the two decades that Streisinger dedicated to zebrafish research before his death, he not only worked on deciphering neuronal development in the fish brain, but also set up techniques for linking mutations in the fish genome to changes in the fish’s appearance.

Streisinger’s goal of bringing zebrafish up to par with model systems of the likes of Drosophila and rodents was carried to fruition by the army of colleagues he had inspired. Zebrafish's ease of maintenance and breeding, year round supply of embryos, external fertilization giving access to embyros from hour zero, and transparent young stages of development makes observation easy. But to really put the animal over the top, it was important to show that it was amenable to mutations, a key tool for biologists.

That’s exactly what Christiane Nusslein-Volhard at the Max Planck Institute in Tubingen and Wolfgang Driver at Massachusetts General Hospital did. They spearheaded the "Big Screen," spread across multiple labs over the two continents, to produce about 4000 fish strains, each of which had a different aspect of early development disrupted. The result of this massive project was published as a collection of 37 papers in a single issue of the journal Development, finally announcing to the academic world that zebrafish was here to stay. On the heels of this accomplishment came the sequencing data of the entire zebrafish genome in 2001, which gave the community the ability to pick out the genes and match them to the changes observed in the big screen fish mutants.

What began as an animal picked up from the local aquarium is now an established vertebrate model system used across thousands of labs to answer questions about the formation of the nervous system, evolution of behaviors, development and treatment of cancers, regeneration of tissues and much more. One can actually look at the activity patterns of every cell in the entire zebrafish brain while the fish swims around. You can screen thousands of candidate drugs by just dumping them into the water with the fish and watching what happens.

“It's a good balance of being simple enough to get a holistic understanding of mechanisms underlying behaviour, while at the same time sharing a lot of conserved similarities in terms of anatomy, genes, molecules, that you can link to mammals and to humans”, says Caroline Wee, a neurobiologist lab at the Institute of Molecular and Cell Biology, A*STAR Singapore.

Julien Vermot, who runs a lab at the Department of Bioengineering, Imperial College London uses these fish for something unique. To study the effects of mechanical forces on the development of the heart, students in his lab stop the zebrafish heart from beating for as long as a couple of days. It’s one of very few animals that can survive this. Despite such unique advantages, the model isn’t everyone’s first choice and certainly not as popular as mice or rats. As Vermot puts it, “It's a fish. And we are not fish. So, you need to convince people that what you do is meaningful for the entire community.” Wee adds, “You can argue they're similar, but it's hard to mentally draw the link between fish and humans.”

While the connection between zebrafish research and humans may not be obvious, the benefits for them are. Rita Fior, group leader at the Champalimaud Centre for the Unknown has shown how these animals can be used to test chemotherapy treatments for cancers growing in actual human patients. Fish injected with cancer cells from patients and given the same treatment as the patient show 84% similarity in the response to the drugs. This sets up precedence for potentially screening drug combinations in fish to look at their efficiency in reducing growth of cancerous cells before administering them to patients.

An exceedingly rare species of orchid, Disa forficaria, found in southern Africa, does not produce nectar. Yet, it is reliably visited by males of the longhorn beetle, Chorothyse hessei, which carry away its pollen packets attached to their underside. Before they depart, though, the beetles exhibit vigorous copulatory behavior perched on top of the orchid flower. They bite the furry antennae-like petals and extend their aedeagus — an arthropod equivalent of a penis — to fit into a floral notch. These visits often end in ejaculation, with sperm being deposited at the floral tip. The beetles are under the false impression that the orchid flowers are females of their species. But why?

Callan Cohen, from the University of Cape Town, who first observed this behavior in the longhorn beetles, investigated the reason behind this unusual sexual encounter. He separated the chemicals released by the orchid flower and tested the response of the beetle antennae, an organ which they use to detect odors, to each of them. One of these compounds, named "disalactone", produced electrical responses in the antennae of all tested individuals. The odor molecule was exceedingly attractive to male beetles, so much so that disalactone beads treated with it not only drew in the beetles, but also enticed them to try and mate with them. While it is presumed that the scent must be the same as that of female longhorns, until scientists catch and examine one, we won’t know for sure.

D. forficaria plants are so scarce that only 11 sightings have been recorded in over 200 years. Last observed in 2019 in the study region, it was thought to be extinct. But this new research shows it is still out there, budding and thriving.

What would happen if you were swallowed whole? Trapped in the pitch black confines of the stomach, with acid squirting from all directions, pushed down and churned by gut muscles, you might be completely digested. But some animals deceive fate, escape towards the light at the end of the intestinal tunnel, and burst out to freedom from the butt.

Consider the land snail. A common and popular prey, it's hopelessly incapable of escaping attacks. Instead, it has developed other defenses like cryptic coloration, withdrawal into its shell, and irritating smell and taste to prevent predation. But its most fascinating survival tactic is coming out alive from the butt of predatory birds. 

In 2012, Shinichiro Wada reported that the land snail Tornatellides boeningi, found in the Hahajima Island in the western Pacific, could survive being swallowed by the Japanese white-eye bulbul and the brown-eared bulbul. Both predators were fed adult snails approximately 2.5mm in shell height. Once the birds had their fill, they rewarded the researcher with a load of data. Wada observed that around 15% of the fed snails passed through the gut alive, were active after their grand escape and survived for at least 1 week after the experiment. Some even gave birth to baby snails after emerging alive from the birds’ intestines.

The tiny proportions of T. boeningi seem to play an important role in the smooth passage of the animal through the gut. Sifting through the poop of other birds on the island showed that remains of larger snail species were always seriously damaged. That small size allowed the shell to remain intact despite the many crushing and cracking parts in a bird’s digestive tract. The whole shell, along with the copious amounts of mucus produced by the snail, could have helped keep the stomach acids from reaching the snail's body. But that’s not all animals need to survive. 

How does the snail breathe in there? Some species of mud snails can survive in waters with little to no dissolved oxygen for nine days or even more. They store gas bubbles in a small cavity, air from which is used in times when oxygen availability is low.

At face value, the act of passing through the gut doesn't seem pleasant. But it comes with perks. Wada and team show that snails might use this journey for their dispersal across the island. They also suggest that passing through the gut may be a cue to give birth in T. boeningi, which may enhance the probability of colonization success at the site of deposition. It's similar to how berry seeds use ingestion by birds to their benefit.

Aquatic mollusks also show great proficiency in butting out of painful situations. Randy Brown, a scientist at the US Fish and Wildlife Service in Fairbanks, Alaska, collected wild, freshwater fish and saw that pea clams and valve snails are abundant in their feces, surviving the passage through the fishes' guts. Many emerged clams opened their shells and extended a foot, and snails emerged from their shells and began moving about. Valve snails have a chalky disk, which they use to seal their shell shut when withdrawn inside.

As prey evolve newer ways to shield themselves, predators also evolve strategies to counter their moves. The spinynose sculpin fish, Asemichthys taylori, has a solution to tear down the hard exterior of a mollusk. In 1988, Stephen Norton at UC Santa Barbara reported that these fish use their teeth to “punch” holes in the shells of their prey, making them more digestible. Norton observed that more 40% of the unpunched mollusks emerged alive from the fish intestines, but none of the punched individuals survived. What was truly fascinating was that the fish could adjust its punching behavior. When given limpets, a prey which has a protective shell but no covering over the shell's exit, fish never resorted to punching. All swallowed limpets, despite being unpunched, did not survive, because the digestive juices could enter beneath the shell. This shows that the fish reserved their energy for punching only when it was absolutely essential.

Copepods, tiny crustaceans found in fresh and marine waters, are also heavily preyed on by many fish species. Many can out-swim predators, but females carrying heavy egg sacs do not have that advantage. But that doesn’t stop them from passing on their genes. Even if the female is eaten and digested, the eggs survive the harsh environment of the fish digestive tract and hatch to produce copepod larvae. Copepods even produce two different kinds of eggs: subitaneous, which hatch soon after spawning, and resting, which have a durable outer shell, designed to survive for long periods. Surprisingly, both types emerge alive out of fish butts. Many copepods which do not produce resting eggs could use this strategy to disperse their larvae using fish as agents. 

Many insects also make a back door exit, using their predators for their dispersal needs. Megastigmus wasp females lay eggs into the seeds of rose plant, which develop into larvae and eat up the soft interiors of the seed. These larvae remain alive even when the rose seeds are consumed and defecated by mockingbirds. Feeble fliers, Megastigmus wasps depend on surviving the gut environment of birds so they can reach and colonize different geographical locations. The hard coating of the seed protects the insects from being digested. Once excreted, the adults chew open the coat and emerge. 

Nematode worms hitchhike on many of their predators to reach far and wide places. In 2015, Carola Peterson and colleagues reported frequent occurrence of living Caenorhabditis elegans worms in the intestines of slugs, even when the slugs were taken from places not suitable for the worm. This led them to speculate that the worms were picked up somewhere else and persisted in slug guts for some time. They tested their theory by feeding fluorescent worms to slugs and looking at the number of worms present in the feces at different times. Still living worms began emerging within a scant 12 hours. Most emerged worms also reproduced later. 

When faced with stress, C. elegans adopt a resting state called "dauer." Peterson observed that most of the worms in the intestine were dauers, which suggests they might be better equipped to survive being eaten and come out the other end alive. Certain characteristics of dauer larvae help make more sense of these observations. These larvae can survive losing 98% of their water by dramatically increasing the quantity of a sugar called "trehalose" in their body. Trehalose helps maintain cell membrane structure and integrity in such conditions. A spike in trehalose levels in dauer larva could give it the means to survive the acidic, low water environment of the slug insides if it got gobbled up.

But what if I told you that sometimes dauer larvae seem to want to get eaten? These worms usually only move two dimensionally, crawling away their whole life, until they turn dauer. Dauer larvae start to lift off the ground, hoist their body vertically, and do a sort of dance. This behavior, called nictation, is thought to increase their chances of being preyed on by animals. Sort of like a giant arrow pointing to the worm. Worms do this only when their food source depletes or they face difficult climates, so as to get transported to a more favorable arena. They take charge of the intestinal reigns and orchestrate their own butt escapes.

To treat neurodegenerative diseases, scientists can create new neurons from stem cells. In no time, new neurons can replace lost ones, and take over their job. A glaring drawback of this method is that these cells are formed outside the body and need to be transplanted into the brain. To date, this is the preferred method to repopulate lost neurons, but it’s far from ideal.

Transferring lab grown neurons into animal brains reduces the cells' viability — their chances of integrating well into the tissue — and the efficiency with which they can restore function. So scientists at Shanghai Research Center for Brain Science and Brain-Inspired Intelligence fashioned a method to regenerate neurons inside the brain. The method is similar to how one would revive a dying plant: by nurturing it with the right conditions for it to grow new leaves.

Building up on a previous study, Haibo Zhou, a postdoctoral researcher in Hui Yang’s lab, and colleagues, set up a method to convert non neuronal brain cells called “glia” into neurons. They did this by turning down a gene called PTBP1 in glia of different parts of the mouse brain, using the gene-editing tool CRISPR. Depending on which brain region was targeted, the glia gave rise to different kinds of neurons.

Reducing PTBP1 levels presumably reverted glia to unspecified stem cells, which adopted varied neuronal identities based on which glia were targeted and the environmental signals they received. This was evident from the team’s successful attempts at restoring two different types of neurons and alleviating the symptoms associated with the loss of each.

Parkinson’s disease occurs due to loss of dopamine-producing neurons and manifests as tremors, stiffness, and loss of balance. To test their method in rejuvenating this group of neurons, the team first got rid of them using a toxic compound in mice. The authors then converted glia into dopamine-producing neurons, and the new cells showed the same activity as their original counterparts. 

This rescue was not limited to just the neuron population. It also partially restored the normal motor behavior of the animal. This is a huge step forward from drug induced alleviation of symptoms because it puts forth a more permanent solution.

The team also tackled retinal diseases caused by death of retinal ganglion cells, or RGCs, which leads to permanent blindness. Turning down PTBP1 in glia of the retina transformed them into RGCs. Astoundingly, these renewed neurons not only responded to light independently, but also sent their projections to the visual cortex correctly, restoring circuit function. This led to a partial recovery of eyesight in the treated mice.

The outcomes from this study are surprising in many ways. Neurons in different regions of the brain vary a lot in their shapes, activity, function, and connectivity. Neurons in young animals acquire these characteristics because of the multitude of developmental signals they receive. These cues might or might not be present in the adult brain. How do the reprogrammed neurons pull this off in the absence of such cues? 

“Maybe the signals still exist in the mice at 8 weeks old. It’ll be very interesting to identify the instructive signals underlying glia-to-neuron conversion in the future”, Yang said in an email. Looking at natural regeneration in animals like zebrafish, where a similar mechanism of glia-to-neuron transformation is observed, could give us hints to what these signals might be.

The high efficiency and flexibility of this technique are appealing. But, given the notoriety CRISPR-based gene editing has garnered in the recent years, the safety of translating the technology into other methods is an open question. How will researchers ensure the system only edits the correct gene? How would one stop the editing once neurons are regenerated?

The authors chose to reduce the levels of PTBP1 by targeting the RNA, rather than DNA. For this they chose Cas13d because it's small, easy to deliver to the cells, yet highly specific and efficient in its action. Compared to conventional tools like Cas9, it's a significant improvement.

According to Yang, CRISPR RNA editing is safer than DNA editing since expression of Cas13d is turned down once neuronal conversion is complete. Unlike DNA editing, which alters the genetic makeup of an animal permanently, RNA editing affects the expression levels of specific genes, temporarily.

“We are now working on monkey model using this approach," Yang says. "Hopefully, we could apply this approach in humans in three to four years.”

If meticulously designed experiments provide evidence for safe therapeutic use in humans, it might open doors for using this method to generate various other cells of the body as well. Treatment options for disease like diabetes and sickle cell anemia could be well within reach. But that is a story for another time.

To find robust methods of pain relief, we need to understand how our bodies resolve pain naturally and how that process is disrupted in case of chronic pain. In a recent study (currently posted as a pre-print) by scientists based in the Netherlands and the US, researchers unraveled how immune cells, called macrophages, relieve pain caused by damage to sensory cells. 

Macrophages are known for their ability to ‘eat’ foreign particles in our body. They also play a substantial role in both the initiation and mitigation of pain. Two types of macrophages are involved in these processes: M1 and M2. The former initially crowd around a wounded area, causing inflammation and pain. As the wound heals they are then replaced by M2 macrophages, which ease these symptoms. The researchers found that an imbalance in the levels of these two types of macrophages can cause chronic pain. 

The way that M2 macrophages alleviate pain is fascinating. A wound disrupts the energy-producing cellular machinery, called mitochondria, of surrounding sensory cells. M2 macrophages actually transfer their own mitochondria into the affected cells in small balloon-like structures, easing the pain sensation. This suggests that therapies aimed at increasing the mitochondrial transfer from M2 macrophages into cells around our wounds, giving them a jolt of energy, could help relieve chronic pain.

Many mammals (like rodents and bears) and birds (like hummingbirds) have the amazing ability to undergo ‘torpor’, during which they slow down their bodily functions to conserve energy. Animals make use of this to survive harsh environmental conditions. However, the mechanism by which animals sense the surrounding temperature and exhibit such a response is not known.

Researchers from Yale University explored this in a recent study published in eLife. They describe how a group of cells called POA neurons in the hypothalamus region of the mouse brain sense cold and get activated to relay the signal forward. 

To understand what sets POA neurons apart from other cells, the scientists looked at the different components they are composed of. All neurons receive information with the help of small pores on their surface, which open only when their partner molecule sticks to them. What makes POA neurons special is the abundance of one such pore, which becomes increasingly likely to open as temperatures drop and it becomes more attracted to its partner. Once open, it allows the neuron to become active and pass on the message. The property of the pore to unlock for low concentrations of the partner molecule at cold, but not warm temperatures, is what makes it a cold sensor.

Findings from this study shed light on one possible mechanism of cold temperature sensing. But in order to fully understand how animals survive frigid conditions, we still need to tease apart the steps from sensing temperature to regulating it.

Every time you eat a bowl of vegetables or fruit, chances are you have a bee to thank for it. 35% of the world’s food crops depend on pollinators like honey bees, bumblebees, stingless bees, butterflies, hummingbirds, wasps and many others. Despite being so valuable, they face unprecedented extinction rates from human actions. Something that each of us can do to combat this is to not only educate others on the contributions of pollinators, but to shed light on how incredibly cool they are.

In that spirit, let me tell you a few things about honey bees that will leave you amazed. 

Honey bees have one of most unique communication systems. When a bee finds a nice, juicy flower patch, it tells its nest mates by doing a waggle dance. This dance relays the location (direction and distance) and perceived quality of the nectar source. Varying dialects of the waggle dance are used by different honey bee species to accommodate for different foraging ranges, likely dependent on food availability in their environment.

Honeybees, as well as a few other species, also have a distinctive way of reproducing called "haplodiploidy". Male drones develop from unfertilized eggs and female workers from fertilized ones, and one queen lays all of them. But in one sub-species called Apis mellifera capensis, the workers also lay unfertilized eggs, which develop into daughters. Years after its description, scientists recently discovered the gene responsible for biological anomaly. 

All of this only scratches the surface of honey bee biology and comes from decades of research. Unfortunately, studies on other bees are grossly lacking. But with pollinator populations dwindling, it’s crucial that we learn as much about them as possible to come up with better solutions for their conservation.

Researchers from the lab of Giorgio Vallortigara have shown that zebrafish do in fact use ordinal counting in order to get to a “reward." Ordinal counting keeps track of a position (as in, the second door out of seven), as opposed to cardinal counting, which tracks an amount ("there are seven doors"). Zebrafish were trained to exit an arena with seven identical exits in a corridor, using only the second exit. This was done by blocking the other exits with a clear sheet of plastic. On the other side of the corridor was a reward of food and other fish. If the fish swam towards other exits, they did not receive any reward. But what happens when all doors are up for ‘swims’? 

Post training, the fish were tested by decreasing the length of the corridor, decreasing the distance between exits, or increasing the number of exits. In the first two experiments, they chose the second exit with a frequency greater than random chance, indicating that they were in fact “counting” to choose which exit to use.

In the last experiment, along with choosing the second exit significantly more than the others, they also chose the second-to-last exit (second from the other end of the corridor) more than chance level. The higher numbers seemed to "confuse" the fish. In such contexts, the fish switched to using spatial feedback, along with ordinal information, to increase their chances of getting lunch with their pals.

Although evidence of numerical skills has been reported in birds, amphibians, mammals and even insects, studying it in a well-established model system like zebrafish opens up avenues to decode the mechanisms underlying this behaviour.