Banded Mongoose: mutualism, cooperative breeding, and vital adaptations

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 Banded mongooses in Kruger National Park, South Africa (Peet van Schalkwyk ©)

“It is the hardest thing in the world to frighten a mongoose, because he is eaten up from nose to tail with curiosity. The motto of all the mongoose family is ‘Run and find out'” —Rudyard Kipling, Rikki-Tikki-Tavi

Cultural inheritance in banded mongooses

The banded mongoose is a bit of an anomaly in the mammal world. Instead of the offspring being raised by their parents (and behaving similarly to their parents), they instead inherit their behaviors from other adult mongooses. The adults are random, rather than closely related to the offspring, but take on a parental role in the sense that they sort of “adopt” a baby/juvenile (about one month old) and show it how to forage, hunt, stay safe from predators, and otherwise be a mongoose properly. These role models or “escorts” will carry around the pups and teach them closely for about two months. The plasticity of mongoose behavior is sufficient to allow for pups to behave more similarly to their role models than to their parents.

This kind of transmittance of behavior is known as cultural inheritance, and is actually quite common in the animal world– but the unique setup in mongooses provides an opportunity to easily decouple the direct genetic inheritance from parents and the cultural inheritance resulting from behavioral plasticity (social learning).

Cultural evolution is becoming one of the most popular topics in biology as more and more scientists are beginning to notice how new behaviors can sweep through a population in less than a generation. The classic non-human example of this would be humpback whale songs changing year to year.

While cultural evolution occurs more quickly than genetic evolution in one sense, it also allows for genetic diversity to persist. Higher behavioral plasticity results in higher variety of trait and higher variety of preference for those traits. It can actually slow down evolution towards physiological adaptation for an environment by slowing the adaptation of physiological change. That being said, it can allow for more rapid adaption and by relying on social learning, only one or a few members of a population need to “discover” a new behavior for it to spread through the population.

It’s possible the mongooses have evolved this escort system as a way to maintain diverse foraging methods and reduce competition in their groups. Maintaining plasticity in foraging behaviors would be useful for social animals that have a wide variety of food sources, as the mongoose does.

Timon and Pumbaa: based on a true story

p02bk7tkSo admittedly Timon is a Meerkat not a banded mongoose, but it’s the same family so it’s close. In a cool example of mutualism, Warthogs (which, by the way, are awesome animals and don’t get nearly enough love) can rid themselves of ticks and bugs by getting groomed by mongooses.

Warthogs–which should look kind of scary to a small mongoose, actually get along quite well with them. Wild pigs tend to have quite a few ectoparasites and bugs inhabiting their skin/fur which can provide an easy snack for the banded mongoose. Warthogs have learned to lay down when mongooses are nearby, so they can pick off the parasites. Besides allowing mongooses to groom them, they also welcome vervet monkeys to snack on their ticks.

Mutualism between mammals is somewhat rare, but wild pigs and mongooses (and vervets for that matter) are highly intelligent and it shouldn’t come as much of a shock that they are able to enjoy the company of other species.

Mutualistic foraging between dwarf mongooses and hornbills

In another species of mongoose, the dwarf mongoose of the Taru desert often cooperatively forages with large birds, particularly hornbills, who share the same prey. The hornbills will wait to start foraging around termite mounds if the mongooses are sleeping and the mongooses will wait for the hornbills to be nearby to begin their foraging. This is true mutualism, as, while many animals have instances of exploiting each other’s coincidental presence for their benefit, the hornbills and dwarf mongoose actually plan their foraging activities around the other.

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The mongooses and the hornbills will warn each other of predators while they forage. The hornbills will even warn the mongooses when there are predators nearby that do NOT prey on the hornbills. The hornbills recognize predators specific to the mongoose as they will not warn against predators that do not prey on the mongoose. This is a pretty unique relationship as most cases of mutualism do not involve so much complex compensative behavior between species. The two species will communicate to one another with different vocalizations, and hornbills will sometimes wake up the sleepy mongooses when they’re impatiently waiting to start snapping up unfortunate insects.

Convergent evolution of neurotoxin resistance

Mongooses are mostly known for fighting cobras (partly because they’re exceptionally quick) but their resistance to the alpha-neurotoxin in cobra venom is what especially allows for this feat.

Acetylcholine is a very important neurotransmitter, so there are acetylcholine receptors all over your muscle cells that need to be free to bind (or not bind) acetylcholine, allowing your muscles to expand/contract. This neurotoxin, called alpha-bungarotoxin (alpha-BTX), works by binding to these acetylcholine receptors and blocking them up resulting in paralysis and eventually death. However the mongoose, the snakes themselves, and several other animals have independently evolved to alter the shape of their acetylcholine receptors so the neurotoxin, alpha-BTX, doesn’t bind.

Tweaks to the nicotinic acetylcholine receptor to prevent snake neurotoxin binding have been shown to have evolved at least four separate times in mammals (the honey badger, pigs, mongooses, and hedgehogs), but in the mongoose, the tweak involves a glycosylation site on the receptor matching the site present in snakes.

Syncing up birthdays

Despite being highly social and altruistic, meerkats are a more vicious member of the mongoose family and are especially well known to participate in infanticide. As meerkats live in a matriarchy with intense dominance hierarchies, many babies do not stand a chance from more dominant pregnant females. Banded mongooses however, have managed to evolve to sync up their birth so they’re all born on the same day. This prevents infanticide as all females are on essentially identical schedules (hormonally and in how they spend their time), so pups are never left alone with other females.

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Photo credit: Feargus Cooney

While most mammals have adapted to differentiate their own offspring very well, the banded mongoose benefits from having all pups be treated equally by the adult mongooses. Syncing up birth to the day or few days is a useful strategy, also seen in flamingos, where both male and female flamingos will even produce and feed crop milk to young who are not their own. However unlike flamingos, syncing up birthdays seems to be more about preventing infanticide and having a more lax dominance hierarchy.

This is a pretty unique strategy as usually species tend to fall on a continuum of high to minimal parental care. In this case, the banded mongoose receives a lot of “parental care” but not necessarily much from their parents. In almost all of nature, the level of paternal parental care is based on certainty of paternity, yet the mongoose has no idea who its close kin are. The behavior where a species mentors and takes care of young they know are not their own is, of course also seen in humans. Mongooses are exceptional in their array of cooperative behaviors– displaying reciprocity, altruism, cooperative breeding, and mutualism. But knowing humans, most will probably continue to believe we are special and entirely disconnected from these evolutionary adaptations.

Sources:

  1. Dwarf mongoose and hornbill mutualism in the Taru desert, Kenya. O. Anne-E. Rasa – Behavioral Ecology and Sociobiology – 1983
  2. How the mongoose can fight the snake: the binding site of the mongoose acetylcholine receptor. D. Barchan-S. Kachalsky-D. Neumann-Z. Vogel-M. Ovadia-E. Kochva-S. Fuchs – Proceedings of the National Academy of Sciences – 1992
  3. Decoupling of Genetic and Cultural Inheritance in a Wild Mammal. Catherine Sheppard-Harry Marshall-Richard Inger-Faye Thompson-Emma Vitikainen-Sam Barker-Hazel Nichols-David Wells-Robbie Mcdonald-Michael Cant – Current Biology – 2018
  4. Reproductive competition and the evolution of extreme birth synchrony in a cooperative mammal. S. Hodge-M. Bell-M. Cant – Biology Letters – 2010
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Bioluminescence- the immense diversity of organisms that glow

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Bioluminescence is a beautiful evolutionary phenomenon which has aided organisms in defending against predators, attracting mates, attracting prey, communicating, and even coping with metabolic stress. A ton of groups contain bioluminescent members (fungi, echinoderms, cnidarians, the list goes on and on) including some real evolutionary stand-outs.

In most cases (but not all!), bioluminescence results from enzyme-catalyzed oxidation of luciferins—light-emitting compounds—by luciferases. There can be many different luciferase compounds used even in closely related species.

New luciferin found in glowworms

A newly identified luciferin was discovered in caves in New Zealand (because of course it would be in a cave in New Zealand) in glowworms. This luciferin uses Xanthurenic acid and tyrosine as the two precursors to the glow. This particular glowworm is Arachnocampa luminosa, a species of fungus gnat that, in its larval stage, produces sticky threads by building a long muscousy tube and moving along the tube sort of vomiting up little sticky threads to trap insect prey. How disgustingly beautiful nature can be!

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Waitomo caves 

Glowworms are not really worms, but rather, larvae of several families of beetle and fungus gnat–however the bioluminescence is not homologous among the groups (so it’s arisen independently many times over). While it’s not always just the larvae that glows, the larvae emits the brightest blue-green glow. The glow helps the glowworms attract insects, attract mates, and protects them from predation (it also inspired James Cameron to make the blockbuster hit, Pocahontas with Glowworms Avatar).

Deep sea Cephalopods like to flash each other

An especially cool evolutionary example is of a deep-sea octopus, whose “suckers,” which still retain a sucker appearance and sucker-like traits, have had many of their muscle cells replaced with light producing cells. Researchers suspect this may have occurred as the result of once being a shallow-water bottom dwelling octopus, and moving to a deep open-ocean environment where suckers were less necessary.

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Deep sea octopus

Now it appears, the octopi use these glowing suckers for communicating to one another via visual signaling. They may also be using them for attracting a favorite prey item of theirs—copepods (small crustaceans). This is an unusual prey item for an octopus, but the copepods are attracted to the bioluminescence.

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Toyama Bay, Japan where firefly squid gather to spawn. Credit: Brian J. Skerry/Getty Images

For a more flashy light show, I’d recommend the firefly squid. Their deep blue lights (produced by photophores) are used for communicating with mates and perhaps rival squid. The light can also be used to break up the body pattern to confuse predators and attract small fish to prey on (because deep sea fish just cannot seem to learn which glowing lights mean danger). The really cool thing about firefly squid though, is not so much the light they produce, but the evolution of their eye that seemed to come with it. They are thought to be one of the only cephalopods to have color vision (by the way, cephalopod eyes: a fascinating topic). They have three visual pigments while other cephalopods only have one, and this may be so they can better distinguish ambient light from bioluminescent light, and perhaps because their light color is pretty unique from other bioluminescence emitted in the deep sea.

Symbiotic bacteria- lux operon helps flashlight fish and bobtail squid

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In perhaps the most of obvious function of bioluminescence: The flashlight fish (Anomalous katoptron in this case, though there are several species), produces light using symbiotic bacteria. The fish’s light organs are located under it’s eyes so it can turn the light on and off by blinking. These organs are packed with bioluminescent bacteria to produce a greenish-blue light. Researchers found that the fish blink less (meaning their organs are open) in the presence of their planktonic prey indicating they use their bioluminescence for finding prey.

 

Quorum sensing and a beautiful tale of symbiosis

One of my favorite bioluminescent evolutionary excerpts is that of Vibrio fischeri and Euprymna scollops (the Hawaiian bobtail squid). V. fischeri is a symbiotic bacterium that produces bioluminescence through the lux operon (which involves another luciferase oxidizing a compound to produce blue-green light). The Vibrio interact with the squid (using type IV pili) which starts the maturation of light organs in the squid. These bacteria help the squid conceal its shadow while its foraging for food under the moonlight. This protects the squid from predators while providing the bacteria with a stable home. 980x

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simplified diagram of lux operon at low and high cell density

What makes this bacterium especially notable, is that it was one of the first bacteria to be discovered to use quorum sensing. Quorum sensing is a gene expression regulation tool (often called “bacteria communication” and totally going to be on your exam tomorrow) where the Vibrio’s gene expression responds to changes in bacteria cell density. A signal molecule- N-acylhomoserine lactone (AHL), is synthesized by LuxI (a protein produced by the lux operon I mentioned earlier) and leaves the bacteria cells. LuxR forms a complex with AHL and binds the lux box causing the activation of luminescence genes. The bacteria colonize the squid’s light organ at a very high density producing lots of this AHL molecule.

Millipedes: Glow first used for coping with climate, co-opted for warning signal

 

If you’re ever in California, be on the lookout for the Motyxia millipedes. They’re pretty easy to spot as they emit a teal glow from their entire body. They also produce poison cyanide which many other millipedes do as well. Instead of concentrating their glow to one light organ and instead of emitting light from a luciferase reaction, they glow all over their exoskeleton using a photoprotein whose homology is unknown.

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M. sequoiae (left), M. bistipita (right)

But what’s REALLY cool about the Mytoxia is that for a while it was thought that bioluminescence evolved in the millipedes as a way to warn predators. However, when researchers discovered that another species (previously Xystocheir bistipita, now reclassified as Mytoxia bistipita) glows, but much more faintly, they looked more into it.

They found that Mytoxia may have actually evolved to cope with hot, dry climates (this species is found in the Sierra Nevada Mountains). The glow of M. bistipita is much less intense and they also have fewer predators than other species. Millepedes have difficulty metabolizing oxygen in hot, dry climates which creates toxic byproducts (like peroxide). Their bioluminescent photoprotein actually helps to neutralize these toxic byproducts. The researchers concluded that the millipedes colonized higher elevations more recently than the bioluminescence evolved, and that with that colonization came more predation. Only then did they co-opt the trait for warning predators of their poison cyanide production. The brighter the millipede, the more cyanide it contained!

Sources:

  1. Paul E. Marek, Wendy Moore. Discovery of a glowing millipede in California and the gradual evolution of bioluminescence in Diplopoda. Proceedings of the National Academy of Sciences, 2015.
  2. Jens Hellinger, Peter Jägers, Marcel Donner, Franziska Sutt, Melanie D. Mark, Budiono Senen, Ralph Tollrian, Stefan Herlitze. The Flashlight Fish Anomalops katoptron Uses Bioluminescent Light to Detect Prey in the Dark. PLOS ONE, 2017.
  3. Quorum Sensing in the Squid-Vibrio Symbiosis. Subhash C. Verma and  Tim Miyashiro. Int J Mol Sci. 2013 Aug.

Botulinum toxin found in new, common bacteria

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Clostridium botulinum, Photo: Eye of Science

Evolutionarily, horizontal gene transfer between bacteria is generally not so groundbreaking. In this case however, it’s a little more newsworthy. A lot of bacteria carry plasmids, which are mobile little DNA structures that are not part of the bacterial chromosome and can be transferred to other bacteria. Often plasmids contain genes that may provide some selective advantage (otherwise why bother keeping them?), such as a toxin or an antibiotic resistance gene. Enterococcus happens to be a frequent plasmid-carrier, which makes it an especially good candidate for frequent horizontal gene transfer. But first, Clostridium. 

Clostridum is an especially fun group of bacteria including some really famous germs:

  • C. tetani (Tetanus),
  • C. difficile (the bacteria in your gut that gives you stomach issues after you take antibiotics as it swarms in on all the spaces other bacteria used to be, before they were killed by antibiotics),
  • C. perfrinigens (perhaps the nastiest of all, gas gangrene),
  • the less famous C. sordelli (which is a rare–but plenty horrific, pregnancy and abortion-associated infection almost always resulting in death by toxic shock syndrome)
  • And of course, C. botulinum, the primary culprit of botulism.
What is Botulinum toxin?

C. botulium is known for releasing botulinum toxin (BoNT), a toxin which interferes with the release of the neurotransmitter—acetylcholine, from axon terminals at the neuromuscular junction resulting in flaccid paralysis (you can’t breathe).

The toxin (a protein) works by binding to receptors at the neuromuscular junction. It is then taken into the cell by receptor-mediated endocytosis. A conformational change occurs inside the early endosome (due to a pH change). A piece of the protein (the light chain) is translocated to the cytosol when another piece of the protein (the heavy chain) forms a sort of channel. This light chain can then cleave these important complex-forming “SNARE” proteins, which are vital to normal vesicular transport and neurotransmitter (which in this case is acetylcholine) release. So without these SNARE proteins, the little acetylcholine vesicles don’t get to where they need to be. In normal neurotransmitter release, SNARE proteins would work to tether the vesicles to the membrane so the cell and vesicle membranes could fuse to allow the release of neurotransmitters.

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Visualized by me on Pymol- PDB file: 3BTA, BoNT, Serotype A. You too, can play around with it in pymol/swissPDB/Chimera/some other visualizer!

Botulinum toxin is the deadliest toxin known, requiring just two billionths of a gram to kill one person. It’s so dangerous that when type H (one serotype of the toxin) was discovered and failed to be controlled by typical botulinum antibodies, the type H toxin became the only example of a genetic sequence that was hidden from public databases due to security concerns. I say “may be” because how would we really know?

Not just in C. botulinum anymore

While we used to take comfort in knowing we could probably avoid Clostridium botulium by just avoiding puffed up canned food, rotten meat, and organic honey, that may no longer be the case. For the first time, the botulinum toxin has been found in a completely different (and very distantly related) bacteria: Enterococcus.

This new variant of the toxin called BoNT/En, was found in South Carolina, in an E. faecium strain isolated from cows. And it wasn’t just the toxin that was found. Several associated proteins that prevent the toxin from being degraded were also found. That being said, the BoNT/En variant didn’t give the cow it was found in, botulism, and it was not actually very harmful initially in mice. Researchers had to manipulate the toxin to better target mice before it was able to actually kill them (I know. Trying to give mice botulism is upsetting, and the reason why I stick to cells and microbes for my research). They are testing the toxin on human neurons to see how toxic it is to humans.

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Enterococcus

What makes this particular jump so terrifying is that Enterococcus is a highly abundant group of bacteria all over our bodies. It is ubiquitous in animals and actually a significant human pathogen. E. faecium is a very hardy bacterium easily evolving antibiotic-resistance and actually pretty difficult to get rid of in hospital surfaces. The thought of a dangerous neurotoxin being easily transferred to a ubiquitous and antibiotic-resistant bacteria is somewhat frightening. That being said, plasmids containing incredibly dangerous neurotoxins would likely need to provide a selective advantage to the host to stick around (and it’s possible in E. faecium’s case, it could even provide a slight disadvantage). BoNT can be carried in a bacteriophage, in a plasmid, or on a chromosome, but carrying a sizable gene cluster you don’t need in evolution has usually resulted in a “you don’t use it, you lose it” outcome. As plasmids by themselves are slightly disadvantageous to carry, what keeps them around is any selective advantage the genes they contain provide.

Where did these toxins come from?

Researchers found that the homolog of BoNT in Clostridium, seemed to be a flagellin gene. These flagellins contain collegenase which breaks down peptide bonds in collagen, so they are also a proteolytic toxin family like the Clostridia neurotoxins. They believe that the neurotoxin and adjacent genesevolved from an ancestral collagenase-like gene cluster.  This gene cluster was likely duplicated and evolved separately to become the BoNT we know today.

My case against Botox: amazing, but maybe take it easy?

Botox can be useful for treating cerebral palsy, urinary incontinence, wrinkles, sweating, spasms, headaches, and tinnitus. While no one’s reportedly died from cosmetic Botox use (presumably because people are probably extra careful with such a terrifying substance), there’s a risk of the toxin spreading beyond the injection site and causing respiratory paralysis. While ordinarily I’m totally accepting of people’s desire to do strange or expensive things in the name of beauty, my (probably illogical) fear is that all it takes is one new guy thinking a smudged decimal point is a comma and you’re dead of flaccid paralysis.

Consider that a muscle with a cut nerve will quickly result in atrophy which will definitely make you look worse, not better. Not using your face muscles isn’t going to prevent you from wrinkling because the issue is not the muscles, but the soft tissue decline that comes with age. Neuromodulators like Botox are very expensive, usually require a high enough dose to actually be effective and wear off in a few months, meaning you would have to get several injections a year to stay smooth and shiny, and the repeated injections are when people tend to see more negative side effects and require a higher dose.

Paralyzing muscles over and over again is not great for you long-term so maybe try sunscreen, a nice skincare routine, and drink plenty of water instead? Mistakes happen, people misplace decimal points, I’d rather not be near it personally. Just a friendly PSA to remind you to definitely do your research if you want to mess around with botulinum toxin!

Sources:

  1. Sicai Zhang et al. Identification of a Botulinum Neurotoxin-like Toxin in a Commensal Strain of Enterococcus faecium. Cell Host and Microbe, 2018
  2. P.K. Nigam, Anjana Nigam. Botulinum Toxin. Indian Journal of Dermatology. 2010 Jan-Mar; 55(1): 8–14.
  3. Doxey AC, Lynch MD, Müller KM, Meiering EM, McConkey BJ. Insights into the evolutionary origins of clostridial neurotoxins from analysis of the Clostridium botulinum strain A neurotoxin gene cluster. 2008.

Cretaceous pterosaur diversification and extinction

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Artist: Mark Witton

Few things are as disappointing as learning that no pterosaurs survived the K/Pg extinction. This has always been especially hard for me to emotionally accept due to their immense diversity. The typical explanation usually told is that they were wiped out with the non-avian dinosaurs after the chicxulub impact, and that they were barely alive by that time anyway because all the birds had filled up the flying niches. However recent evidence indicates that pterosaurs actually were doing very well up until 65 million years ago. Why they went extinct may have nothing to do with birds or a failure to diversify. Serial size reduction allowed for smaller pterosaurs to survive through other extinctions. Reaching sexual maturity before being fully grown allowed for smaller hatchlings maturing more quickly, allowing for more reduction in size by accelerating evolution somewhat. So if there were smaller pterosaurs at the end of the Cretaceous, AND pterosaurs have previously proven to be capable of relatively rapid phylogenetic size decreases, why did no pterosaurs survive?

The Cretaceous is more known for its giant, “small-plane sized” pterosaurs (Arambourgiania, Quetzalcoatlus, and one that’s been in the news more recently for “terrorizing” Transylvania: Hatzegopteryx). For background pterosaurs are split into two major suborders, with Rhamphorhynchoids being a paraphyletic group characterized by having teeth, long tails, and a cruropatagium that stretched between the feet (like how bats have it). Most were small and lacked bony head crests. They appeared in the Triassic and went extinct during the Cretaceous though there is no strong evidence to indicate they were outcompeted by pterodactyloids which is a common assumption.

Pterodactyloids, the other suborder, did not appear until the late Jurassic and were much more successful and diverse in the Cretaceous. While all pterosaurs are outstanding creatures, the pterosaurs this post is concerned with would all be pterodactlyoid members.

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Rhamphorhynchoid on left, Pterodactyloid on right

No fossils of pterosaurs have been found from after the K/Pg extinction (and I don’t believe there ever will be 😦 ). But while there are certainly no pterosaurs alive today, there is a lot of evidence indicating that pterosaurs were actually quite diverse even at the end of the Cretaceous, and that some were even very small. The discovery of small pterosaurs from the late Cretaceous does seem to indicate that the reason for their clade’s total extinction was not simply because they were just “too large.”

Small pterosaurs may have been more abundant in Cretaceous than previously thought

A small azhdarchoid (azhdarchoids being the most recent common ancestor of Quetzalcoatlus and Tapejara, and all its descendents) pterosaur was discovered from the Campanian Northumberland Formation of British Columbia. With an estimated 1.5m wingspan, the pterosaur specimen is described as being about the size of a large seagull. The specimen found might not actually be an azcharchoid, but it certainly was from a pterosaur. Researchers were able to analyze the bones to determine whether or not it was juvenile or adult and found that the specimen was either fully grown or very close to being fully grown. For more on that, read the paper here.

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Pterosaurs preserve terribly. They’re bones are hollow, their skeletons are fragile, they didn’t routinely die in nice, preserving environments. During the Cretaceous, pterosaurs shifted from marine to more non-marine habitats. This may account for the lack of data on small, difficult to preserve pterosaur fossils in the late Cretaceous. Terrestrial habitats do not preserve fragile fossils. Even much larger, denser bones do not often preserve well in terrestrial environments. The fossils that have been found from pterosaurs of this period are usually in very bad shape and are only fragments of the entire skeleton. Often times, fossils have to be looked at by many bird and pterosaur specialists before it can even be determined that the bone WAS from a pterosaur.  There is a lot of growing evidence suggesting that smaller pterosaurs in the late Cretaceous were not as rare as once believed.

Birds not the cause of pterosaur extinction

Pterosaurs were excellent fliers, almost definitely warm-blooded like birds (due to the energy expense of their lifestyle) and seemed able to adapt to a wide variety of niches. So it’s strange to imagine them going extinct due to their failure to diversify in the presence of birds. A study showed that pterosaurs actually diversified more after birds appeared. Pterosaurs had about a 160 million-year run on Earth and were relatively similar morphologically for the first 70 million years. They then began to experiment, trying out many modes of life. As birds became more successful, the pterosaurs actually responded by diversifying more. The emergence of birds (at least 50 million years after the first pterosaurs), encouraged the pterosaurs to try out new diets and feeding styles as seen by the rapid diversification of skull shapes in the fossil record. The general direction they went towards was much larger bodies. This was when the famous giant Quetzcoatlus types emerged.

sources:

  1. A small azhdarchoid pterosaur from the latest Cretaceous, the age of flying giants. Martin-Silverstone, Elizabeth, et al. Royal Society Open Science. 2016.
  2. Evolution of morphological disparity in pterosaurs. Katherine Prentice, Marcello Ruta, Michael Benton – Journal of Systematic Palaeontology – 2011

 

 

 

Hantavirus may pose bigger zoonotic threat than we thought

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The adorable host of a virus that causes your lungs to fill with fluid.

A small, innocuous looking virus with just three genome segments, causes one of the most deadly infections in the United States. Hantaviruses circulate worldwide causing either hemorrhagic fever with renal syndrome (HFRS) or, in the case of the North and South American strains, Hantavirus pulmonary syndrome (HPS). Famously recognized in 1993 in the Four Corners region of the U.S., Sin Nombre Virus, a strain of hantavirus, still infects at least a few people in the U.S. every year.

Hantaviruses are thought of as a virus people only get directly from rodents, which cannot be transmitted person-to-person. Infections result from exposure to contaminated excretions/secretions of rodents infected with the virus, though the rodents themselves show no signs of disease. These rodents also transmit the virus to each other.

Coevolution with hosts

While many species may be drivers for the evolution of another, the term coevolution is applied when two species influence each other so much that they are evolving together, where one undergoes genetic change the other responds with genetic change. They are undergoing speciation together. It was thought for a while that rodents were unharmed by the virus due to long, ongoing rodent-hantavirus coevolution. Significant phylogenetic congruities have been shown, for example, the phylogeny shown:

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Host species phylogeny on left, virus phylogeny on right, lines indicate which host virus infects.

New research might be indicating that’s not as true as we thought, phylogenetic analysis studies may be flawed, host range my be bigger, and rodent speciation doesn’t match up. While I’m not enough of a hantavirus or rodent expert to weigh in on this, certainly “whoa if true” to the coevolution theory.

Person-Person Transmission

In 1996, an outbreak of hantavirus in Argentina occurred, yet there was especially low rodent density and there was strong evidence for person-person transmission.

Then in 2011, a similarly unusually outbreak in Chile occurred. An Andes hantavirus, a close relative to the North American Sin Nombre virus (meaning “no name” as the native Americans), was shown to be transmitted person-to-person. In an outbreak of 5 human cases, symptoms developed in 2 household contacts and 2 healthcare workers after exposure to the first patient patient. Analysis of isolates from each patient supported person-person transmission for the all secondary-case patients.

Hantavirus found in human saliva

You might optimistically tell yourself that maybe this Andes hantavirus was a unique case. And maybe hantavirus was still really just a rodent disease that rarely spilled over to a person. But in Sweden in 2008, a Puumala hantavirus that causes hemorrhagic fever with renal syndrome (nephropathia epidemica) was found in human saliva of 10 patients. Whether or not this is actually a mode of transmission or not remains to be seen, but it does seem like hantaviruses are becoming more adept at infecting and transmitting between human hosts.

Climate change’s effect on hantavirus?

Hantaviruses frequently jump hosts and seem to circulate amongst bats, moles, shrews, and rodents, but climate change and human impact generally decreases rodent diversity. Intuitively you may assume hantaviruses would be less able to jump hosts as global warming/human impact goes on.

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Perhaps colder areas will actually see a decrease in hantavirus outbreaks as a result of global warming, due to the expected decrease in vole/northern rodent species populations. Yet that doesn’t seem to be what’s happening. Hantavirus surveillance has indicated an INCREASE, not only in outbreaks, but in genetic diversity and abundance in rodent populations.

If climate change does end up resulting in low rodent densities, this may also present another hantavirus risk– providing selective pressure for the virus to change transmittance route.

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deer mouse dusted with fluorescent powder to identify which mice got in most fights/matings thereby spreading more hantavirus. It was big, old mice.

Sources:

  1. University of Utah. “Big, Old Mice Spread Deadly Hantavirus.” ScienceDaily. ScienceDaily, 9 January 2009.

2. Phylogeny and Origins of Hantaviruses Harbored by Bats, Insectivores, and Rodents. Wen-Ping Guo-Xian-Dan Lin-Wen Wang-Jun-Hua Tian-Mei-Li Cong-Hai-Lin Zhang-Miao-Ruo Wang-Run-Hong Zhou-Jian-Bo Wang-Ming-Hui Li-Jianguo Xu-Edward Holmes-Yong-Zhen Zhang – PLoS Pathogens – 2013

3. An Unusual Hantavirus Outbreak in Southern Argentina: Person-to-Person Transmission? Rachel Wells – Emerging Infectious Diseases – 1997

4. Hantavirus RNA in Saliva from Patients with Hemorrhagic Fever with Renal Syndrome. Lisa Pettersson-Jonas Klingström-Jonas Hardestam-Åke Lundkvist-Clas Ahlm-Magnus Evander – Emerging Infectious Diseases – 2008

5. Person-to-Person Household and Nosocomial Transmission of Andes Hantavirus, Southern Chile, 2011. Constanza Martinez-Valdebenito-Mario Calvo-Cecilia Vial-Rita Mansilla-Claudia Marco-R. Palma-Pablo Vial-Francisca Valdivieso-Gregory Mertz-Marcela Ferrés – Emerging Infectious Diseases – 2014

 

Salty Antarctic Lake Provides Clue to Viral Evolution

In the Vestfold Hills region of Antarctica, a team of researchers have discovered a unique method of genetic exchange happening in a deep lake—so salty it remains unfrozen down to minus 20 degrees. In it, lives members of Haloarchaea, a class of Euryarchaeota that thrive in high salt conditions. These extremophiles are able to thrive by having extremely high rates of horizontal gene transfer, swapping genes with other genera even, to more rapidly evolve. Despite the shockingly high rate of gene sharing, the lake still maintains distinct species with no one dominant species winning out. The lake is incredibly cold, providing very little energy, so the archaea in this area only produce about six generations a year because they have to metabolize and reproduce so slowly.

While people have been aware of the archaeal extremophiles there for some time, it was only recently that anyone noticed their plasmids.

HalosPlatte3
Haloarchaea colonies

The team discovered plasmids in one strain that were not behaving like regular plasmids. Plasmids are pieces of DNA independent of the host genome which replicate independently and are kept around usually only if they have some beneficial gene to the organism (e.g. antibiotic resistance). What differentiates a plasmid from a virus is the method of transmitting genetic information.

For background, a plasmid typically relies cell-cell contact or “conjugation”–when a sex pilus of a bacterial cell containing the plasmid will combine with another bacterium to transfer the plasmid, or is picked up as naked DNA. Other horizontal gene transfer methods would be transduction (genetic transfer via a virus) or transformation (the collecting of naked DNA from the environment).

Viruses travel, encased in a protein coat, and rely on lysing or budding off their host cell and finding new cells to attach to and enter (or, in the case of retroviruses and lysogens, integrating in the host DNA and being activated later in any of that host’s progeny).

But these plasmids are acting like viruses. The pR1SE (plasmid) encodes proteins that go into the host membrane and allow the membrane to bud into vesicles containing plasmid DNA. These vesicles could then infect more of the archaeal species, plasmid-less members. The plasmids could then replicate themselves in their new host cell.

Besides this just being cool because it’s a way we’ve never seen before of transmitting DNA (and because anything involving archaea in extreme environments is cool), it also may be representative of some early stage of viral evolution.

Viral evolution is a hugely debated topic with no one really agreeing on how viruses came about, whether they evolved many times or once then diversified, which came first in the evolution of life etc., but this does seem to support the idea that at least some groups of viruses may have started as plasmids.

Some people think the obvious answer to viral evolution is gene reduction (a lot of giant virus fans), others think it’s gene addition (what this supports). I think the answer is gradually proving to be both—that viruses have evolved independently many times throughout history, and you could probably find at least a few examples to best support each major theory.

Source:

  1. Susanne Erdmann, Bernhard Tschitschko, Ling Zhong, Mark J. Raftery, Ricardo Cavicchioli. A plasmid from an Antarctic haloarchaeon uses specialized membrane vesicles to disseminate and infect plasmid-free cells. Nature Microbiology, 2017

2. High level of intergenera gene exchange shapes the evolution of haloarchaea in an isolated Antarctic lake. Ricardo Cavicchioli et al. PNAS. 2013

Echinoderms’ deviation from the universal code

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The very strangeness of Echinodermata is partly responsible for the dedication that specialists in the group feel. We revel in their weirdness.
-Rich Mooi

Given that every biology student in the world has been introduced to the standard genetic code, and likely uses it frequently, it is kind of baffling that so few of us ever bother to think much about it. As a longtime lover of systematics/molecular evolution, the knowledge that the “universal genetic code” is not actually universal has always caused me some level of concern when imagining how scientists cope with such an issue or if they even cope with the issue at all.

Usually when you look this up you find a lot of “the code is essentially universal, only a few exceptions have been found” which would imply that maybe one or two extremely obscure microorganisms violated this rule slightly. But mammals mitochondria actually contains four out of 64 codons that do not match the universal code. Echinoderms, yeast, platyhelminth worms, all follow slightly different mitochondrial DNA codes and protozoan and some bacteria even follow different nuclear DNA codes (nuclear being the only DNA bacteria have).

While there are 64 codons, there are fewer than 64 tRNAs, which use an anticodon sequence to recognize a codon on mRNA and carry the appropriate amino acid at the other end. Different tRNAs with the various amino acids will sort of float in and out until the right one’s bound. The third position of the anticodon (the ‘wobble position’) however, binds very loosely to the DNA which is why the tRNA usually relies on recognizing the first two nucleotides. Some amino acids can have multiple tRNAs recognizing them but RNA modifications in the anticodon region of tRNAs can result in the evolution of a deviation to the universal genetic code. The echinoderm’s genetic code evolution is particularly intriguing which is hardly surprising given everything else about them.

A recent Nature paper shows an example of how this works in echinoderms. In echinoderm mitochondrial DNA, the codon AAA, which according to the “universal code” should code for a lysine, actually codes for an asparagine. Analyzing the tRNALys isolated from a sea urchin, they discovered a modified hydroxylated nucleoside; hydroxyl-N6-threonylcarbamoyladenosine. This modified nucleoside adjacent to the anticodon prevents the mt-tRNALys from misreading AAA as lysine, allowing AAA to code for an asparagine.

Mitochondria generally use a codon-anticodon pairing rule that allows unmodified uridine at the anticodon first position to pair with all four nucleotides at the third codon position. When an amino acid only has two codons corresponding to it, the G forms a base-pair with pyrimidine, and modified uridines (5-carboxymethylaminomethyl-uridine being a commonly heard modification to the wobble position base) can discriminate purines from pyrimidines. The presence of a pseudouridine in starfish mt-tRNAAsn in the middle of the anticodon allows the tRNA to decode the AAA codon more efficiently than the unmodified tRNA. Also interesting, the mt-tRNAs possessing anticodons similar to tRNAAsn, but which only decode two codons each (tRNAHis, tRNAAsp and tRNATyr) all possess unmodified U (position 35), further indicating pseudouridine (Ψ35) is important for decoding the three codons.

While certainly not all examples of a modified genetic code work quite this way, it’s intriguing to realize how something generally portrayed as being set in stone, is relatively labile and dynamic.

Given that systematics has favored mitochondrial DNA for many phylogenetic analyses, this could have an effect on the results if using an amino acid alignment or a distance matrix where each amino acid change is weighted a certain amount. You could imagine an alignment between mammals, echinoderms, and reptiles for example, where an AAA to an AAG would be a synonymous mutation (as in, not changing the protein) in mammals and reptiles, but a nonsynonymous mutation (changing the amino acid) in echinoderms, thus deserving a different score. AGA and AGG which both code Arginine in the ‘universal’ code, code for a stop codon in our mtDNA, while our nuclear DNA’s stop codon (UGA), codes a tryptophan. An AUA isoleucine in our nuclear DNA is read as a methionine in our mtDNA. There are likely many more “exceptions to the rule” that we have no idea exist.

Sources:

  1. Hydroxylation of a conserved tRNA modification establishes non-universal genetic code in echinoderm mitochondria. Asuteka NagaoMitsuhiro OharaKenjyo MiyauchiShin-ichi YokoboriAkihiko YamagishiKimitsuna Watanabe Tsutomu Suzuki. Nature Structural & Molecular Biology (2017).

2. Tomita, K.Ueda, T. & Watanabe, K. The presence of pseudouridine in the anticodon alters the genetic code: a possible mechanism for assignment of the AAA lysine codon as asparagine in echinoderm mitochondriaNucleic Acids Res.2716831689 (1999).