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.
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.
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
Phytoestrogens are simply plant-derived xenoestrogens (mimics of estrogen). They’re abundant in legumes (soy, notably), but also present in many other plants. Despite their presence in certain plants being touted as scary, I’d say they’re pretty misunderstood.
Phytoestrogens help breeding success of kākāpō, the flightless nocturnal parrot
The darling flightless parrot of New Zealand has a struggling population partly because it only breeds once every few years. They seem to only breed during mast years (when plants produce a ton of edible fruit/seeds) and seek out fruit from the native rimu tree, which suggested the birds breeding success may rely on the presence of phytoestrogens found in the native plants. The hypothesis is that kākāpō don’t produce enough estrogen to make a fertile egg but the phytoestrogens act as supplements.
The scientist conducting this study tested the native plants for estrogenic content and found high levels of phytoestrogens. They looked at the ligand binding region of the progesterone receptor, the androgen receptor, the estrogen receptor 1, and estrogen receptor 2 in four native parrot species, and non-native parrots and compared them with chicken receptors. They found that in most receptors there was more then 90% homology except in the estrogen 1 receptor. Parrot estrogen receptors are actually genetically different, containing an extra 8 amino acids in the hormone binding region, which changes the binding strength to estrogen.
Soy probably pretty good for you
Active compounds of soy include isoflavones- daidzein, genistein, and glycitein. They act as phytoestrogens, a word which seems to frighten some people. A popular belief amongst anti-soy people is that men who ingest too much soy are going to re-enter puberty and turn into estrogen-filled feminized men (heaven forbid).
But this is not really what’s going on.
Phytoestrogens are structurally similar to estradiol so they have the ability to cause either estrogenic or antiestrogenic effects by blocking estrogen receptors. Phytoestrogens have weak estrogen activity in your body, so they may also bind weakly to estrogen receptors. They don’t displace estrogen, they supplement it.
Plants like soy have evolved phytoestrogens to protect from harmful microbes and to help form nitrogen-fixing root nodules.
So the expectation is that they act like antiestrogens in high estrogen concentration environments, and act like estrogen in low estrogen environments.
There are actually a lot of different estrogen receptors in the human body so the same chemical could be and agonist on one estrogen receptor type and an antagonist on another. So the phytoestrogens in plants could trigger an increase or decrease in endogenous estrogen through feedback loops.
It is almost certainly a serious oversimplification to say phytoestrogens are estrogen mimetics. Lots of compounds have partial agonist activity, meaning that at one concentration they are agonists and at a different concentration they are antagonists. It is possible they could affect the different receptors differently.
Reasons to even get excited over Phytoestrogens
Certain hormonal cancer (uterine, prostate, breast etc.) risks could possibly be lowered with phytoestrogen consumption. If they do actually compete with and block estrogen (an antagonist) at estrogen receptors in the breasts, cervix, or uterus, or if they depress estrogen production, they could tend to inhibit estrogen dependent tumors.
Phytoestrogens may even provide some sort of benefit to women undergoing menopause and experiencing hot flashes, and post-menopausal women at risk for developing osteoporosis and issues in cognitive function which can sometimes be experienced due to dramatic hormone changes.
If phytoestrogens are agonists at estrogen receptors on osteoblasts and osteoclasts they will help reduce osteoporosis. These estrogen receptors are quite different from the receptors on breast tissue.
From a meta analysis on the effects of isoflavones on bone mineral density in menopausal women: “Isoflavone intervention significantly attenuates bone loss of the spine in menopausal women. These favorable effects become more significant when more than 90 mg/day of isoflavones are consumed. And soy isoflavone consumption for 6 months can be enough to exert beneficial effects on bone in menopausal women.”
Soy phytoestrogens are associated with much less negative effects than synthetic endocrine disruptors. And while results of most of these soy studies are dubious—varying with age, level of consumption, and the composition of the individual’s intestinal microflora, soy studies are just as well supported as pretty much any other “eat/drink more of (vegetable, tea, “superfood” etc) and (some health benefit) happens” claims.
While most people tend to be skeptical of simply ingesting a plant and deriving benefits (especially when they are comparing the plant to the highly powerful and concentrated drugs we’ve developed), underestimating and understudying plants has brought about, and continues to bring about, death and illness to plenty of people. So maybe it provides small benefits, but at the very least research does seem to have debunked the myth that soy is dangerous for people.
Constituents of soy if you’re still worried
Oil- large amounts of polyunsaturated fatty acids (i.e. linoleic acid (omega 3))
Vitamins and minerals- K, P, Ca, Mg, Fe, B-Vitamins, antioxidants
Phytosterols– Disogenin –sterol- is converted to progesterone in body
Saponins*- being looked at especially
Ferritins- Soybean is a good source of iron
Glyceollins- antiestrogen activity
Unique oestrogen receptor ligand-binding domain sequence of native parrots: a possible link between phytoestrogens and breeding success. Catherine E. J. Davis A , Adrian H. Bibby A , Kevin M. Buckley A , Kenneth P. McNatty A and Janet L. Pitman. 11 July 2017.
2014 Jul 7. Do soy isoflavones improve cognitive function in postmenopausal women? A meta-analysis. Cheng PF1, Chen JJ, Zhou XY, Ren YF, Huang W, Zhou JJ, Xie P.
2003 Jan-Feb. Effects of soy and other natural products on LDL:HDL ratio and other lipid parameters: a literature review. Hermansen K1, Dinesen B, Hoie LH, Morgenstern E, Gruenwald J. .
Soy intake and risk of endocrine-related gynaecological cancer: a meta-analysis. Myung SK, Ju W, Choi HJ, Kim SC; Korean Meta-Analysis (KORMA) Study Group.
Soy intake and cancer risk: a review of the in vitro and in vivo data. Messina MJ1, Persky V, Setchell KD, Barnes S.
2014 May 28. Effects of isoflavones and amino acid therapies for hot flashes and co-occurring symptoms during the menopausal transition and early postmenopause: A systematic review. ThomasIsmail, Taylor-Swanson Cray, Schnall, Mitchell, Woods
Clinical studies show no effects of soy protein or isoflavones on reproductive hormones in men: results of a meta-analysis. Hamilton-Reeves JM1, Vazquez G, Duval SJ, Phipps WR, Kurzer MS, Messina MJ.
Soy isoflavone intake increases bone mineral density in the spine of menopausal women: meta-analysis of randomized controlled trials. Ma DF1, Qin LQ, Wang PY, Katoh R.
Soy isoflavones for osteoporosis: an evidence-based approach. Taku K1, Melby MK, Nishi N, Omori T, Kurzer MS.
“Do you think God gets stoned? I think so — look at the platypus.”
Venom isn’t very special in the animal kingdom, but our anthropocentric mindsets tend to focus more on large mammals than anything else, so to us it seems pretty mystical. Only a dozen or so mammals deliver venom, almost all of which deliver it via a bite for defense or predation. The platypus is unique in that it is so far the only animal known to use venom for a purpose other than defense or predation.
Only the male platypus has venom. And the male platypus only seems to have potent venom seasonally. The season when they have a lot of venom is unsurprisingly mating season, as the males actually use their venom, injected via venomous spurs on their hind legs, for intraspecific competition with other platypus males to keep territories and mates. While technically the echidna has venom, it can’t erect it’s spurs, and simply excretes a milky secretion.
Their venom, though nonlethal, causes excruciating pain for hours or days and is essentially nonresponsive to morphine. Only nerve-blocking agents (or antivenom) can provide relief.
A 2010 study found 83 peptides in platypus venom, many of which resemble venom genes from snakes, sea stars, and spiders. The platypus and reptiles have independently co-opted the same genes for venom usage making the platypus venom a cool example of molecular convergent evolution.
And just so the monotremes can continue to follow their pattern of general nonconformity and being surprisingly different from each other, the echidna venom gland transcriptome looks very different from the platypus one. You can read this poston their weird sex chromosomes for more.
The venom induces Ca2+ influx in cells, which results in neurotransmitter release. Defensin-Like peptides (defensins being immune proteins that usually defend the host from microbes), C-type natriuretic peptides (OvCNPs), nerve growth factor (OvNGF), and hyaluronidase have also been found. These peptides cause muscle relaxation, inflammation by promoting histamine release, and form ion channels in the lipid membranes of cells. The venom also contains a D-amino acid (as opposed to just all L-amino acids, which is the isomer previously thought to be the only conformation manufactured by cells).
First venomous animals were mammals
The platypus having venom and laying eggs isn’t even that weird, as it seems to be that that was the norm for the ancestors of mammals. Euchambersia mirabilis, a therocephalian therapsid from the end of the Permian (~255 mya), which were some of the “almost-mammals” (the term “mammal-like reptile” is horribly outdated and silly but for some reason people still use it), was determined to have venom glands. Venom glands which appeared way before snakes and lizards evolved them, and actually millions of years before any snakes even existed.
So while venom in mammals is very rare now, it may actually be an ancestral characteristic. Venom relatively expensive to have as it requires some method of injection into another animal, a gland, and then the making of proteins. It’s also suspected to be expensive because the loss of venom in animals that are no longer under pressure to produce any, is very common. Venom has a weak phylogenetic signal—similar types of venom are not necessarily found near each other on a phylogenetic tree, so genetically it seems not very “difficult” for various venoms to arise.
Monotreme venom as diabetes treatment?
The hormone, glucagon-like peptide-1 (GLP-1), is secreted in the gut, stimulating the release of insulin to lower blood glucose. But GLP-1 typically degrades within minutes in humans.
People with type 2 diabetes can’t maintain a normal blood sugar balance, but maybe they could if they had a less rapidly degrading GLP-1.
However in the platypus, there’s conflicting functions of the GLP-1. Not only is it a regulator of blood glucose in the gut, it is also in their venom. This conflict between the two different functions has resulted in the evolution of a dramatically changed GLP-1 system. GLP-1 in monotremes is resistant to the rapid degradation that occurs in other animals, and degrades by a completely different mechanism.
The function of GLP-1 in the venom seems to have resulted in the evolution of a stable form of GLP-1 in monotremes. Stable GLP-1 molecules can potentially be used as a type 2 diabetes treatment.
Both platypus and echidnas have evolved the same long-lasting form of the hormone GLP-1 despite echidnas not having spurs.
Kita, Masaki, David Stc. Black, Osamu Ohno, Kaoru Yamada, Hideo Kigoshi, and Daisuke Uemura. “Duck-Billed Platypus Venom Peptides Induce Ca2 Influx in Neuroblastoma Cells.” Journal of the American Chemical Society50 (2009)
Enkhjargal Tsend-Ayush, Chuan He, Mark A. Myers, Sof Andrikopoulos, Nicole Wong, Patrick M. Sexton, Denise Wootten, Briony E. Forbes, Frank Grutzner. Monotreme glucagon-like peptide-1 in venom and gut: one gene – two very different functions. Scientific Reports, 2016
Julien Benoit, Luke A. Norton, Paul R. Manger, Bruce S. Rubidge. Reappraisal of the envenoming capacity of Euchambersia mirabilis (Therapsida, Therocephalia) using μCT-scanning techniques. PLOS ONE, 2017
If, like me, you’ve been reading about the unusually horrific outbreak of cholera in Yemen, you may be wondering how it got so bad. While an understanding of ecology is central to fighting any disease, if feels especially important when discussing cholera, as the current Yemen outbreak is being almost entirely blamed on war resulting in collapsing infrastructure resulting in millions of people losing access to clean drinking water. On top of that, the malnutrition of many children in the area results in them being more susceptible to Vibrio infection.
To add to that, access to rehydration therapy (the common treatment for cholera when intravenous fluids and antibiotics aren’t an option) is low, and the vaccine campaign has been dropped with the justification being that the limited amounts of vaccine would not be as effective in Yemen as they would in areas where less people are infected.
The varieties of Vibrio
The most important vibrio species to human disease are Vibrio parahaemolyticus, Vibrio vulnificus, and Vibrio cholerae. Vibrio species have flagella and pili which are important virulence factors–notably the toxin co-regulated pilus. The cell walls of Vibrio contain lipopolysaccharides consisting of lipid A (endotoxin), core polysaccharide, and an O polysaccharide side chain. Vibrio can then be divided into serogroups based on this O polysaccharide (200 serogroups in V. cholerae’s case).
V.cholerae O1 and V. cholerae O139 both produce cholera toxin (which causes a rise in cAMP resulting in the cell losing nutrients, which is why you not only need tons of water, but also need to replenish lost electrolytes). These are the serogroups associated with cholera epidemics. Many strains of V. cholerae do not have this toxin and do not cause epidemics though they may still cause illness.
The O1 serogroup is further subdivided into three serotypes: Inaba, Ogawa, and Hikojima. There are then two “biotypes” of V. cholera O1: Classical and El Tor. These biotypes can be further subdivided but let’s just stop here.
The cholera that were famous for killing lots of people in the 1800s were all of the Classical type. The cholera that is responsible for today’s pandemic is of the El Tor biotype.
The CTXφ phage
V. cholerae secretes cholera toxin. This is the toxin that causes the “rice-water” stool (not diarrhea really, as it’s just mucus and water), resulting in dehydration of the host. Colonization of the small intestine required the toxin co-regulated pilus (coded by the vibrio pathogenicity island).
The genes for cholera toxin are not in the Vibrio genome unless the bacteria has been infected by a CTXphi (CTXφ) filamentous phage, which inserts it’s genome into the V. cholerae genome. The CTXφ can transmit cholera toxin genes from one V. cholerae sstrain to another (via horizontal gene transfer).
Infectious CTXφ particles are produced when V. cholerae infects humans. Phages are then secreted from the infected bacteria without lysing the cell.
Seasonal epidemics inversely correlated with environmental cholera phage presence
Cholera seasons usually make sense as they tend to coincide with monsoon season. But perhaps less obvious (or totally obvious if you’re into viruses) cholera phages have a very dramatic influence on seasonality.
The presence of viruses infecting V. cholerae O1 or O139 inversely correlates with the occurrence of viable V. cholerae in the environment and the number of cholera cases. Both epidemic and nonepidemic serogroups have been shown to sometimes carry lysogenic phages which reproduce and kill epidemic strains. Lysogenic phages integrate into the genome so it replicates with every reproduction of the bacteria
One common O1 phage can use several V. cholerae non-O1/non-O139 strains as alternative hosts.
Having alternative hosts present combined with the lysogenic V. cholerae strains can result in a cholera phage “bloom,” thus lowering the transmission of phage-sensitive, more virulent cholerae strains.
Phage and Vibrio waves controlling epidemics
Cholera outbreaks occur in waves with different serogroups dominating at different times.
The absence of one phage specific for one cholerae type provides an opportunity for that serogroup to begin the seasonal epidemic. However, the phages for that serotype will eventually amplify in the environment and attack this serogroup, ending that epidemic.
A different cholerae serogroup would then be resistant to that first phage or carry it as a prophage in the genome—so it isn’t killing that bacteria. A second epidemic wave from the new dominating serogroup can now occur until phages specific to this new serotype bloom, thus ending the epidemic.
Some serotypes will be resistant to all the phages that were killing the virulent phages in the environment, and these serotypes will occupy the interepidemic periods. These strains usually lack typical virulence factors that would make them particularly good pathogens, but are instead more environmentally adapted than the other more virulent strains.
These resistant serotypes may ALSO harbor prophages—phages integrated in the genome—which kill virulent serogroups and may pick up virulence factors via horizontal gene transfer.
If this happens, new serotypes that were previously not very virulent may emerge as the new epidemic serotype.
Self-limiting seasonal epidemic also probably caused by phage
A naturally occurring lytic phage, JSF4 (lytic meaning it simply lyses the cell), infects and kills Vibrio that are sensitive to it.
In a study from 2005, it was shown that the peak of cholera season was preceded by a peak in V. cholerae presence which was then followed with a peak in JSF4 phage presence as the epidemic ended. JSF4 phages would then also be excreted in the diarrhea of sick cholera patients. So the patients at the end of the epidemic end up ingesting both a lot of V. cholerae as well as JSF4 phage which kills the bacteria. The increase of phage results in the decrease of V. cholerae and the epidemic ends.
This is likely why outbreaks are self-limiting.
V. cholerae O139 spread by turtles
While O1 causes the majority of outbreaks, O139 is confined to Southeast Asia. Recently however, it’s been discovered that soft-shelled turtles in China are big carriers of O139. While a lot of aquatic animals spread cholera, the soft-shelled turtles have been definitively linked to human disease and make excellent hosts as they are unaffected by the bacteria which clings to many of their surfaces and intestines. These turtles are then consumed by people, to spread more cholera to new unsuspecting hosts. If turtles being cute wasn’t a good enough reason to stop eating them, maybe this is?
Jiazheng Wang, Meiying Yan, He Gao, Xin Lu, Biao Kan. Colonization of Vibrio cholerae on the Soft-shelled Turtle. Applied and Environmental Microbiology, 2017
Faruque, S. M., I. B. Naser, M. J. Islam, A. S. G. Faruque, A. N. Ghosh, G. B. Nair, D. A. Sack, and J. J. Mekalanos. “Seasonal epidemics of cholera inversely correlate with the prevalence of environmental cholera phages.” Proceedings of the National Academy of Sciences 102.5 (2005)
Faruque, S. M., M. J. Islam, Q. S. Ahmad, A. S. G. Faruque, D. A. Sack, G. B. Nair, and J. J. Mekalanos. “Self-limiting nature of seasonal cholera epidemics: Role of host-mediated amplification of phage.” Proceedings of the National Academy of Sciences 102.17 (2005)
Murray, Patrick R., Ken S. Rosenthal, and Michael A. Pfaller. Medical microbiology. Philadelphia, PA: Mosby/Elsevier, 2016.
A fan favorite, and probably the most successful genus on the planet–at least on land—the bacteria, Wolbachia infects an estimate between 40 to 65% of all arthropod and nematode species. This microbe is constantly drifting across the line between mutualist and parasite to it’s host. Some hosts are unable to survive and reproduce without a Wolbachia infection whilst others are killed by it.
Wolbachia as a mutualist
Plenty of species have become reliant on this microbe. The caterpillar of the spotted tentiform leaf miner uses Wolbachia to create green islands on yellowing leaves which remain fresh for munching on.
It provides a benefit to certain nematode worms, such as Brugia malayi and Wuchereria bancrofti which cause elephantiasis, and which cannot survive without a Wolbachia infection.
Some Wolbachia bacteria provide metabolic advantages to their hosts such as in bed bugs who use it to synthesize B-vitamins that are absent in their blood meals. Wolbachia can even mediate iron metabolism in Drosophila.
But most exciting given the recent explosion of flavivirus infections (Zika traveling farther and farther north every summer for example), Wolbachia provides flies with resistance to many RNA viruses.
Wolbachia as a sex-determinator
In leafhoppers, Zyginidia pullula, females have two X chromosomes while males have only one X chromosome, yet when infected with Wolbachia, the X0 genetic males appeared to be female.
Some females of the Japanese butterfly, Eurema mandarin have a sex chromosome system where the males are (ZZ) and the females are (ZW). This incongruence between chromosomal and phenotypic sex can be explained by feminization of genetic males induced by Wolbachia. Two strains of Wolbachia, wCI and wFem, have been found in E. mandarina and the females having male chromosomes (ZZ) are consistently infected with both wCI and wFem. However females with only wCI are true females (ZW). Despite having male chromosomes, ZZ females are physically female and fully fertile.
A similar thing happens in woodlice (pillbugs? Roly-polys?), where all the ZZ males infected with Wolbachia develop as female. The W chromosome is sometimes lost entirely in these populations and sex is entirely determined by presence or absence of Wolbachia.
Who needs males?
Wolbachia has evolved into an intracellular parasite, and while it can infect many different organs, it is most famous for infecting the testes and the ovaries. Wolbachia are too large for sperm, but fit nicely into mature eggs so the infection is inherited maternally through the eggs.
So now the evolutionary dilemma that keeps Wolbachia on the balance between parasite and mutualist is, if males are an evolutionary dead-end, how does this intracellular parasite that needs its host to survive and reproduce, and it’s host species to continue thriving, evolve to both spread throughout populations but not allow evolutionary cheater strains to ruin everything? Wolbachia has developed numerous ways of targeting males to help itself spread such as:
Male killing- infected male larvae die, so more infected females are born
Feminization- where infected males develop as females or infertile pseudofemales
Parthenogenesis- when females reproduce without males
Cytoplasmic incompatibility (CI)- when Wolbachia-infected males can’t successfully reproduce with uninfected females or females infected with another Wolbachia strain.CI-causing Wolbachia interferes with the chromosomes during mitosis so they no longer divide in sync.
Mosquitos carrying Wolbachia have a higher reproductive success when present in a population with mosquitoes not carrying Wolbachia. When a male mosquito carrying Wolbachia tries to mate with a female who is not carrying Wolbachia, the female’s eggs won’t hatch. However females with Wolbachia do not have this issue and produce perfectly healthy offspring which are all also carriers of Wolbachia. So you can imagine how the Wolbachia is able to sweep through a mosquito population. The female Wolbachia carriers have a much higher fitness than the non-carriers.
Scientists have taken advantage of this evolutionary strategy in fighting mosquito-transmitted viruses such as Dengue and Zika. The Aedes aegypti, a black-and-white striped species of mosquito infects people with Dengue virus which has no vaccine or real treatment and causes pains, fevers, rashes, and headaches. A plan (credited to evolution/ecology biologist, Scott O’Neill) to release Wolbachia infected mosquitos into the wild to lower dengue spread is becoming more and more popular. Wolbachia stops Aedes mosquitoes from carrying degue virus. Wolbachia carrying females have a selective advantage and should sweep through the population.
Wolbachia to rescue us from Dengue (and others?)- The original plan
An unusually virulent strain of Wolbachia the ‘popcorn’ strain, essentially halves the mosquito lifespand (it’s pretty gruesome, the bacteria essentially reproduce like crazy in the brains, eyes, and muscles filling up neurons). Dengue takes a long time to be able to reproduce and make it to the salivary glands so it can be transmitted, so only older mosquitos can transmit it.
Unfortunately Aedes (and Anopheles which transmist malaria) are not natural hosts of Wolbachia infections, so Scott O’Neill carefully developed a new symbiosis by injecting eggs. This took forever to work, until one lucky grad student was able to make it a success. Finally, an egg was stably infected and a line of Wolbachia-carrying Aedes was created. But after all that work, the strain was too virulent and the females did NOT have a selective advantage and actually had lower numbers of eggs with lower viabilities (honestly, they should have seen this coming really).
But none of that even ended up mattering because some other scientists figured out that Wolbachia stops dengue virus from replicating. Simply the presence of a nonvirulent strain of Wolbachia in the population was enough to stop the spread of dengue. So the team switched to a less virulent strain, wMel, and successfully started a line of wMel carrying Aedes mosquitos.
wMelwAlbB update and some critiques of the data
As amazing as Wolbachia is, it will take at least a few years to get significant results and many years to eliminate any particular mosquito-transmitted pathogen with this method. Some papers say Wolbachia was able to make not only dengue, but also Plasmodium and other flaviviruses less able to replicate, but others said the opposite. It would be kind of important to figure out how the Wolbachia is inhibiting the virus because no one seems to agree if it’s general or specific. But now with significant selective pressures on all these diseases I’d suspect it’d be easy to switch host vectors because mosquitos bite hosts, geographically spreading infections very far (potentially) exposing the virus to a wide variety of new potential hosts vector species.
In a 2016 paper looking at the progress of the wMel strains, they collected Ae. Aegypti after one year and it continued to have low levels of dengue (which implies it was passed around through tons of mosquitos and not a whole lot of apparent evolution has taken place in terms of resistance) but what if the some of the dengue viruses switched species?
They could try passing the dengue through many mosquitos perhaps in a mixed host population. Or basically just try to provide the virus with as many opportunities as you can for it to evolve in the hopes that you may understand potential mechanisms the different diseases may have to get around this one Wolbachia infected species of vectors.
While the paper shows wMelwAlbB, the superinfection, that strain of Wolbachia actually doesn’t appear to inhibit DENV very much. But later in the paper, it’s very dramatically different so it’s difficult to say if the data is actually supporting that the superinfection sweep will work.
As far as how they ensure the right strain is dominating all the time given selective pressures towards different mosquito sex alteration methods, that remains unanswered. Combined male-killing CI strains readily become extinct following invasion so CI strains are more selected for but sex-ratio distortion decreases male infection and therefore reduces the occurrence of CI meaning that you might expect selective pressure for evolution from CI to CI/sex ratio distortion to sex ratio distortion only.
Using Wolbachia’s ability to stop mosquitos from carrying Zika, Dengue, Chikungunya, Plasmodium—the parasite responsible for malaria, may mean the eventual elimination of these diseases in humans.
It may even be used to someday stop nematode worms from causing blindness, disability, elephantitis etc in many millions of people every year.
Particularly inspiring about this story is how ecologists and evolutionary biologists ended up being the ones to figure out a way to eliminate viral infections. Yet more evidence that pre-med students or medical researcher hopefuls shouldn’t blow off biodiversity/ecology/evolution classes in college.
Kageyama, Daisuke, Satoko Narita, and Masaya Watanabe. “Insect Sex Determination Manipulated by Their Endosymbionts: Incidences, Mechanisms and Implications.” Insects 3.4 (2012): 161-99.
I contain multitudes: the microbes within us and a grander view of life. Ed Yong, 2016
Bacterium offers way to control dengue fever. Natasha Gilbert – Nature – 2011.
Establishment of a Wolbachia Superinfection in Aedes aegypti Mosquitoes as a Potential Approach for Future Resistance Management. D. Joubert-Thomas Walker-Lauren Carrington-Jyotika Bruyne-Duong Kien-Nhat Hoang-Nguyen Chau-Iñaki Iturbe-Ormaetxe-Cameron Simmons-Scott O’Neill – PLOS Pathogens – 2016
Since it’s pride month, I thought the evolution of homosexuality warranted some attention. It turns out homosexuality is common throughout the animal kingdom, while homophobia is only seen in one species.
While sexuality is complex and seems to have a lot to do with epigenetics, as well as conditions in the uterus during fetal brain development, this variety is not limited to humans. Instead of thinking of humans as unique and separate from other animals, try to consider that brains, social structure, and cognitive ability exist on a spectrum with humans simply sometimes possessing a “higher degree” of whatever special unique thing we think we have. Such as love and sexuality. Homosexuality is especially common in primates and marine mammals (it’s correlated with intelligence in species). Same-sex relationships amongst animals strengthen social structures and can be particularly useful in systems with a lot of parental care, systems where the females outlive the males (humans?), and systems where not all males get an equal number of mates. Bottlenose dolphins for example are well-known for their bisexual behavior which strengthens social bonds.
When talking about homosexuality in nature, brief periods or episodes of homosexuality are actually pretty common. Male dominance mating (which is very common in giraffes), isn’t really “true homosexuality” because the males do not form any kind of bond, and the males will usually mate with females if they can. Cases of males or females rejecting the opposite sex and forming permanent pair bonds is more rare but absolutely happens.
A classic female-female coupling that actually makes a lot of evolutionary sense from a reproductive point of view, is the Laysan Albatross. The Laysan Albatross is monogamous and mates for life, and almost a third of the parent pairs are both female. This is useful as sometimes males will mate with more than the just their one female mate (basically he cheats on her in the hopes of making more offspring) and as the Albatross has evolved to require high parental care from both parents, female-female parents are actually a necessity in many cases where the father is absent.
Macaques are also rather known for their “lesbianism,” which in this case, has nothing to do with parenting and more to do with them just preferring sex with other female macaques. The males just can’t keep up.
Not all dominant mounting is males
While males mating with other males is very common, scientists have sometimes argued that a lot of that “mating” is simply the males exerting dominance over each other. Females do it to though, especially in the case of the female spotted hyenas who live in a matriarchy. The female hyena is even larger and more terrifying than the male hyena and leads the family.
A study of gay sheep, was actually pretty historical as it really confirmed that there is a biological basis for sexual preference in animals. Sheep do seem to have a much higher rate of homosexuality than other animals where as many as 1 in 10 rams can be gay. Rams have undergone a lot of selective breeding which may provide some evidence that genes are involved in sexual preference. A region in the hypothalamus which is generally much bigger in rams than in ewes was found in gay rams to be the same size as the female’s. The hypothalamic region size variations effected levels of aromatase, an enzyme which converts androgens into estrogens. This supported the theory that hormones present during fetal development plays a role in determining sexual preference.
Bonobos are so closely related to us that it hardly seems worth it to mention them, but they are fascinating none the less. They exist in a peaceful (compared to chimps and humans) matriarchal society where sex occurs between basically every pairing you can imagine, excluding close family members (evolution doesn’t favor inbreeding). If you want to learn more about these super gay cousins of ours, I highly recommend primatologist, Frans de Waal’s books. He’s basically the top authority on bonobo sex. Really the best of the best.
Adoptive gay vulture dads
In what may be one of the cutest stories I’ve read all year, two male griffon vultures from Amsterdam have recently been given the opportunity to raise a chick together. These two males are long-term mates who had been building nests together for months but were unable to produce an egg together (obviously). The zookeepers remarked that it was unfortunate as they were one of the most devoted culture couples observed.
Vultures are monogamous and have biparental care systems, so the males together could still make great parents. When a vulture egg was abandoned, and no heterosexual vultures would agree to incubate it, they gave the egg to the long-term male couple. The males ended up being very enthusiastic helicopter parents, proving that they could successfully hatch an egg even without a female helping. They carefully took turns incubating it, and when it hatched they proved to be protective, loving parents. The fathers have split their jobs equally, taking turns caring for their baby, looking for food, defending the nest, and feeding the baby.
Possibly the most famous gay couple in the animal kingdom is the penguin couple from the central park zoo, Roy and Silo. The two chinstrap penguins, where internationally celebrated for successfully hatching and caring for an egg they were given. Their caretakers noticed that they engaged in mating behaviors with one another and seemed to instinctually want an egg of their own, once seeming to try and hatch a rock that resembled an egg. Other gay penguin couples have been observed actually trying to steal eggs from other penguins, a behavior that’s not uncommon in heterosexual penguins either. Penguins typically engage in multiple long term relationships (kind of like humans do), and interestingly, many of them will switch around between male and female partners in their lifetime.
Oregon Health & Science University. “Biology Behind Homosexuality In Sheep, Study Confirms.” ScienceDaily. ScienceDaily, 9 March 2004.
Polyploidy is the condition where an organism possesses more than two sets of chromosomes. Most people probably only associate it with plants, as polyploidy in animals has been relatively understudied, and unisexuals—animals that are entirely female, are typically ignored because they use hybridization and parthenogenesis (though personally I think it may be male refusal to accept that they aren’t as permanent or resilient as they may have hoped—see the degenerate Y chromosome). The most famous female-only species are probably the New Mexico whiptails, Cnemidophorus neomexicanus, or “lesbian lizards,” a hybrid species of lizard that no longer involves males in their reproduction but still often perform courtship rituals to stimulate ovulation.
Both parthenogenesis (when eggs develop with no fertilization) and hybridogenesis (fertilization occurs but paternal DNA isn’t passed on) are pretty common in amphibians. A more intriguing example than the lizards, though one that’s gotten less press until now, is the unisexual Ambystoma hybrid salamanders. This salamander ranges from triploid to pentaploid with Ambystoma nothagenes using genes from males from three different salamander species– Ambystoma laterale, Ambystoma texanum, and Ambystoma tigrinum.
The Ambystoma females always require sperm from a related species to fertilize their eggs and initiate development and generally just discard the sperm genome. Sometimes the unisexual sexually reproduces instead and there is a genome addition or genome replacement event where the maternal genome is discarded or the female acquires the male’s genes and then keeps only some of the genes after mating.
What’s kind of intriguing about this case of “kleptogenesis”, or gene stealing, is that the females basically express genes from the different males at a relatively equal rate. How exactly they choose which genes to use and which to throw away is not known, nor is how these genes come together to make a good hybrid.
Why do it?
How Ambystoma, a six-million-year-old lineage, and how other polyploids/unisexuals/hybrid species survive when in competition with “regular” diploids living in the same spatial niche, is also not understood. It’s generally considered that polyploidy is a short-term strategy evolved in environments that are less stable. Which is why Ambystoma being a polyploid for so long is especially surprising.
While polyploidy can be advantageous, it’s initially unstable before becoming a competitive strategy. The presence of duplicated genes can help fuel diversification and evolutionary success.
Heterosis, gene redundancy, and asexual reproduction can all be considered advantages of polyploidy. Heterosis is essentially the ability to make better use of heterozygosity. Gene redundancy allows you to better diversity and provides a protection from harmful mutations. And asexual reproduction enables you to reproduce without a sexual mate around.
Polyploidy in animals is a case of convergent evolution where many fish and amphibians have acquired it separately. All the polyploids have acquired their genomes differently and in different ways. The unisexuals and males in the salamander group have higher gene exchange than other polyploids which may explain the “balance” in the genome not seen in other polyploids. Instead of gene silencing or dominance evolving, it seems natural selection has favored a more balanced genome because that’s just what worked for these girls. If you lose some gene contribution it’s less dramatic this way than if you’d put almost everything into one male salamander only for him to do something inconvenient like die or not show up to mate.
There’s some serious selective pressures for salamanders to survive injuries. They have the ability to regenerate tissue, so if part of their tails snap off, they can grow back. A study published in the Journal of Zoology showed that these polyploid all-female salamanders regenerate lost tissue 36% faster than other salamander species.
Within 10 weeks, after having had 40% of their tails cut off, the all-female salamanders had full length tails. The diploid sexually-reproducing relatives needed another 5 weeks to finish growing their tails.
The explanation may have to do with more genes meaning more proteins meaning faster regeneration. And if you can’t regenerate you don’t do so well so this could have been an added pressure to explain how this lineage was able to stay polyploid for six million years.
J. Saccucci, R. D. Denton, M. L. Holding, H. L. Gibbs. Polyploid unisexual salamanders have higher tissue regeneration rates than diploid sexual relatives. Journal of Zoology, 2016;
Comai, Luca. “The advantages and disadvantages of being polyploid.” Nature Reviews Genetics11 (2005)
Kyle E. McElroy, Robert D. Denton, Joel Sharbrough, Laura Bankers, Maurine Neiman, H. Lisle Gibbs. Genome Expression Balance in a Triploid Trihybrid Vertebrate. Genome Biology and Evolution, 2017
Evolutionary Significance of Whole-Genome Duplication. Mcgrath-M. Lynch – Polyploidy and Genome Evolution – 2012