Did inbreeding kill the mammoths? Don't believe everything you hear

Whenever people hear about inbreeding, many think of cousins marrying and having mutant babies. People think of inbreeding as a repulsive idea because our genes want us to reproduce with individuals not closely related to us, to decrease the chance of recessive, deleterious traits killing our offspring.  This would ultimately reduce the fitness of the population, a process called inbreeding depression.

Here's the thing, inbreeding is the mating of pairs who are closely related, genetically.  It can lead to homozygosity, which is when a cell has two identical alleles of the same gene on both homologous chromosomes.  In the punnett square below, the individuals with BB and bb alleles are homozygous for that particular trait.

Homozygosity is not necessarily a bad thing.  It's how some of us end up blonde - because blonde is a recessive trait (not dominant), and a person needs to be homozygous recessive for hair color to end up with blonde hair.  A person heterozygous for hair color would carry one copy of the dominant allele (brown) and one copy of the recessive allele, but would express the dominant allele and be brunette.  In reality, heredity is far more complex than this, what I've described here is a simplification of the process.  A lot of genetic disorders are recessive though.  That means that people can be carriers but not express a disorder.  When two carriers have a child, the child has a chance of being homozygous recessive for that trait, since both parents carry a copy of the allele.  It's the reason why purebred animals often have health problems.

Royal families have historically been inbred to maintain "pure" blood lines.  Because of its isolation, the population of Iceland was also historically inbred.  Inbreeding is never going to lead to mutant children with two heads, or something ridiculous like that, because humans do not carry genes for two heads.  In fact, no animals do.

But inbreeding depression in a population can be a really serious issue.  A new open access paper published this past week suggests that woolly mammoths (Mammuthus primigenius) may have inbred themselves into extinction.  See, there's a strong conservation across vertebrate species for the number of cervical vertebrae, which is typically 7.  There are interspecies variations, just like there are for any other trait, but intraspecies variation is limited.  The most typical variation in vertebral number is the presence of ribs in the seventh vertebra.

It looks like this:


The presence of a cervical rib is, in itself, harmless.  But still, 90% of people born with a cervical rib die before reaching reproductive age, thus presenting a huge selective pressure against cervical ribs.  Cervical ribs are often associated with multiple major congenital abnormalities.  The selective pressure against cervical ribs is thus a selective pressure against the other defects it is often associated with.

Three cervical vertebrae of the woolly mammoth were recently found in the North Sea during infrastructural work, and were donated to the Natural History Museum of Rotterdam.  Two of those three cervical vertebrae contained facets of cervical ribs.  The authors looked through other fossil records to find the prevalence of this trait in other mammoths, and in the closely related extant species of African and Asian elephants.

The authors found that 33% of samples from mammoths contained cervical ribs, compared to 3.6% for the two extant elephant species.  This is a statistically significant finding.  The authors then concluded that, with this high incidence of cervical ribs, coupled with the limited genetic diversity of the time, it is likely that inbreeding is what caused the development of these protrusions.  As you can imagine, the internet went bananas over this.

But I have a serious problem with the methodology of this study.  They looked at a total of 16 samples of mammoth cervical vertebrae, and 28 samples of the cervical vertebrae of extant elephants.  This sample size is too small to be considered valid and to support the generalizations that were made.  Furthermore, data was unavailable for 7 of the 16 samples from mammoths.  So they found 3 cases in 9 samples (33%), and reported this as statistically significant.  To be honest, I don't even understand why they would have reported that they looked at 16 samples, when they really could only measure 9 of them.  This was flagged in the peer-review process.  In fact, another group has recently been reported to have ruled out inbreeding among the dwindling mammoth population altogether.  While I'm not going to deny the findings, I'll reiterate that I think the authors have jumped the gun in terms of generalizing their results, and I think that the way this study was reported has now spread a huge amount of misinformation regarding the extinction of woolly mammoths.

This week in biology/medicine (March 24-30, 2014)

A European group has identified a fossil of a new, whale-like species that filtered plankton, showing that Cambrian ecosystems were closer to modern ecosystems than has been previously thought.

A photographic exploration of the oldest living things in the world.  Not research findings, but worth checking out anyway.

Being underweight is as much of a mortality and health risk as being obese.

Crows understand water displacement at the level of a 5-7 year old child. (Open Access)

Speaking of intelligent animals, goats are pretty smart too. (Open Access)

And a public health win!  Public smoking bans have been linked with substantial reductions in preterm births and asthma-related hospital admissions. (Open Access)

Ever had a migraine just after a stressful event?  Apparently that's normal.

Huntington's-associated neurodegeneration linked to depleted levels of an enzyme (cystathionine gamma-lyase) that makes cysteine.  Shameless self-promotion: if you want to know more about CGL or cysteine metabolism, check out this paper!

And a Dutch hospital used a 3D printer to make a plastic skull, which they then transplanted onto a patient.

Don't hit me with your best shot: self-vaccination against the flu

Well, we may be ramping down flu season up here in the northern hemisphere (if winter EVER decides to go away!), but the idea of self-vaccination against the flu is interesting nonetheless, and will be useful in the future as it continues to develop.

Seasonal flu is an infectious disease caused by a virus, and it is estimated to affect 5-10% of adults, and 20-30% of children.  The seasonal flu causes 3 to 5 million cases of severe illness annually (that's globally, fyi), and up to 500 000 deaths.  The most effective way to avoid getting the flu and spreading it to others is through vaccination.  Now, the way flu vaccines work, is that organizations like the CDC and WHO monitor what flu strains are going around.  While the northern hemisphere is experiencing its flu season, the southern hemisphere is not, and vice versa.  That means that whichever flu strains are going around the southern hemisphere in July are being monitored to try to predict which flu strains will be going around the northern hemisphere in January.  This process involves hundreds of research labs, all testing and identifying flu viruses from infected patients world-wide, year-round.  The WHO then consults with experts on which strains should be covered in the next flu shot.

Vaccination coverage against the flu is actually not as high as they should be, and the reason is not that flu shots are dangerous, but that a lot of people have trouble finding the time (I'm guilty of that this year...).  In the US, annual influenza vaccination coverage hovers around 42%, and in Europe it's about 12% for the general population.  To address low coverage and the costs of annual flu shots, researchers from Atlanta, led by James Norman, hypothesized that microneedle patches could be used to get people to vaccinate themselves.  This may sound like a weird concept, but keep in mind that when you take over-the-counter or prescribed medication in your own home, you are self-administering your medicine.  This self-vaccination would be the same thing.  This is what a microneedle patch looks like:

(source)

These have been used before for cosmetic applications and for hormone delivery, but data generally is not available.  This paper reports a study on the usability and acceptability of these patches for self-vaccination.

All participants were shown how to use the patch, and then self-administered three separate times.  The researchers found that there was a learning curve to self-administering, with the number of insertion sites increasing each time the patches were used.  The insertions were also generally well-tolerated, with only very mild redness and swelling of the skin.  About 51% of the participants who regularly get flu shots said they would be vaccinated against influenza if given the choice of having a microneedle patch instead of a needle and syringe.  Of the participants who don't get flu shots, 30% expressed willingness to be vaccinated if they were offered a microneedle patch, which went up to 38% when they were given the choice to self-administer their vaccine.  That means that almost 1/3 of normally non-vaccinated people would get one with this new method!  Participants were asked to rate the pain level between the use of a microneedle patch and an injection using a needle and syringe.  Microneedle patches scored 10 times lower on the pain scale!  

The most significant predictors of vaccine uptake were beliefs about the convenience and reliability of microneedles, and support for microneedles from doctors and family.  Ultimately, the researchers found that the use of microneedles could improve vaccination coverage in the US from 42% to 65%, which could have a significant impact on reducing hospital admissions, productivity losses, and deaths.  

Obviously this technology isn't ready to be rolled out for the 2014 flu season, but it's an interesting start and could have significant implications in the near future.

Let's talk about (plant) sex, baby!

You'd think with all my thesis studying, I'd have had enough of thinking about how awesome plants are.  But you'd be wrong.

When I was in the second year of my undergrad, I took a class on comparative plant physiology.  For some reason, I found this to be one of the more boring classes ever (until I had to sit through comparative animal physiology....zzzzzzzzzzz).  While studying for a final, one of my roommates told me that I needed to think of it like a soap opera.  Not 30 seconds later, I'm in my room reading about how in angiosperms (flowering plants), the pollen tube (the male reproductive organ) swells and bursts during reproduction.

  

And that is when I realized that plant sex can be quite raunchy.

Like I mentioned in my last plant post, many people do not actually think of plants as having these crazy, complex lives.  But they do, and they compete for mates just like animals do.  A new study published a few days ago in the New Phytologist (which I believe is open access), found that the pollen of milkweed actually use weapons to get an advantage over competitors.

It was previously believed that the only type of sexual selection plants like milkweed could participate in was just sending out massive amounts of pollen, in the hopes that one of those grains would be the first to reach the stigma - a part of the female reproductive organ, it looks like this:

(source)

Pollen is generally captured by the stigma either through the air or by pollinators.  Milkweed pollen develops in a pollen sac (technical term pollinium), which attach to the feet or mouthparts of pollinators, like bees, wasps, and butterflies, who then unknowingly contribute to a no-holds-barred sexual competition between plants.  Two pollinia are attached to form a complex (which is confusingly called a pollinarium).  There are five pollinaria per milkweed plant.  The pollinators pick up one of these complexes, then go off to another flower where they pick up another complex, and so on, and these pollinaria attach to each other like a chain, which is called concatenation, and it looks like this:

(source)

Basically what this diagram is showing you is that once the pollinaria attach, it leaves some pollen sacs more likely to leave their pollen on a stigma than the other pollen sacs.  This study looked at sexual selection in milkweed mediated through physical male interference, like where one pollen sac is located in the chain, and through the effect of physical traits, like the horn-like extensions, that contribute to one pollen sac maintaining its coveted position.

Alright, so the authors, led by Andrea Cocucci, studied four species of milkweed.  They analyzed pollen donation efficiency, and they found that there may be a competition for a "coveted spot" in the chain, but the chance of pollination is pretty similar no matter where the pollen sac is.  This position may only give a slight advantage, but not enough for it to be a sexually selected competitive trait.  Then, the authors looked at these horn-like extensions, called caudicle horns, that prevented concatenation in ancestral species.  

       

(horns)                                                    (no horns)

The horns on the pollinarium make it hard for the pollinaria of other species to attach in a chain.  That pretty much gives that plant a selective advantage over another plant, whose pollinaria allow for concatenation.  

Plants are not typically known to use these types of "weapons" and interference strategies in reproduction the way animals do.  This shows that there is a confrontation process in milkweed plants during reproduction that involves a direct physical interaction, and traits like these horns are an adaptive trait likely evolved from male-male competition in plant reproduction!  This is the first-ever report of an active competitive interaction among pollen before landing on the stigma, and the authors go as far as comparing these horns to those of bucks, who violently compete for mates:

(source)

This study also shows that sexual selection is possible even without the ability to move around, see, and smell.  The only thing that's needed for sexual selection is proximity and physical contact.  

Note: I grabbed most of these figures from the research paper.  If you're going to use them, please cite the original paper

If you're interested in learning about animal sexual selection, I'd suggest checking out Dr. Tatiana's Sex Advice to All Creation.  This was one of my "textbooks" for my biology of sex class in second year, super funny and informative!

This week in biology/medicine (March 17-23, 2014)

Scientist find a new mechanism for how body clocks work - could be used in the future to alleviate the effects of chronic shift work and jet-lag.

The loblolly pine genome has been sequenced - that's a loblolly pine below, it's the largest genome sequenced to-date: over 7 times the size of the human genome! (Open Access)

Can't remember where you put your keys?  Blame your genes.

Paternal age causes widespread alterations in gene expression, especially with those genes associated with inflammation, which is implicated with autism. (Open Access)

HIV viral protein is a neurotoxin associated with memory and learning impairment, even under conditions of limited viral replication. (Open Access)

Half of Americans believe in medical conspiracy theories.  Wow!

Effective leaf mimicry was achieved as early as the Early Cretaceous period.  Fossil of the earliest known stick insect discovered. (Open Access)

(source)

Predicting Human Facial Features From DNA Sequence

Alright, with the emotional rollercoaster of submitting my PhD thesis for defense over, and with my second dose of caffeine hitting my bloodstream, it's time to talk some science.

Just this morning, I came across a gem of a paper, published two days ago, that may just revolutionize forensic sciences and paleontology/anthropology (and it's open access! Bonus!).  This paper discusses the creation of a 3D model of human faces based only on their genome sequences.  I'm going to be talking about this paper in a forensics context: even though we've sequenced the human genome, generally only a few physical characteristics can be inferred from any DNA left behind at a crime scene.  Before 2012, forensic scientists could derive ethnicity, ancestry, and in some cases hair colour, but that was pretty much it.  In 2012, a Dutch group of researchers reported finding five candidate genes that influenced human face shape, or facial morphology.

Human face and head shape (or the technical term craniofacial shape) is determined during embryonic development through a series of precisely-timed gene expressions and interactions.  Then, as humans grow and develop, environmental factors and hormones continue to affect facial development.  Part of the reason why identifying the genes involved in human facial morphology has been so difficult is because through the use of genome-wide association studies, we've been trying to define facial development as univariate (meaning it only has one set of variables that define it), rather than the mutlivariate trait that it really is.  But this American group, led by Peter Claes, used a novel method that combined a bunch of different 3D modeling and gene analysis procedures, to look at between-population facial variation using participants with mixed West African and European ancestry from North America, Brazil, and Cape Verde.

The researchers used SNP (pronounced snip) genotyping to identify variance in the gene sequence of participants. SNPs are single nucleotide polymorphisms, which means that they are variations in the sequence of a gene at a single point in the DNA region being observed.

This may seem like it's just a tiny, insignificant change, but SNPs are actually responsible for the majority of genetic variation between humans, and are hugely important in the development of disease, and in response to pathogens, vaccines, and drugs.  In a human genome, there are many many SNPs, no one has just one.  They are also important in crop and livestock breeding, since they introduce the genetic variation that farmers and scientists select for (or against).  In my lab, I tried to work out a really interesting way to use SNPs to identify gene copy number, as an alternative to using Southern blots.  But that's a story for another day (unless it never gets published).

Anyway, Peter Claes and his colleagues selected 50 genes that were potentially related to craniofacial development, and a set of SNPs that had a high frequency of variation in these genes, to test these for their associations in facial shape variation.


Their method jointly modeled ancestry, sex, and genetic makeup (the technical term is genotype), in order to identify their independent effects on facial development. Once they created their 3D model they had another set of participants come in and look at the faces, and try and discern important characteristics from them.  Ultimately, the researchers found a set of 20 genes that significantly influence facial features, particularly in terms of face length and width, strength of the brow ridge, eye distance, nose width, and philtrum size and shape.  Obviously this is just a start, and there needs to be more study with other populations before this model is generalizable.  But the authors are confident that in 5-10 years, this model will be helpful in the prediction of human faces, especially the effect of other factors (age, temperament, adiposity) on facial features.  The construction of a 3D model of a person's face from DNA left at a crime scene could be used to help identify a suspect - although once apprehended, a sample of their DNA would have to match that found at the crime scene.  At the moment, this technology is too new to be used as evidence in a criminal trial.  Interestingly, this technique can also be used to make detailed facial reconstructions of our ancestors, which hasn't been possible to-date.

Thesis Writing, BRB

Hey science lovers,
I'm just putting some finishing touches onto my thesis to submit this week.  I'll be back with some more science soon.  In the meantime, enjoy this bit of whimsy:

GMOs take 3: what does Roundup actually do?

Alright, at the risk of typecasting myself as a one-trick pony, I have decided to write a piece about Roundup and how it works.  Given the recent traffic I've been getting on my GMO-related posts though, it seems there's a dearth of easily accessible, good scientific information out there on what really goes on when it comes to GMOs, and people really want to know more.

So, first of all, Roundup is the name of an herbicide that is sold by Monsanto.  I understand that everyone thinks Monsanto is the worst thing to ever happen to the planet, but lets put that aside for now and just focus on the science.  Roundup is the trade name for a chemical called Glyphosate, it looks like this:

(source)

What this chemical does is it inhibits an enzyme (5-enolpyruvylshikimate-3-phosphate synthase, or EPSPS for short), which is involved in making the precursor to the biosynthetic pathways of the amino acids tyrosine, tryptophan, and phenylalanine.  For reference, human beings do not have these pathways, we need to get our aromatic amino acids from our food.  That means that if you were accidentally sprayed with Roundup, nothing would happen to you.  This inhibition is competitive, which means that the glyphosate binds to the site in the enzyme where its substrate would go.  Anyway, this basically inhibits plant growth because those amino acids are necessary for plants to grow.  Idealy, the only plants that are able to grow in the presence of Glyphosate are those that have been genetically modified to be glyphosate resistant, or Roundup Ready.

Glyphosate-resistant plants have been genetically modified to over-express bacterial EPSPS.  That means the plants express the bacterial form of the gene, which is resistant to the effects of the inhibitor, at amounts that are higher than normal gene expression for the plant.  Scientists do this kind of over-expression all the time, including for something as simple as purifying proteins or for making vaccines.  When we over-express a gene, we're basically asking the host organism to make as many copies of it as is possible.  That's it, that's all there is to it.  The bacterial gene isn't bad for humans or other animals, because a) we don't have the necessary biochemical pathway anyway, and b) like I said in my first post on GMOs, the food we eat every single day is covered in bacteria which means that at many, many points in your life, you've consumed bacteria that has EPSPS in its genome, and you've lived to tell the tale!  Eating Roundup Ready plants is no worse than eating bacteria-covered plants, you're exposed to the same genes.

Ok, so most people argue that Roundup is a toxic chemical and they don't want to be eating crops that are completely doused in herbicides and pesticides.  See, people think that because something kills a plant, it's automatically dangerous to people.  But that's simply not true.  Another commonly used herbicide is 2,4-D (aka 2,4-dichlorophenoxyacetic acid), which is a synthetic auxin.  Auxin is a plant hormone that mediates plant growth and development.  Sidebar: plants only have 5 types of hormones that basically do EVERYTHING!  Plants are amazing!

Anyway, every time I debate with people about GMOs, the conversation is always derailed by the evil practices of Monsanto.  And that's because as soon as you really understand the science behind GMOs, it's hard to argue against it.  Monsanto is a company that wants to make money (GASP!), and so yes, it charges people to use its products.  But that doesn't mean GMOs are bad or will kill you.  Glyphosate and the products of its degradation have been shown to have low toxicity when ingested, inhaled, or applied to skin.  It's not a toxin that kills everything it touches except for Frankenplants.  It's a little bit less effective now because the improper and/or widespread use of glyphosate has led to the development of resistant weeds - this is the same problem we're starting to see with the widespread, improper use of antibiotics.

GMO take 2: stop using bad science to justify your fearmongering!

 

I am often on I F*cking Love Science! because in fact, I do.  And every time they post something interesting on GMOs, there's a huge amount of backlash from followers.  I always answer them with my previous post on GMOs, but now I feel like we need to have another talk.  This one is about all the fearmongering that people are spreading regarding GMOs using bad science!  

This is what came up in the comments:

That first comment is addressed in my previous post on GMOs.  But that second one?

Well, I followed that link, which led me to a newspaper article, which led me to another newspaper article, and eventually I found the study that they were referring to.  Which, by the way, is the one up at the start of this post, and has been RETRACTED!!!!  It was retracted because after its publication, several members of the scientific community began raising questions about the validity of the findings, the proper use of animals, and even allegations of fraud.  The editor-in-chief of the journal Food and Chemical Toxicology, who, by the way, has a Ph.D. and research experience, reviewed all of the data that the authors of the article had collected.  While he found no fraud, he did think that the number of animals used in the study was such a small sample size (which was also flagged during the peer-review process), that NO CONLUSIONS COULD BE DRAWN between exposure to Round-up and tumor development.  PLUS, the strain of rat that was being used in this study (Sprague-Dawley) has a known high incidence of tumor development.  So that means the strain chosen for this study confounds the results based on having a high background rate of natural tumor development.   The results are not necessarily incorrect, but they are considered inconclusive. Plus, people are under the impression that because this research was funded by an independent scientific research council means that it's completely legit.  Well, CRIIGEN may be independent, but they have their own agenda, and it's very anti-GMO.  Research being funded by this organization may be just as biased as research being funded by Monstanto, yet no one is up-in-arms about that.  This is a French organization, and France is notoriously anti-GMO.  (I've listened to French scientists tell stories about their fields being burned down and their labs being ransacked because they were involved in GMO research).

But the damage is done, just like the bad science that has led people to firmly believe that vaccination is harming their children.  But seriously folks, do some thinking and some research before you start misinforming and fearmongering.  GMOs are NOT going to kill you. 

Extraterrestrial origins of life: more than science fiction?

 

I am never opposed to a wacky idea just because it seems a bit "out there."  As such, I've always been open to the idea of panspermia, or the idea that life exists throughout the universe, and that life on Earth comes from an extraterrestrial origin.  Star Trek did it.  And Star Trek has been right about A LOT of things.  But joking aside, I like the idea of non-terrestrial origins of life.  We already accept the fact that the water on Earth came from space.  Is it so far-fetched to think that maybe life did too?

Not long ago, I came across an article on cracked.com, that made fun of scientists for believing in really wacky, non-sciency ideas.  Dr. Francis Crick (of Watson and Crick, the "discoverers" of the structure of DNA) apparently believed in panspermia. The author of the article, who completely misunderstands the idea behind panspermia and extraterrestrial origins of life, pokes fun at Crick for being as crazy as a scientologist.  Well, I'm here to challenge him.

Panspermia is not that crazy an idea.  Let me first summarize the arguments of Wickramasinghe and Trevors.  These guys first state that any paradigm shifting idea in science receives a lot of push-back from the scientific community, but the very process of challenging existing ideas is what science is all about.  The prevailing concept is that of a terrestrial "primordial soup" as the origin of life on Earth.  This idea states that all of the organic molecules that are life's chemical building blocks were originally formed entirely in terrestrial clouds through UV radiation from the sun and electrical discharges from lightening.  This has been replicated in laboratory work.  But what's lacking from this idea is how did life arise from the soup of organic compounds?  How did this system of amino acids and sugars develop into a self-replicating living cell?  Even without answering that, the primordial soup concept has achieved paradigm status, and is the predominant idea most people have on the origins of life on Earth.  This idea was challenged in the early 1900s, by Svante Arrhenius, who posited that bacterial spores containing genetic information could have been lifted off other planets and been propelled through space to Earth.  This idea was unpopular because it was untestable, because he basically said that the movement of extraterrestrial cells to Earth at the present time would be too small to be detected.  So the primordial soup idea remained as the favoured paradigm.

In the 1950s, the consensus among astronomers was that the dark irregular patches in the Milky Way were the result of ice particles.  But Wickramasinghe challenged this idea in the 1960s, showing that these "dust" particles were actually made of carbon, which is, of course, the signature element of life.  In characterizing this dust, he received a lot of criticism from both astronomers and biologists because this was a hugely paradigm-shifting idea.  In the 1980s, Wickramasinghe and his co-author Hoyle estimated that the random assembly of the simple amino acids and sugars in the primordial soup into even the simplest of self-replicating microbes involved probabilities so incredibly, infinitesimally small that they would not reasonably be thought to have happened in the context of the primordial soup in that amount of time.  Instead, they have posited a hypothesis that microbial life arrived on Earth around 4 billion years ago, which coincides with the an epoch of intense bombardment of the developing Earth.  This isn't so hard to imagine when we think about the discoveries of extremophilic microbes that can fit into every conceivable environment, no matter how inhospitable they might appear.

For example, waterbears (Tardigrades):

These guys are a micro-animal that can withstand temperatures at just around absolute zero (-273 Celsius, -460 Fahrenheit) and pressures about six times higher than what we would find in the deepest trenches of the ocean, AND ionizing radiation at doses hundreds of times higher than the lethal human dose, AND the vacuum of space.  Why would it need to have these traits if it was not exposed to these stressors regularly on Earth?  That doesn't seem to fit with the idea of evolution through natural selection, since there would be no suitable selective pressures for these traits on Earth.  Hmmmmm.

Then there's the Cyanobacteria:

These guys made the news last year for surviving over 550 days in space.  These little blue-green guys photosynthesize, just like plants do.  They hitched a ride on the outside of the International Space Station for 553 days, and survived!  In the cold vacuum of space.  If you're interested in learning more about Cyanobacteria, click here.

Other types of microbes have been taken into space and survived.  That's a pretty big deal!  So is it really that crazy to think that life on Earth might have originated in space?  The only way we'll ever be able to find out for sure if the origin of life on Earth is extraterrestrial is to find life out there, or traces of life, that has the same genetic code as terrestrial life.  All terrestrial life has the same genetic code, so this would be the best way to prove the idea of panspermia.  Of course, there would be huge implications for human psychology, even health, and our concepts of evolution, star formation, and even genetic engineering.  Now all we have to do is find extraterrestrial life!

New evidence that plants have decision-making capabilities based on the perception of risk

Plants are amazing.  That is a fact.  As a plant scientist, that is the answer I've always given to the typical question: "why do you even like plants?  They're so boring!"  NO!  Plants are unbelievably complex, animals are boring!
Sidebar: I am so into plants that this will likely be the first of a series of posts on how cool plants are.  Prepare yourselves.

Animal behaviour and adaptation is based on movement.  Stressful environment?  Cool, I'll just migrate.  But plants can't move around, so they've had to develop all these super amazing and complex strategies for surviving and thriving in stressful and changing environments.  Case: wild tobacco plants in the U.S. were pollinated by a type of moth that would also lay its eggs on the plants.  This attracted caterpillars that started eating the plants, so what did the plants do?  The plants stopped producing the chemicals that attract its usual pollinator and started flowering during the day instead of at night, to attract a different kind of pollinator!  That would be like a woman being able to actively decide when she ovulates.  It's bananas!  See, plants are cool!

Plants have a really complex secondary metabolism.  Every living creature has primary metabolic pathways, which are necessary for life.  This is the metabolic network that allows organisms to grow and reproduce, maintain structures, and respond to the environment.  Secondary metabolism refers to the network that also helps organisms survive, but they're not absolutely necessary for survival.  Secondary metabolism is what makes plants so awesome!  In plants, secondary metabolism supports primary metabolism by keeping the primary metabolic network working.  It's also extremely important for plant defense.  A lot of the volatile compounds (a fancy way of saying compounds that vapourize at room temperature) are produced during secondary metabolism.  Volatile compounds are what makes herbs and spices smell and taste good.  They're used to deter herbivores, and are often used in signalling from one plant to another.  One really cool defense mechanism that plants have is through methyl jasmonate, which is a compound that plants release when they're being eaten by caterpillars.  This heightens the plants own defenses, but it also warns the plants around it that there are herbivores around, so they might want to heighten their own defenses.  There are other insects that prey on these caterpillars that have adapted to recognize methyl jasmonate.  They then sweep in and lay their eggs inside the caterpillars.  But because plants aren't wasteful, jasmonates are also used as a signal for flowering and aging.

 

(I thought this was fitting)

Anyway, that's my attempt to convince you, dear reader, that plants are pretty amazing.  This post is actually about a new paper that outlines the seed abortion decision-making process in plants that is based on both internal and external cues.  Seed abortion in this case basically means that plants are selectively deciding whether or not a seed will develop.  In the context of this paper, that means that if there is a high amount of parasite infestations in the surrounding environment, then producing a seed, and the fruit to protect the seed and help in its dispersal, is energetically too costly for the probability that the seed will survive.

The authors used Tephritid fruit flies, which lay their eggs in the fruit of the European Barberry.  Larvae eat the fruit and seeds.  There is usually only one larva per fruit, and each fruit has two seeds.  That means that the larvae probably need more than one seed to survive.  So the plant can let both seeds die, or it can selectively abort one of the seeds, leaving the other to develop.  This increases the likelihood that one of the seeds will survive and grow into a plant.

What the authors found was that this selective abortion of seeds was strategic.  Seed abortion was higher when there were two viable seeds per fruit (neither was damaged), increasing the odds that one would survive.  It was also higher when water constraints and predation by the fruit flies occurred together; exposing a plant to one stressor decreases its likelihood of survival, exposing it to two stressors is even worse.  Basically, the plants are strategically deciding, based on environmental cues, what the likelihood of offspring survival is, and how best to increase the odds.

This has led a lot of people to describe the results in the context of plants "thinking", which ends up in a philosophical debate about thinking that derails the conversation about a really interesting discovery.  If we think of human thought as a process that allows human beings to reflect on and interpret their environment and to make plans and predictions about the world, then can we really say that this process in plants is any different?  Just some food for thought.

Resurrected 30 000 year old virus provides clues for viral diversity

By now lots of people have probably heard the news about the 30 000 year old virus from the Russian Arctic that was discovered and brought back to life.  A group of scientists from France initiated a survey of the Siberian permafrost, and discovered a large DNA virus that maintained its ability to infect its host after thawing.  Reports have been clear about the fact that this virus does not affect humans or animals.

We all know of viruses that affect humans, like influenza and varicella, but people may be more unfamiliar with giant viruses.  Large DNA viruses are viruses that contain DNA, and whose particles are large enough to be seen using a light microscope (the ones we all used in high school).  Considering that most bacteria are 1/10th the size of bacteria, that makes these large viruses huge!  Virus particles (or virions) contain genetic material (either DNA or RNA), a protein coat to protect the genetic material, and an envelope around the protein coat. (x).

There is debate as to whether or not viruses can be considered "alive".  They do carry their own genetic material, they reproduce, although they need a host cell to do it, and they are able to evolve (that's why antiretroviral drugs for HIV treatment that worked well in the last decades don't work as well anymore).  What keeps them from truly being classified as "alive" is that they lack key characteristics such as cell structure.  Viruses are often described as organisms on the edge of life.

 Regardless of the type of virus you're dealing with, the life cycle will be the same.  Viruses attach themselves to a host cell and releases its genetic material inside.  That genetic material essentially hijacks the host cell's enzymes to make more viruses.  The viral particles assemble into viruses, which eventually lyse, or split, the cell.  Proteins are classified by what type of genetic material they have, and which enzymes they take over in their host cell.

DNA viruses carry DNA as their genetic material.  One example of a DNA virus is varicella, or chickenpox.  This type of virus hijacks DNA polymerase, the enzyme that copies and replicates DNA, and is used in cell division.  I wrote a bit about DNA polymerase in relation to telomere erosion last month.  Basically, what happens is the enzyme copies the DNA from the virus, which is then copied into RNA like the rest of the host cell's genome.  Influenza is an RNA virus.  That means that its genetic material is RNA.  The classification system for RNA viruses is a bit more complicated than I want to get into.  The simplest way to think of it is this: in our cells, DNA is transcribed into RNA, which is then translated into proteins.  For RNA viruses, their genetic material enters the cell as RNA, so it hijacks the translation enzymes, or the enzymes that are used in making proteins.  In a sense, RNA viruses skip one of the steps that DNA viruses use.  There are also retroviruses, such as HIV, which is also an RNA virus, but the difference is that it requires the reverse transcription of RNA into DNA.  The virus has its own enzyme that does this (called Reverse Transcriptase - scientists are creative!), the resulting DNA is then incorporated into the host genome.  Then the host cell treats the viral DNA like its own DNA, replicating it and making lots of viral particles.  Viruses are a really important means of horizontal gene transfer, the process of transferring genes from one organism to another by a means other than reproduction.  As such, viruses are an important contributor to genetic diversity.

The large DNA virus that was found in the Siberian permafrost infect a type of protist of the genus Acanthamoeba.  These are a type of amoeba that are most often found in fresh water.  The amoeba are mostly bacterivores, which means they eat bacteria, but some opportunistically infect humans and animals too.  The researchers found the large DNA virus, called Pithovirus sibericum, by using Acanthamoeba as bait.  The Pithovirus was then identified using a light microscope, and was collected from deep permafrost layers, whose oldest sediments date back to the Pleistocene, which ranges from 2.5 million to 11 000 years ago.  The sediments in which Pithovirus was found are 30 000 years old.  The virus was used to infect Acanthamoeba in order to amplify viral particles, which were then observed.  That means that the virus was still able to infect its host cell (aka, still virulent) even after 30 centuries!  The researchers were able to look at a full replication cycles, which lasted around 10-20 hours.                                           

                                                                                                                                               (x)                

There are other types of large DNA viruses that have been identified that infect Acanthamoeba.  They are Mimivirus, Moumouvirus, Megavirus, and Pandoravirus.  Prior to the discovery of Pandoravirus, large DNA viruses displayed the same distinctive features: they all had similarly shaped and sized capsids (the protein coat surrounding the genetic material), a large, adenine-thymine (AT)-rich genome, and they encode their own full transcription mechanism.  Pandoravirus shook things up with its large amphora-shaped capsids, and its cytosine-guanine (CT)-rich genome.  It basically has no resemblance to the other large DNA viruses.  So it was believed that large DNA viruses that infect Acanthamoeba were segregated into two families.  The discovery of Pithovirus now shows that large viruses are more diverse than originally thought.  DNA sequencing of Pithovirus found an AT-rich genome that is remarkably small, about 5 times smaller than that of Pandoravirus.  The genome of Pithovirus also encodes 5 times fewer proteins than the genome of Pandoravirus, although interestingly, the number of proteins that are used to make viral particles are similar between the two types of virus.  That pretty much means that large and complex  viral particles don't necessarily always have to come from larger genomes.  

The authors mention that this is the first time an ancient virus like this has been revived.  There have been other ancient viruses identified, ranging from 7000-140 000 years old, but no mention has been made of their viability.  The authors also stress that the thawing of the Siberian permafrost due to climate change, drilling, or mining, may cause the release of ancient and viable pathogens like Pithovirus that we're not ready to deal with.  Pithovirus may not infect humans, but it has a genome structure and replication cycle similar to that of other large DNA viruses that do infect humans and animals, and their release into our ecosystem could have devastating effects on human health.