Relatedness is relative: How can I be 85% genetically similar to my mom, but only related to her by half?

First of all, no. I am not the lovechild of star-crossed siblings, or even cousins, or even second cousins. 

This is a gee-whiz kind of post. But the issues are not insignificant.

Hear me out with the background, first, before I get to the part where my eyes bug out of my head and I pull out my kid's Crayola box and start drawing.

If you've learned about sociobiology, or evolutionary psychology, or inclusive fitness, or kin selection, or the evolution of cooperation and even "altruism," or if you've read The Selfish Gene, or if you've been able to follow the debate about levels of selection (which you can peek at here)...

... then you've heard that you're related to your parents by 1/2, to your siblings by 1/2 as well, to your grandparents and grandchildren by 1/4, to your aunts and uncles and nieces and nephews by 1/4 as well, and to your first cousins by 1/8 and so on and so forth.  (Here's some more information.)

So, for example. For evolution (read: adaptationism) to explain how cooperative social behavior could be adaptive in the genetic sense, we use the following logic provided by Bill Hamilton, which became known as "Hamilton's Rule": 

The cost to your cooperation or your prosocial behavior (C) must be less than its benefit to you (B), reproductively speaking, relative to how genetically related (r) you are to the individual with whom you're cooperating. That could have come out smoother. Oh, here you go:

C < rB, or B > C/r

If you're helping out your identical genetic twin (r=1.0), then as long as the benefit to you is greater than the cost, it's adaptive.

C < B, or B > C

If you're helping out your daughter (r = 0.5) then as long as the benefit to you is greater than twice the cost, it's adaptive.

C < (1/2)B, or B > 2C

So already, the adaptive risk to helping out your daughter or your brother is quite higher. And it's even harder to justify the cooperation between individuals and their sibs' kids, and grandkids, especially ESPECIALLY non-kin. But, of course creatures do it! And so do we.

As relatedness gets more distant and distant, we go from 2 times the cost, to 4 times, 8 times, 16, 32, 64 etc... You can see why people like to say "the math falls away" or "drops off" at first or second cousins when they're explaining where the arbitrary line of genetic "kin" is drawn.  If you offer up a curious, "we're all related, we're all kin," someone out of this school of thought that's focused on explaining the evolution of and genes for social behavior may clue you in by circumscribing "kin" as the members of a group that are r = 1/8 or r = 1/16 but usually not less related than that.

This has long bothered me because we're all genetically related and so much cooperation beyond close kin is happening. And it's been hard for me, as someone who sees everything as connected, to read text after text supporting "kin selection" and "kin recognition" (knowing who to be kind to and who to avoid bleeping), to get past the fact that we're arbitrarily deciding what is "kin" and it seems to be for convenience. I'm not doubting that cooperation is important for evolutionary reasons. Quite the contrary! It's just that why is there so much math, based in so many potentially unnecessary assumptions about genes for behavior, gracing so many pages of scientific literature for explaining it or underscoring its importance? 

(It could just be that as an outsider and a non-expert I just don't understand enough of it and if I only did, I wouldn't be gracing this blog with my questions. But let's get back to my reason for posting anyway because it's potentially useful.)

Right. So. Even for folks who aren't part of evolution's academic endeavor, it's obvious to most that we're one half dad and one half mom. The sperm carries one half of a genome, the egg another, and together they make a whole genome which becomes the kid. Voila!

There's even an adorable "Biologist's Mother's Day" song about how we've got half our moms' genome... 

... but there's biology above and beyond the genes we get from mom (and not from dad). And that song is great for teaching us that the rest of the egg and the gestational experience in utero provide so much more to the development of the soon-to-be new human. So "slightly more than half of everything" is thanks to our mothers. Aw!

But, genetically, the mainstream idea is still that we're 50% our mom. 

I teach very basic genetics because I teach evolution and anthropology.And I'm not (usually) a dummy.* I get it. It's a fact! I'm half, genetically, my mom and I'm also half my dad. 

r = 0.5

Okay! But, given these facts about relatedness and how it's imagined in evolutionary biology, facts that I never ever questioned, I hope you can see why this report from 23andMe (personal genomics enterprise) blew my mind:

Percent similarity to Holly Dunsworth over 536070 SNPs (single nucleotide polymorphisms or, effectively/rather, a subset of known variants in the genome; Click on the image to enlarge).
I am 85% like my mom and I am at least 76% like my students and friends who are sharing with me on 23andMe. Names of comparisons have been redacted. As far as I know, this kind of report is no longer offered by 23andMe. I spat back in 2011/12 and the platform has evolved since.

Okay, first of all, it is a huge relief that, of all the people I'm sharing with on 23andMe, the one who squeezed me out of her body is the most genetically similar to me. Science works.

But that number there, with my mother, it is not 50%. It's quite a bit bigger than that. It says I'm over 85% the same as her.

What's more, I am also very similar to every single person I'm sharing with on the site, including example accounts from halfway around the world. Everyone is at least 60-ish% genetically similar to me, according to 23andMe. I know we're all "cousins," but my actual cousins are supposed to be 1/8th according to evolutionary biology. How can my mom be related to me by only one half? How can my actual cousins be only an eighth (which is 12.5%)? 

What is up with evolutionary biology and this whole "r" thing?

Hi. Here is where, if they weren't already, people just got really annoyed with me. Evolutionary biology's "relatedness" or "r" is not the same as genetic similarity like that reported by 23andMe.

Okay!

But why not? 

Let me help unpack the 85% genetic similarity with my mom. Remember, it's not because I'm inbred (which you have to take my word for, but notice that most everyone on there is over 70% genetically similar to me so...).

It's because my mom and dad, just like any two humans, share a lot in common genetically. Some of the alleles that I inherited from my dad are alleles that my mom inherited from her parents. So, not only is everything I got from her (50%) similar to her, but so are many of the parts that I got from my dad. 

Let me get out my kid's arts supplies.

Here is a pretty common view of relatedness, genetically. In our imagination, parents are not related (r = 0) which can lead our imagination to think that their alleles are distinct. Here there are four distinct alleles/variants that could be passed onto offspring, with each offspring only getting one from mom and one from dad. In this case, the sperm carrying the orange variant and the egg with the blue variant made the baby.

1. (Please, if you're horrified by the "r" business in these figures, read the post for explanation.)

But few genes have four known alleles, at least not four that exist at an appreciable frequency. Some could have three. What does that look like? 

The green allele doesn't exist in the next example. As a result of there being only three variants for this gene or locus, mom and dad must share at least one allele, minimum. That means, they look related and that means that, depending on which egg and sperm make the kid, the kid could be more related to mom than to dad. 

2. (Please, if you're horrified by the "r" business in these figures, read the post for explanation.)

Now here's where people who know more than I do about these things say that the kid is not more related to mom than dad because she got only one allele from mom and that keeps her at r = 0.5. 

Well, that's just insane. What does it matter whether she got the allele from mom or dad? I thought genes were selfish? (Sorry, for the outburst.)

Again, I realize I'm annoying people and probably much worse--like stomping all over theory and knowledge and science--by mixing up the different concepts of genetic similarity (e.g. 50%) with "r" (e.g. 0.5) and horribly misunderstanding all the nuance (and debate) about "r," but I'm doing it because I'm desperately trying to know why these two related ideas are, in fact, distinct. 

One last pathetic cartoon. 

In this third example, as is common in the genome, there are only two alleles/variants in existence (at an appreciable frequency, so not accounting for constant accumulation of de novo variation). An example of such a gene with only two known alleles is the "earwax gene" ABCC11 (there's a wet/waxy allele and dry/crumbly one). Here, the two alleles are orange and blue. Most humans in the species will have at least one allele in common with their mate for a gene with two alleles, and it's not because most humans are inbred, unless we want to redefine inbreeding to include very distant relatives (aside: which may be how the term is used by experts). 

3. (Please, if you're horrified by the "r" business in these figures, read the post for explanation.)

But as a result of the chance segregation of either the blue or orange allele into each of the gametes, two people with the same genotype can make a kid with the same genotype. 

And of course, making a kid with your same genotype is the only possible outcome if you and your mate are both homozygous (i.e. where both copies are of the same variant so that leaves no chance for variation in offspring unless there is a new mutation). 

So, I wandered a little bit away from my point with these drawings, but I had to because I wanted to get down from where my imagination has me (us?) with "r" versus how things really are with reproduction. We are baby-making with vastly similar genomes to ours, so we are making babies with vastly similar genomes to ours. 

So, I do see why biology says I'm related to my mom by one half. But, on the other hand, what does it matter if I got the thing I have in common with my mom from my mom or whether I got it from my dad? Because I got it. Period. It lives. Period. 

[Inserted graf January 20, '17] Saying it matters where I got the similarity to my mom keeps us at r = 0.5. Saying it matters only that I inherited DNA like hers keeps us always, all of us, at r > 0.5 with our parents and our kids because any two babymakers share much of their genome.

And the fact that this (see 2 and 3) happens so often is why I'm a lot more than 50% genetically like my mom, and the same can be said about my genetic similarity to my dad without him even spitting for 23andMe. 

So, here we are. I don't understand why our relatedness to one another, based on genetic similarity, is not "r."

I hope it's for really beautifully logical reasons and not something political. 

Because...

If "r" was defined by genetic similarity, then would cooperating with my 76% genetically similar students and friends be more adaptive than the credit I currently get from evolutionary biology for cooperating with my own flesh and blood son? 

If "r" was defined by genetic similarity, then could we use the power of math and theoretical biology to encourage broader cooperation among humans beyond their close kin? 

So many questions.

Maybe I should re-learn the math and learn all the other math.

Nah. Not myself. At least, it wouldn't come fast enough for my appetite. Maybe someone who already knows the math could leave a comment and we could go from there... 

And it would be worth it, you know, because despite my relatively weaker math skills, I bet we're more than 50% genetically similar.

*from 23andMe: "You have 321 Neanderthal variants. You have more Neanderthal variants than 96% of 23andMe customers."

What if Rev Jenyns had agreed? Part II. Would evolutionary theory be different from a population perspective?

In yesterday's post I noted some general differences between Darwin's individual-centered theory of evolution, and AR Wallace's more population-focused ideas.  Of course they both developed their ideas with the kinds of knowledge and technology then available, so we can use them to represent differing points of view we might hold today, but must realize that that is symbolic rather than literal. They were who they were, both skilled and perceptive, but their ideas were subject to modification with subsequent knowledge. One major piece of knowledge that emerged after their time was that genes are point causes of biological function, that is, single locations in DNA with distinct activity.
But that knowledge was derived from Mendel, Morgan, Watson, Crick and a host of others, who, following Mendel, pursued genetic function with independent point causation as the assumed starting point that drove their study designs.  DNA may be atoms on a string, but the assumption was misleading then, and still is today.

Alfred Russel Wallace

The modern theory of evolution, population genetics, is based on genes as point causes, and it recognizes the local nature of evolution in time and space.  A genetic variant's chances of spreading in a population are, naturally enough, seen in population perspective.  But by and large that perspective is about a genetic variant, and indeed attempts to explain functional and adaptive evolution from a single gene's point of view.  The variant's success depends on the relative success of other variants at the same locus--competition.  Of course that success depends on many things, but this perspective basically just 'integrates' away all factors other than the gene itself, computing a net-result picture.  It is very 'Darwinian' in the sense of being strongly deterministic and considering genes as points individually competing with each other for success.

This is not a fallacious picture, but I think it's not terribly relevant to the kinds of questions most people are asking these days, both in evolution and in biomedical genetics.  One needn't deny that individual genetic variants don't have their differential success over time, or that we can't or shouldn't be aware of nucleotide differences.  To do so would be something like denying that a house is made of bricks, the bricks can be identified and enumerated, and they have something to do with the nature of the house.  The question is the degree to which you can explain or predict the house from the enumeration of the bricks.

There are those who suggest that evolution is more about interaction at the genome level than it is about single alleles; enumerating bricks is not enough. However, the allele-focused view would have it that it is only the 'additive' aspect of each individual allele's effect on its own, that is transmitted. The idea is that even if the combination of alleles at and among loci affect an individual's traits (roughly, this is called 'epistasis'), s/he only transmits a roughly random half of those to each offspring.  Thus, the combination effect is not inherited.  Epistatic holism is an evolutionary hoax.

This venerable riposte to those arguing for a more 'holistic' or complex genomic viewpoint may be mathematically true in the abstract, but misses an important point.  In fact, the fitness (reproductive success) of a given allele entirely depends on the rest of the genome and the external environment.  If you just think about how life works (that is, metabolism, morphology, and many other complex interactions), the dependency is very unlikely to be simply additive. Things work, things adapt in combinations.  But we'll see below how this squares with the additive-only view.

In fact, the collective context-dependency of each allele's functional effects means that the evolution of a population is dependent on its mix of genomic variation--which brings us back to Wallace, and is what group selection is properly about.

Group selection: why a bad reputation?
Group selection got a bad reputation in part when a book by VC Wynne-Edwards was published in 1964 that claimed that in many species, individuals restrained their reproduction essentially for the good of the group (whether or not this was done knowingly for that purpose).  This was a kind of fitness-related altruism that was ridiculed on the grounds that if I restrain my reproduction for the good of the group, others may not be so restrained and any genetic variant that led me to do what I did would thus be out-competed.  So group selection was out, but WD Hamilton introduced concepts of extended kinship to explain altruistic behavior, such as why I might help someone at a cost to myself--if that someone were a relative, for example.  Hamilton's rule became dogma and explains much of the sociobiology of our era still today (though the rule doesn't really work very well when closely tested).

In this sense, group selection was viewed or modeled as driven by single genes and the argument was how an individual 'altruism' gene could possibly sacrifice itself and still get ahead, the one coin of the realm recognized by the most strident of Darwinists.  In recent years, various defenses of the idea and proposed mechanisms have been offered, usually with no reference to Wallace's more ecological concept.  The reason his views might be relevant is not that he thought about this in modern terms, but because he recognized that the collective qualities of the group--its overall members' traits--are what affects the group's chances of confronting the environment or other populations that it faces.

But in fact I think that while the evolution of altruism is an interesting question, it is a red herring that has given group selection a bad name.  Because there is a lot more about group selection than that gene-centered, restricted argument would suggest, and it's fundamental to life.  Indeed, it is possible that Wallace's idea, that the properties of the group determine its success, is more cogent than the gene-focused version--but for different, wholly non-mystical reasons.

Group selection, more properly conceived
The answer in brief is not a new fact but a different way of weighing the facts.  It is based on the indisputable fact that DNA is, by itself, quite an inert molecule. Anything it does is only in context.  The chance of an allele being successful depends on what else it finds itself combined with.  If in that context, the allele's effects are harmful, it has reduced prospects.  But if it finds itself in genomic and environmental circumstances in which it functions well, it can proliferate.

But what determines those genomes?  It's the relative frequency of their alleles in the population.  This is the result of the genomic history of the population as a reproducing unit.  Unless quickly removed, our new allele will see itself, probabilistically, in the company of other variants in the individuals who carry it.  If the number of those variants, and/or their frequencies, in which it can have positive effect is high enough, it has an increased chance of proliferating.  This is, in a legitimate sense group selection, because genomewide the success of the group depends on its collective distribution of alleles.  (Here we're not considering how that collective success operates, whether in terms of mating, avoiding predators, finding food, dealing with local climate, etc.).

The same variant that does very well in one genomic or environmental setting may do very poorly in another.  This is another manifestation of the central fact that a variant has no predetermined effect on its own.  It's why personalized medicine, based on predicting disease from genotypes, has a long way to go, at best, for other than very severe, largely early onset traits.

It is not that the individual variant, or the individual person, isn't important, or that we can't trace the frequency change of the variant, just as has been done for decades by population genetics theory.   But it misses the important collective aspect of an allele's success.  It's like the fact that we can count the bricks that make up our building, but we are hard-pressed to understand the building that way.

Over time, a successful population accumulates enough variants in enough genes that enough newly arising alleles are in favorable 'soil' to confer viable effects on individuals who bear them.  A population depauperate of enough of an allelic mix, genomewide, dies out.  This is, in every meaningful and non-mystical sense, a group phenomenon and if the term hadn't already been abused, group selection.  If a population perspective is really the most important one for understanding genome dynamics, then our usual genetic reductionism is misplaced.  

The Normal (bell-shaped) distribution of so many traits, like stature; UConn WWI recruits

Everyone in a population differs a bit but most people, for most traits, are rather near the middle.  The roughly Normal (bell-shaped) distribution of traits like human stature is a reflection of this.  There are those in the high- or low-end tails (very tall or very short), but most are near the middle.  There is a strong 'central tendency'.  Where does that come from?  It is a direct reflection of an evolution that makes most people inherit what in their collective ancestry has evolved as a 'fit' state for that population's circumstances.  There are always new mutational variants arising, and if the population--the 'group'--had not evolved this central tendency, it would not be a healthy one, and that would affect the likely fate of new mutations.  There are exceptions, but the restricted variance of natural populations, the tendency of most individuals to be quite similar, reflects what is, in fact, a form of group-selection history.

A major way in which this can arise, given that we have genomes made of multiple chromosomes and there is recombination and we are diploid but pass on only half our genome complement, is for many different genomic factors to affect a trait--for it to be 'polygenic'.   I think that it is the assembly of many more or less equivalent parts, independently segregating, that enables most individuals to inherit what the population's previous history has proved viable, that is, multiple independent contributors is why such central-tendency, limited-variance characteristics are so widespread.  Gene duplication and other processes help generate this state of affairs.  It's the way molecular interaction works; if things had been too genetically unitary, survival would have been more precarious.

From this perspective, the standard 'selfish gene' viewpoint's denial of the importance of epistasis and other contextual elements of gene function is off the mark.  It misperceives the nature and vital importance of the population in which these combinations exist, and the necessity that those factors be there, in enough numbers and/or with high enough frequency.

So, Wallace again?  But wait--isn't it individuals who reproduce or not?
But what about those individuals, on whom a century of population geneticists and countless popular science writers, have placed their hyper-competitive hyper-individualized stress?  The individual, driven by some critical genetic variant survives or not.  Individuals as wholes are viewed (or should we say dismissed), essentially, as mere carriers of the gene whose evolution is being tracked.  The context of population may be real, as discussed above, but the individual, basically a manifestation if its genotype, is what selfishly acts and determines success. No?

Sure, in a sense.  But the variant's prospects depend on the collective, and it's mutual, or relative.  Variant One is affected by Variant Two--but Variant Two is affected by Variant One, and so on.  The individual, or worse, individual gene focus is something one can compute, but it is misleading.  And, in fact, the situation is even more problematic in respect to what individuals actually are, genomically.

In Part III, I'll discuss how individuals, too, are being misperceived as the ultimate functional units based on their individual genotypes, either as wholes or in terms of specific genes.  Again a group or population perspective has an important, largely unrecognized role to play in individuals' and hence groups' success.

Wallace was onto something that's rather absent in Darwin, and still absent today as a result of the fact that the particularist aspect of Darwin's and Mendel's view prevailed.

Plant sociality and solidarity

Plants aren’t nearly as passive as their stationary state might lead one to think.  They have similar immune system needs to animals, because they are routinely attacked by hungry microbes and larger creatures intending to munch their way around a leaf.  And, like animals, they have ways of battling the ever-evolving attackers, that allow them to adapt to changing assailants.

We've blogged recently about how plants communicate through their roots and in other ways (here) and about how they may even be altruistic (here).  Here’s another interesting paper, in PNAS, about sophisticated responses and sociality among plants ("Intake and transformation to a glycoside of (Z)-3-hexenol from infested neighbors reveals a mode of plant odor reception and defense," Sugimoto et al.).  The authors report that tomato plants affected by cutworms produce a volatile chemical called Hex Vic ((Z)-3-Hexenylvicianoside) that diffuses through the air to neighboring plants.  When the neighbors detect this, they then express genes that produce a substance that makes them resistant to cutworm attack, as well as weakens the worm.

In response to herbivory, plants emit specific blends of volatiles. When undamaged plants are exposed to volatiles from neighboring herbivore-infested plants, they begin to defend against the impending infestation of herbivores. This so-called “plant–plant signaling” has been reported in several plant species. For example, a study on the expression profiles of defense-related genes when Arabidopsis was exposed toseveral volatiles, including green leaf volatiles and a monoterpene, showed that the manner of induction varied with the gene monitored or the volatile used, suggesting that the plant responses were specific to the individual volatile compound.

Unlike defenses against microbial infection, this is a mechanism related to a mega-scale predator, an animal that is too big for the plant easily to defend itself, unless it evolves some form of toxin to kill the worms.  

Here, one might speculate about why plants under attack would help other plants, rather than just do their best to beset the cutworms on their own. Normally, one would say they ‘should’ (from a Darwinian perspective) raise their defenses as best they can, but not tip-off their neighbors, and hence competitors of the danger.  Let them fend for themselves, and if they fail, the plant with the best defenses wins an evolutionary skirmish.

Micro Toms;  Wiki source

Of course if the neighbors are clones from the same artificial domestic strain, as these appear to be (the authors say they are Micro-Toms, a hybrid strain), the evolutionary issues are moot, since whatever led to the plants' behavior didn't occur in a field of clones.  So one wouldn't be able to say this evolved so they could help their close-kin neighbors in the usual sense.  But if natural tomato seed dispersal isn't distant, then nearby plants would be close relatives, and the kinship argument might work, that the attacked plant may be harmed or even doomed, but by warning its neighbors it’s warning its kin.

But, if natural tomato seed dispersal is distant, spread in the droppings of birds that ate the fruits, e.g., than the explanation must be something different.  And indeed, if the volatile emissions are detected by non-kin, plants of other species, as Sagimoto et al. seem to suggest, below, then the kinship explanation doesn't work at all.

Because (Z)-3-hexenol is a common volatile compound emitted by most herbivore-damaged plants, andbecause we found that a wide range of plant species could accumulate (Z)-3-hexenyl glycosides after exposure to volatiles, absorption and glycosylation of exogenous airborne (Z)-3-hexenol might be a general response in plants.

In any case, here we have yet another example of a more complex living world than traditional understanding of botany has generally allowed.  It's a reminder that we should curtail our hubris when it comes to assuming we higher animals do everything best.  

"Roots": the saga of (plant) families caring for each other

We did a post a few weeks ago about plant intelligence.  We wrote primarily about a recent Michael Pollan piece in The New Yorker that discussed the issue at length, we thought in a nicely thought-provoking way.  A piece in The Scientist, "Plant Talk" by Dan Cossins, pushes the issue a bit further.



Cossins describes an experiment that demonstrates that plants communicate through their root systems.  They send warning signals about insect infestations, and share nutrients.  A PhD student in Scotland, Zdenka Babikova, tested the role of mycorrhizal fungi in this communication system, and published the results in Ecology Letters in July.  She planted 5 bean plants in 8 different pots; one was a 'donor' plant, and the other four were 'receiver' plants.  One formed root and mycorrhizal contact with the donor, another only mycorrhizal contact, and two had neither.  Cossins writes:

Once the mycorrhizal networks were well established, Babikova infested the donor plants with aphids and sealed each plant in a separate plastic bag that allowed for the passage of carbon dioxide, water, and water vapor but blocked larger molecules, such as the VOCs [volatile organic compounds] used for airborne communication.

Four days later, Babikova placed individual aphids or parasitoid wasps in spherical choice chambers to see how they reacted to the VOC bouquets collected from receiver plants. Sure enough, only plants that had mycorrhizal connections to the infested plant were repellent to aphids and attractive to wasps, an indication that the plants were in fact using their fungal symbionts to send warnings.

Figure 1. Experimental mesocosm (30 cm diameter; n = 8) showing the donor plant, which was colonised by aphids, and four aphid-free receiver plants. All plants were grown in the mycorrhizal condition but one plant was prevented from forming mycelial connections to donor plants (0.5 μm mesh), another was allowed to form connections initially but the connections were snapped after additions of aphids to the donor (rotated 40 μm mesh), and two other plants were allowed to form shared mycorrhizal fungal networks (non-rotated 40 μm mesh allowing fungal contact only; no barrier allowing fungal and root contact) with the donor plant for the duration of the experiment. Ecology Letters, Babikova et al., 2013

Cossins adds, with respect to plant communication, "Moreover, plants can “talk” in several different ways: via airborne chemicals, soluble compounds exchanged by roots and networks of threadlike fungi, and perhaps even ultrasonic sounds. Plants, it seems, have a social life that scientists are just beginning to understand."

A lot of the work on communication between plants was dismissed by most botanists until recently. Now botanists acknowledge that there may well be signaling going on, but some still are not willing to consider plants to be social organisms, or altruistic, and see all this signaling as an offshoot of a plant's ability to alert healthy cells of insect attack from damaged cells, or of a plant's response to drought, and so forth.  Is that just a bias because plants don't do it the same way we do?

Plus, the inter-plant communication doesn't seem to do the sender of the signal any good, so some wonder how this could have evolved.  The same debate has been going on with respect to animals for a very long time, and the same kinds of answers are coming up -- plants seem to most effectively receive signals from related plants, so they may be protecting copies of their own genes when they signal to neighboring plants, because related plants share many of their genotypes.  Kin selection is controversial especially if it involves risk to the helping organism, such as a plant when it helps another.

This is all interesting for its own sake.  But there are possible important applications.  For example, Babikova et al. note that it has been found that some commercially bred maize no longer produces the VOCs induced by insect infestation. That is, a natural early warning system may be being bred out of crop plants, and thus increasing the need for pesticides. As Babikova et al. say, "...our data suggest a pressing need to determine the extent to which manipulation of common mycorrhizal mycelial networks can provide sustainable solutions to manage insect pests. The role of mycorrhizal fungi in mediating multitrophic interactions in agricultural ecosystems has largely been overlooked, but our findings suggest that there may be potential to develop fungal treatments to enhance crop protection." So indeed learning about inter-plant communication is of more than whimsical interest. 

As for how apparent altruism could have evolved in plants, or whether these communication mechanisms are helpful to other plants purely by accident, this is only a problem when the assumption is that evolution is about competition rather than cooperation.  The argument can be made -- we made it in our book "The Mermaid's Tale" and elsewhere, but more and more evolutionary biologists are making the argument as well -- that cooperation is more fundamental to life and to evolution than competition.

This is a serious problem if one individual makes a big reproductive sacrifice that serves to help another's reproduction.  It is that aspect of altruism that has attracted so much theoretical attention over the years (in animals).  But, again, it is a serious problem mainly if one views each organism as an independent actor, ignores mutuality and things like recombination and population change over time, and ignores the almost automatic kinship among nearby individuals in many species.

Whether human culture-derived words like kin or altruism should be applied to plants in a way that skirts so close to anthropomorphizing, this depends, we think, on whether you think of humans as exceptions, or more representative of the rest of nature than we generally like to accept. Or if you think that our kind of wet-ware (neurons and interconnections that form our unitary sense of existence) is the only one that counts.  But that's somewhat like saying trains or planes are not vehicles, because they don't work like cars do.  The same sorts of questions can be asked of consciousness -- are we really the only organisms that have self-awareness?

Cooperation might actually be ... cooperation

Cooperation, altruism, anything but self-interest, have long been perplexing to true Darwinians.  According to theory, cooperation can't happen unless it has a payoff in terms of increased fitness because it's costly to the donor.  So, cooperation is redefined as ultimately just a form of competition, or as selfish only being done when those who cooperate can expect reciprocity, or only practiced among kin.

A new paper in Current Biology, Social Evolution: Reciprocity There Is, Taborsky, challenges the idea that cooperation only happens among kin, supporting instead the idea that it is evidence of reciprocity; you pat my back and I'll pat yours.  But such arguments basically make the competition viewpoint a tautology, an assumption, from which any explanation can be -- must be -- just a kind of mathematically different way to express competition.  However, cooperation is so ubiquitous, at all levels of life, that it should stand alone, without being remolded and forced to fit classical Darwinian theory.

Vampire bat; Wikimedia

Taborsky cites a recent paper on food sharing among vampire bats.  These animals often feed roost-mates by regurgitation of a blood meal, and the question has been why such behavior would have evolved. 

The original explanation for this costly helping behaviour invoked both direct and indirect fitness benefits. Several authors have since suggested that food sharing is maintained solely by indirect fitness because non-kin food sharing could have resulted from kin recognition errors, indiscriminate altruism within groups, or harassment.

The authors tested these alternate explanations by looking at food-sharing over several years among a group of bats.  They determined that sharing was initiated more often by the donor than the recipient, so clearly it wasn't due to harassment.  And, they found that bats who were given food were more likely to share, and that this reciprocity was more often involved in sharing than was relatedness between bats.  Food sharing was also correlated with social grooming.  The authors conclude that food sharing has direct, mutual fitness benefits that is more about reciprocity than kinship. 

Questionable assumptions
Well, maybe.  The assumption underlying the idea that cooperation, or altruism, are in fact selfish behaviors is that everything organisms do must be optimized to reduce energetic costs and to increase fitness.  This in turn largely also implies the assumption that evolution arrives somewhere, that organisms have finished evolving, and that energy expenditure for a given lifestyle must be as low as it can be and fitness as high as it can be.

There are problems with these assumptions.  The first is that evolution never arrives, organisms are always in process -- there is clear-cut genetic evidence for this. Dead genes, called pseudogenes, litter most genomes, relics of gene duplication events in the distant past, or functions the organism no longer has (chickens still have genes that could produce teeth, if asked to at the right time and place in development, e.g.).   

And, whether you come down on the ENCODE end of the "junk DNA" debate and accept that 80% of non-coding DNA has function, or the Dan Graur side of the debate and accept that most DNA is in fact junk (that is, doesn't do anything relevant), there does seem to be at least some of the genome of most species that has no function, whether or not it once did.  The point is not to rehash the junk DNA debate, but instead to point out that whether it's 20% or 95% of our genome, we seem to be spending a significant amount of energy making DNA that has no function.  That's not optimal.

Further, we've got a lot of DNA repair enzymes floating around in our cells, and the reason is that the processes of chromosomal replication, DNA transcription and translation are not error-free.  When the wrong nucleic acid is incorporated in a new stretch of DNA or mRNA, the cell has ways to detect this, and then correct it.  Why should these error-prone mechanisms have been maintained by selection, if optimal energetics is its goal?

There are numerous examples of imprecision at the cellular level.  Gene transcription can be stochastic, somatic mutations occur and proliferate, during development superfluous cells and tissues are made, such as webbing between the digits, and then programmed to die before birth, and so on.  If energetic optimization were a rule that evolution was supposed to be following, evolution didn't get the message.

Similarly with cooperation -- if  cooperation were only competition or selfishness in disguise, it's hard to know what to make of the interaction between cellular organelles, genes, gene products, cells, tissues, organs, organisms.  Sexual animals can't even reproduce themselves alone.  We're dead without our microbiomes.  Ecosystems are built upon cooperation.

The slime mold Dictyostelium discodeum, collections of cooperating amoeba: The Mermaid's Tale

The selectionist problem
As we've been discussing recently, this relates to the selectionist assumption, that there must be a selective reason, that is, one based on raw competition, for everything organized about life.   If cooperation leads to proliferation of whatever is responsible for it, then that means something isn't proliferating and that implies competition -- or, rather, that is an instance of redefining cooperation as just another form of competition.

Since differential proliferation is a fact of life, and proliferation is necessary for a species or lineage to persist over time, one can take a cold mathematical view and say that it is perfectly legitimate to show that everything can be translated mathematically in to proliferation based on competition.  This is not really accurate, but is actually beside an important point here.

That point is that cooperative interactions at various levels from genomes to cells to organs to individuals in a species and species in ecosystems, are how life works on a daily basis. Even if one were to grant that this arose because of some version of competition, that doesn't help understand how or why the cooperative organization works today.  Yes, there may always be a Darwinian component of variation and behavior, but that won't help understand the 'emergent' nature of the cooperative interactions.

Cooperation in the sense we're talking about is so ubiquitous that it is at least as important a feature of life as the competition that occurs.  Indeed, natural selection, as Darwin clearly noted, is usually very very slow, almost undetectably so.  But cooperation is manifest all around us all the time.  It deserves more careful attention on its own terms.

Darwin vs Wordsworth: Is Nature cruel or beneficent?

In what looks an awful lot like cooperative behavior, groups of birds often get together to 'mob' a predator.  That is, they swarm predators together, in an attempt to chase them away from nests or from a food source, and so on.  Birds often make mobbing calls, that alert nearby birds to danger, and solicit their aid.




A new paper in Biology Letters suggests that "long-term familiarity" is a factor in whether or not birds choose to help each other when faced with threat from a predator.  A.M. Grabowska-Zhang et al. show that "neighbours that shared a territory boundary the previous year are more likely to join their neighbours' nest defence than neighbours that did not share a boundary before."

Predation is a major cause of death in nestlings, so driving predators from an area in defense of the nest is crucial.  And, the more birds that can mob a threatening predator, the more likely they'll drive it away, so soliciting the help of neighboring birds is also crucial.

Grabowska-Zhang et al. "tested the hypothesis that long-term familiarity between territorial neighbours is positively related to joining behaviour in predator mobbing."  They did this in a population of great tits breeding in next-boxes in Oxfordshire, in the UK. These birds have been tagged and followed in previous years, so that their ages and familiarity are already known.  The researchers served as predators, by approaching a nest and making noise, and then assessed the birds' response.

For pairs of nests where each contained at least one familiar individual, in 12 out of 16 trials (seven out of eight nest pairs), at least one neighbour joined the mob. Individuals from the unfamiliar group joined the mob in just two out of 16 trials (one out of eight nest pairs). No neighbours joined the mob in first-years' nest.

That is, they report that they've demonstrated a significant influence of familiarity on taking part in solicited mobbing behavior.  The idea that birds decide who to cooperate with is interesting one -- apparently, they don't help just anyone.  But, what interests us more is that the authors conclude that they can't tease out from this study whether the birds cooperate because they are good neighbors (altruistically), or because they figure they'll get help from their neighbors when they need it themselves (selfishly).  The same behavior can be interpreted in two very different ways.

This is not new to this study, of course -- altruism has long been explained away as selfish.  And similarly, cooperation as competition.  There is a danger in reading ourselves into what we see in Nature.  It's a problem of subjectivity intruding where we hope and strive to be objective to the extent possible.  The issue first of all can affect study design itself, and then the interpretation of results.  Thus, if competition is the lens of your view of Nature, you can design studies to find competition or evaluate organisms' success in comparative terms.  If cooperation is your bent, you can study what happens when organisms work together for whatever reason.   The truth, as this study shows, is typically a mix.

The danger extends to reading other work, in science but even in other areas.  One can mine important thinkers for statements supporting one's bias, just as can be done with Biblical exegesis.  For example, at about the same time, and totally unbeknownst to each other, two famously brilliant authors wrote about the awesome splendor of Nature.  Darwin looked upon Nature's 'grandeur' (his word) and saw beneath it a relentless, impersonal, and savage 'struggle for survival' against limiting resources.  In an 1838 notebook, he denigrated philosophers who were trying to understand life by saying that one would learn "more towards methaphysics than Locke" by understanding baboons.  But last night Ken was writing on something for Evolutionary Anthropology that referred to Darwin's quote.  He has also been reading the famous pastoral poems written at almost the same time by the poet laureate William Wordsworth.  Like Darwin, Wordsworth denigrated stuffy academics, remarking that one who wished to understand life should turn not to the work of philosophers but to Nature's magnificent panoply reflecting God's beneficent intent.

Birds may not think about competition vs cooperation in ways that we do, but in their own way they show us the nuances of Nature.

Altruism -- can we do good just for the sake of it, after all?

Ant colony; Wikimedia Commons

Altruism, organisms being good to others even at their own risk, has perplexed true Darwinists for 150 years.  It even perplexed Darwin, who brilliantly anticipated numerous potential challenges to his theory, including the possibility that the existence of altruism, in a world he painted as red in tooth and claw, could destroy it.

The March 5 issue of The New Yorker addresses the issue in a piece (subscription required) by Jonah Lehrer, "Kin and Kind."

According to legend, the biologist J.B.S. Haldane was several pints into the evening when he was asked how far he would go to save the life of another person.  Haldane thought of a moment, and then started scribbling on the back of a napkin.  "I would would jump into a river to save eight cousins, but not seven."  His drunken answer summarized a powerful scientific idea.  Because individuals share much of their genome with close relatives, a trait will also persist if it leads to the survival of their kin.  According to Haldane's moral arithmetic, making a sacrifice for a family member is just another way of promoting our own DNA.

That settled it.  Altruism is selfish after all.  Evolutionary biologist, William Hamilton, formalized the idea in an equation published in 1975, in what came to be called inclusive fitness:

      rb > c

where

      r is "degree of relatedness",
      b is the reproductive benefit to the recipient of the altruistic behavior, and
      c is the reproductive cost to the altruist.

In very basic terms, you and your sib, parent, or child share half your genes.  This is on average and it's statistical.  You can't say in advance which genetic variants you'll share, just that overall it'll be half of them.  That's because everyone gets half their genes from their father, half from their mother.   So, if you do something for your sib that puts you at risk, say, of having one of your own children, but your assistance leads your sib to have at least 2 children s/he that wouldn't have had without your help, then the genetic variants you carry will, on average, proliferate--via your sib's children who will carry those variants.

Under these conditions, if a variant in question leads you to this helpful rescuing behavior, the variant will (statistically) proliferate, because helping your sib to have more children than you give up will increase the frequency of those helping-variants in the next generation.  Likewise, you share 1/8 of your variants with your cousins, so to give up a child of your own by helping your cousin, that cousin would have to have at least 8 more children than without your help.  That's what Haldane meant.  This may make little sense in slow reproducers like humans, but could actually work, in principle at least, in fast reproducers who produce hundreds or thousands of offspring--like ants.

So, Hamilton's rule seemed to explain why vampire bats feed each other, why bees will sting, and die, to defend the hive, and why Ken dove into a pool to save a drowning stranger years ago.  It even came to explain things that had nothing to do with altruism, such as homosexuality, which could evolve because homosexuals cared for the offspring of their kin, thus perpetuating their own genes even if they themselves didn't reproduce.

This would seem to show clearly that, by itself, Hamilton's rule simply cannot explain human (or even primate) sociality.  In all human societies people routinely help their cousins and other more lineally distant relatives.  But primates simply cannot have 8 or more additional children as a result of being helped.  So those who have thought about this have had to devise various escape-value explanations to preserve the essence of Hamilton's rule; one is 'generalized reciprocity' the idea that I may help you because some day you may return the favor.  But with such escape valves, and the complexity of society, it should long ago have been clear that all bets are off.

And, the entomologist, E.O. Wilson, became enchanted with the idea, and used it to explain ant behavior, as well as human, in his book that got Sociobiology -- the idea, essentially, that behavior can be explained genetically -- up and running. His last chapter, which anthropologists knew at the time was very ill-advised if not downright naive, applied all of this to humans, in very superficial ways.  But he started a fad -- or ideology, or even a cult of sociobiology that was nowhere so fervently applied as it was to humans.

But now Wilson has changed his mind, and thinks inclusive fitness doesn't explain altruism, or much else, after all.  And this is making a big splash in the field of evolutionary biology and even in the popular press, as the Lehrer piece shows. This is part of the cult of the celebrity science, and the good fodder it makes for the popular media.  It's interesting that we were supposed to believe Wilson when he was a Hamilton devoté, and now again when he's decidedly not.  It's like Francis Fukuyama, who wrote The End of History in 1992, arguing that liberal democracies were the final stage in the development of governmental form, and then changed his mind.  He was also a leading neocon, until he wasn't.  And he's still a media darling.  Why do those who were anointed shepherd remain shepherds forever, no matter what they do to destroy their own credibility, and the rest of us are sheep forever?

In any case, the signal, and among the strongest, theoretical examples of the way that what appears to be nice can be shown to be calculatedly nasty,  that was the particular genetic relationships among the different classes of members of a hive in many ant species, simply isn't right.  It doesn't explain what it was held, fervidly and combatively, to show.

Haplodiploidy in bees; Encycl. Britannica

In the supposed canonical case of ants, this had to do with what is called 'haplodiploidy', too much to go into here unless we're requested to do that, but can easily be found in sources like Wikipedia.  The gist is that there are genetically sterile castes....and how could that happen?  What genetic variation, that led to your being sterile, could possibly proliferate in the presence of more 'selfish' variation?  The answer is that the sterile caste members are related to the Queen for whom they sacrifice their own chances at reproduction.

However, this genetic situation simply is not closely associated with sociality even among insects: some have haplodiploidy but don't live in social hives, some in social hives don't have haplodiploidy.  Many behavioral-evolutionary anthropologists seem to be  unaware of any of these unsupportive facts -- clear and repeated exceptions. It is these facts that led E.O. Wilson to abandon his prior strong advocacy of inclusive fitness and, indeed, his coined field of Sociobiology.  But Wilson, now in his dotage, is as simplistic in his new statements as he was in his strong advocacy of sociobiology.

Why is the demise of Hamilton's rule as Gospel such a big deal?  Because it shouldn't have been a Big Deal in the first place.  And yet why should we care what Wilson says this time around anyway?

The problem with all of this is the desire or even deep hunger, to find some precise, competition-centered pat explanation for observations about life. Anything that looks organized is assumed to be due to systematic, force-like Darwinian competition.  Even group selection, which Wilson is now advocating, is a simplistic notion, that orthodox Darwinians cannot accept because it doesn't work strictly at the level of the individual which they insist, for some good reasons, it must, since it is only individuals who carry genes and either do or don't reproduce.  From that point of view, everything that looks cooperative simply must have arisen and/or work strictly to the advantage of the individual.  Or, to be even more precise, it has to work at the level of individual genes.  It has to, to seem like real science!

This is a reverse kind of logic.  If you view the world as horribly selfish and cruel, then of course anything can be explained by selfishness.  On the other hand, if you see cooperation as being important, you can argue that things good for a group advance even if genetically they arise only in one member of the group.  You can argue that over time, the kindliness genes will spread and advance: each kindliness mutation will add to the group's success.  Even those without kindliness variants will do well, but they won't out-do their nicer peers.  Arch Darwinists who seem to be convinced the world is full of cheaters (does this imply that they know they're cheaters themselves, and is some sort of tacit confession?), will always devise (again post hoc) reasons why kindness for unselfish reasons will never win.  Or they will always be able to find reasons why kindness is just competition in disguise.

Cooperation, and we wrote our book Mermaid's Tale largely about it, is pervasive and ubiquitous.  Life is about molecules interacting, cell compartments interacting, cells, organs, and organisms interacting.  Cooperation means co-operation, and only in some social animal contexts is it about cozy kindly interactions including the sort of interactions referred to as 'altruism'.  If an enzyme and its substrate interact to bring about a reaction, that is cooperation.  If one component has the wrong structure or isn't present when the other is, the interaction doesn't occur.  One can't just evolve by out-competing the other.  Things may arise individually, but in various ways must advance in prevalence by successful interactions.  If this is extended to the thousands of interactions in a cell, and among cells in an organism, then why not among organisms in a population?

Sometimes inter-individual competition does certainly occur and sometimes this seems clearly to be related to genetic differences.  And even if there may be some elements of competition -- in the restricted sense simply of some things proliferating faster than others, that fact doesn't gainsay the predominance of cooperation as a fundamental part of the road to success.  Much more of the time what goes on in life is about successful interactions.  Why we resist that recognition is unclear, unless it has to do with the legacy of capitalism and colonialism, and things like that, as some historians and sociologists of science, or opponents of religion, have argued.

Well, the big debate is merely scientists' egos and tribalism speaking.  The obvious truth is that there aren't rules of this simple form for life.  Instead, life by its very nature only has to do what it does.  So if local groups are made of close relatives because individuals are born, live, and die in a general local area, then all one has to have is some sense of parental feeling to be easily extended to sociality.  This is so widespread that in a sense it doesn't require any special explanation or theory at all.  It doesn't require rigid, ubiquitous, or formalized theory--no matter how urgently mathematical biologists want it to be.  And mathematical models are by their own very nature law-like, rigid types of relationship that are far from fitting the realities of Nature--even if those models show how Nature would work to the extent the circumstances resemble the model.  Just as Hamilton's rule, taken properly as a generic guide, is informative.

The idea that if you help kin to an extent as predicted by Hamilton's principles, you'll statistically advance copies of your genes is simply a fact.  But it's also a huge 'if', and the many subtleties and nuances and other sources of variation are so great that, as with  most things in evolution, the theory can't be expected to apply rigidly or always.  Most things drift in or out of populations with little, or perhaps only occasional, help from classical natural selection.  We've discussed this in many posts on MT.  The essential cooperativity is entailed, among other things, by the nature of life as being organized around polymers (DNA and proteins) as we described in a series of recent posts, too.  Again, just because something is plausible and mathematically sound, doesn't mean it happens in real life.

In this sense, which we think is truly profound, life is not like physics and is not a science that requires the kind of rigidity or formal rigor that physical sciences do.  The reason, in a sense, is that life is by its very nature all about differences!  Differences are what enable evolution.