Field of Science

Sunday Protist - Lacrymaria: 'swan-necked' ciliate

[scheduled post; written 27.08.09]

Lacrymaria, Phil Gates @

Go check out the post in Beyond the Human Eye, a really cool microscopy blog I just came across! Also contains links to pages with movies...

(no time for makeshift review articles, completely swamped with stuff. You're safe this time around =P)

Blogging intermission for a week...

My spontaneous burst of posting will pause for a bit as I'll be away from reliable internet connection next week. Then there'll be the usual mayhem associated with the start of the term, but I should be able to squeeze something in every once in a while. I do still owe that Eukaryogenesis post, and I was also gonna blog about multicellularity eventually. I'll try to update at least once a week, hopefully stuff in addition to the Sunday Protist.

That said, I will have something scheduled for this Sunday, but don't expect anything grand. I only have time to make another 'protist appreciation' post amidst all the usual end of summer/start of term chaos.

Enjoy what's left of the summer!

Sunday Protist - Perkinsela: Life as an organelle

ResearchBlogging.orgWe've all heard of the primary endosymbiosis of bacteria that eventually became mitochondria* and plastids, on two separate occasions (three if you count Paulinella plastid origin). Some have heard of secondary, and maybe even tertiary, plastid endosymbiosis (eg. brown algae with red algal plastids). There's a fascinating case of tertiary endosymbiosis where an entire diatom inhabiting a dino (Kryptoperidinium), etc. Another interesting phenomenon is the endosymbiosis resulting in other essential 'organelles', eg. Polynucleobacter in Euplotes(Görtiz 2006 in Prokaryotes 1:364-402). While plastids have been transferred about the tree several times, secondary endosymbiosis of mitochondria or whole non-photosynthetic eukaryotes seems to be extremely rare. Thus, the following case of an endosymbiosis of a kinetoplastid by an amoeba I find to be rather interesting.

*Well, there's still remnants of a
crackpot adherence to the autogenous model of mitochondrial origin...

Meet Perkinsela (formerly Perkinsiella; Dyková et al. 2008b), an endosymbiont of amoebae that took until Hollande 1980 to be recognised as an organism rather than organelle! (although Grell 1973 Protozoology (p.363) does suggest a link to the endosymbiosis theory that was just becoming established at that time). Here's the amoebozoan host Neoparamoeba with an arrow pointing to Perkinsela:

(Eva Dyková, Tolweb Perkinsiella page)

This endosymbiont's life cycle has become completely confined within the host cell, as it is perpetrated along with nuclei upon host cell division. It is often found in a strange 'bipolar' form, with nuclei opposite of each other across the massive mitochondrion (which contains the kinetoplast - a dense disk of mitochondrial DNA unique to Kinetoplastids, which include Trypanosomes, the cause of African Sleeping Sickness), and in close association with the host nucleus:

(Dyková et al. 2003 Eur J Protistol; 8 shows Neoparamoeba with its endosymbiont (NN - host nucleus, K - kinetoplast (mitochondrial DNA), n - Perkinsela nucleus; 9 - Perkinsela itself. Note the two nuclei across the kinetoplast from each other (c- cytoplasm))

The nature of this endosymbiotic relationship remains unknown, although it seems to be mutualistic as the host and the endosymbiont both die without each other (Dyková et al. 2008b).

The endosymbiont is a sister group to Ichthyobodo, and even contains the splice leader sequences characteristic of Euglenozoa (the larger containing group of kinetoplastids, diplonemids and euglenids (remember Euglena?)) (Dyková et al. 2003; 2008b). Here's a tree to orient yourselves: (because everyone knows what Jakobids and Diplonemids are...feel free to go here for the bigger picture ^.^)

(Simpson et al. 2006 Trends Parasitol.; family tree of creatures with 'hockey puck' mitochondrial DNA...the intelligent designer was definitely tripping out on some serious stuff when he made this clade ^.^)

(Let's just say Neoparamoeba is an Amoebozoan. I have no desire to sort out Amoebozoan taxonomy at this hour, as it's a fucking mess. I have three trees before me from various periods, and the burning urge to rip all my hair out is a little too much. Seriously, Amoebozoa are just fucked up, as morphology-based classification failed more abysmally than usual there. It's hard to determine morphological features of something so...amoeboid ^^. I challenge a certain taxonomist who reads this to blog about their phylogeny! Have fun =P)

Interstingly, both Neoparamoeba and Ichthyobodo are fish gill parasites. While Neoparamoeba is an opportunistic parasite (Young et al. 2007) (ie it can also live freely; a more vicious example of opportunistic parasitism is Naegleria, which is harmless until it accidentally gets into a brain - it happens to love neural tissue!), Ichthyobodo is an obligatory ectoparasite. ('ectoparasite' means it attaches to the surface of the host cell to drain it of its 'juices', instead of going completely inside).

Fish gills seem to be rather fertile ground for parasites of all levels of devotion; for the chances of passing by one when you live in water are pretty good. It seems like the long-term close association between Neoparamoeba and Ichthyobodo parasitising off the same host has led to this intimate endosymbiosis - would be interesting to know the approximate timescale of the divergence between Perkinsela and Ichthyobodo, to see how long it can take for such relationships to evolve.

Here's the Neoparamoeba opportunist in action:

(Lovy et al. 2007 Vet Pathol; A - amoeba, E - fish epithelial layer; bar = 3um)

To summarise what I'm talking about:

(M - mitochondrion with kinetoplast; N - nucleus; HN - host (Neoparamoeba) nucleus)

If we were to analyse the Perkinsela genome, it would likely show signs of substantial genome reduction, due to it being no longer necessary to keep the entire set (depending how old the relationship is, of course). What would be even more exciting is if gene transfer to the host nucleus has already occurred! Perhaps the mitochondrion-targetting genes may go first; as far as I know, whether host-to-endosymbiont-nucleus targetting genes exist is still poorly understood. There are cases of host-to-endosymbiont-plastid targetting (dinoflagellates Karenia, Karlodinium...), however; and endosymbiont mitochondria tend to disappear rather early in endosymbiosis, so it's surprising to find it so prominent here.

Which makes one wonder...perhaps the host is keeping the endosymbiont for its mitochondrion? The cytoplasm is extremely reduced, so that the cell appears to be little more besides a nucleus or two and a kinetoplast. Could the kinetoplastid mitochondrion be capable of something the Amoebozoan one is not, that also happened to be useful for the amoeba? Doesn't seem very likely, but who knows... perhaps the ancestral Perkinsela was engulfed by the predatory Neoparamoeba as prey, and led to the mitochondrial analogue to kleptoplasty ('stealing of plastids' from prey practised by some predatory protists; sometimes they'll keep photosynthetic (algal) cells around for their plastids until they die - could be how cyanobacterial endosymbiosis first started)?

Or is Perkinsela just a really good parasite, successful to the point of no longer needing to even try, enjoying its free ride along with the host? This doesn't explain why Neoparamoeba dies without it, though. I guess all it would take is for the host to lose a gene or two essential for producing something that is made and exported by the endosymbiont/parasite; thereby fixing a dependency upon it. But I'm just rambling at this point...

There seems to be no mention of basal bodies/centrioles in Perkinsela ultrastructure studies; this worries me. kDNA replication is molecular cell biology on potent hyperhallucinogenic acid, and is a susbtantial topic best left for another day. In Trypanosomes, the final steps of kinetoplast replications require a system of fibrils attached to the flagellar root; the mitochondrion is tightly associated with the basal bodies (Liu et al. 2005 Trends Parasitol). If Perkinsela evolved from a 'stuck' amastigote kinetoplastid (ie. one in a non-flagellar stage of its life cycle, although that doesn't seem to happen in modern Ichthyobodo...), it could still retain a pair of centrioles, devoid of flagella. However, those should be fairly visible in EM.

I'm have this nagging feeling that I'm not making much sense anymore... >_> To wrap this up, there's also potential endosymbiotic association between the amoebozoan Thecamoeba and a labyrinthulid species. The labys seem to be able to proliferate at will without destroying the host, thereby seeming rather non-parasitic at the moment (Dyková et al. 2008a) Interesting...

Microbial diversity is amazing as is, but as soon as you start treating a cell as a potential ecosystem in its own right, the hidden universe of intracellular parasites and symbionts is overwhelming. This is where those popular charts showing the majority of biodiversity as invertebrates are just abusrd - each and every one of them is a possible ecosystem for microbial life, both bacterial and eukaryotic, and each and every cell thereof is yet another niche. And every protist is a possible ecosystem for some other protists, or prokaryote. Sometimes, those relationships persist and develop, and, on occasion, blur the line between organism and organelle.

So I wonder: is Perkinsela now an 'organelle'?

(This is why you should support basic biological research in addition to biomed; one cannot tackle cancer before understanding how single cells work in the first place. The 'higher' biology lies in the fundamentals, not select, limited cases like humans or mice...)

DYKOVA, I. (2003). -like endosymbionts of spp., relatives of the kinetoplastid European Journal of Protistology, 39 (1), 37-52 DOI: 10.1078/0932-4739-00901

DYKOVA, I., FIALA, I., DVORAKOVA, H., & PECKOVA, H. (2008). Living together: The marine amoeba Thecamoeba hilla Schaeffer, 1926 and its endosymbiont Labyrinthula sp. European Journal of Protistology, 44 (4), 308-316 DOI: 10.1016/j.ejop.2008.04.001

DYKOVA, I., FIALA, I., & PECKOVA, H. (2008). Neoparamoeba spp. and their eukaryotic endosymbionts similar to Perkinsela amoebae (Hollande, 1980): Coevolution demonstrated by SSU rRNA gene phylogenies European Journal of Protistology, 44 (4), 269-277 DOI: 10.1016/j.ejop.2008.01.004

Liu, B., Liu, Y., Motyka, S., Agbo, E., & Englund, P. (2005). Fellowship of the rings: the replication of kinetoplast DNA Trends in Parasitology, 21 (8), 363-369 DOI: 10.1016/

Lovy J, Becker JA, Speare DJ, Wadowska DW, Wright GM, & Powell MD (2007). Ultrastructural examination of the host cellular response in the gills of Atlantic salmon, Salmo salar, with amoebic gill disease. Veterinary pathology, 44 (5), 663-71 PMID: 17846238

SIMPSON, A., STEVENS, J., & LUKES, J. (2006). The evolution and diversity of kinetoplastid flagellates Trends in Parasitology, 22 (4), 168-174 DOI: 10.1016/

YOUNG, N., CROSBIE, P., ADAMS, M., NOWAK, B., & MORRISON, R. (2007). Neoparamoeba perurans n. sp., an agent of amoebic gill disease of Atlantic salmon (Salmo salar)☆ International Journal for Parasitology, 37 (13), 1469-1481 DOI: 10.1016/j.ijpara.2007.04.018

Two rants on endosymbiosis

ResearchBlogging.orgFirst off, quick point: Can we please stop using headlines like "Darwin was wrong about [x]"!? Srsly, big deal, some dead dude from the 19th century was wrong about something. Well shit. Evolutionary biology as we know it is now fundamentally flawed. Because Darwin didn't have PCR or fancy sequencers or GFP-tagged whatever. Tragic. What about all the shit Mendel was wrong about? Are we gonna ignore him now? /rant #01

Sometimes when writing up a post on something, I come across 'interesting' sites and papers. I mention my reaction in brackets, and find more crap to rant about. I then move the contents of the brackets to a footnote and unleash an off topic at the bottom of the post. But sometimes, this rant would be -really- off topic, and would be rather distracting if it becomes longer than the post itself. Today, we have come across one such case.

Warm-up - (excessive endosymbiosis)
Before embarking on a little journey of "Did he seriously just write that/get a faculty position/get a degree", a warm up paragraph from this week's Nature:
"In the former, the peptidoglycan layer is sandwiched between the outer and inner membranes, so that it surrounds the inner membrane: in contrast, in the latter there is no inner membrane, and the peptidoglycan layer, located outside the cell, surrounds the outer membrane." (Lake 2009 Nature) (via Catalogue of Organisms, who beat me to it, grrr XP)
That, my friends, is a wonderful example of epic semantics and topology fail. What he's talking about is that double membraned bacteria in question have cytosol-Inner Membrane(IM) - murein wall - Outer Membrane(OM) - outside. Single membraned bacteria have a cytosol-OM-murein wall-outside arrangement [sic]. Ie, somehow OM-M became IM-M-OM, raising the question of how the outer membrane end up on the other side of the murein. Thus, Lake invoked endosymbiosis to explain this 'conundrum' - an OM-M endosymbiont entered another OM-M prokaryote, and the endosymbiont OM became the inner membrane, while the host lost its murein wall. Very complicated stuff.

It may be quite evident at this point what the real 'conundrum' is there. Instead of comparing biochemical properties of the membranes to each other, he compared their relative positions. There is a very interesting topological property where if you have an double membrane and lose the outer layer, the former 'inner membrane' becomes the outer one. I think I may be onto something here...anyone wanna collaborate on a Nature paper? Any mathematicians out there wanna contribute a proof?

So how could someone who's probably a decent scientist fall for something like that? In fact, this seems common as soon as you put the 'hype' into 'hyp[e]othesis' - in this case, the guy seemed desparate for endosymbiosis, to the point of overlooking this very simple point in semantics. The reviewers and editors were no better - they too were getting carried away with the endosymbiosis hype (of course, they've still got ways to go to reach Margulis levels thereof...) For some reason, the fact that there's only one confirmed case of prokaryote-prokaryote endosymbiosis in the literature seems to worry no one...

(Coming from the TC-S camp of eukaryotic evolution, it was probably the double membrane state that was ancestral, with the loss of the outer membrane leading to what TC-S calls 'negibacteria', which eventually gave rise to us Neomurans. Even if you propose that single membraned bacteria came first, there's still no need for endosymbiosis, for they could have perhaps devised a way to form the outer membrane on their own. That would still be more parsimmonious, and more likely, than Lake's hypothesis above...) /rant #02

The big rant - (insufficient endosymbiosis)
We have some major endosymbiosis people in our department, so I never really came across any skeptics of mitochondrial endosymbiosis. The endosymbiotic theory of mitochondrial and plastid origins is pretty much beyond dispute these days, and the evidence is simply overwhelming. However, there always has to be someone to blow against the wind gale. Very rarely, they happen to be right; but even in those cases, their argument tends to be well-reasoned and supported by at least some data from the start. The other 99% of crackpots remain just that - timeless testament to our innate irrationality.

There's some guy who seems mildly annoyed by mitochondrial endosymbiosis. To the point of dedicating an entire website to the topic:

So there's a whole page 'critiquing' the endosymbiotic mitochondrial origin theory. I know this is only half a step up from bashing creationists, but it got me a little irritated. Not because I feel threatened, but because it seems to be so easy to get employed as a crackpot, and I'm a little envious of their capabilites. See, if you actually try to abide by proper reason and the scientific method and all that crap, you'll be dirt poor and socially marginalised for the rest of your life. Thus, I shall enjoy one of the few advantages we do get - the feeling of intellectual superiority as you rip into some crackpot's drivel with a barrage of citations and proper data. It's a sport.
"The extensive gene transfer that is needed in the endosymbiotic theory would wreak havoc in a complex genome since frequent insertion of random pieces of mitochondrial DNA would disrupt existing functions."
Uhhh...heard of transposons, by any chance? I'm sure those are a few orders of magnitude more plentiful and more violent than the occasional piece of mitochondrial DNA. Yet they still...happen. And genomes have generally been able to deal with it. Random gene insertions do disrupt functions, but then you've got a few million other genomes to take their place! Isn't evolution awesome?
"Most pictures in textbooks of mitochondria resemble bacteria, but in reality, mitochondria form a dynamic network of interconnecting tubules (reticulum)"
May we introduce you to bacteria that don't look like 'bacteria'? Say hi to Streptomyces and Planctomyces, for example.

I'm just making shit up hypothesising here, but it seems like the stereoptypical bacterial morphology may be limited by the fact that it swims. There are certain shapes optimal for a flagellate lifestyle, and netlike/mycelial/branching forms are not among them. Once a bacterium has become commited to living exclusively in the intracellular environment, it no longer needs to be hydrodynamic, and can start taking on whatever other form it likes. I'd imagine that >800my is plenty of time for drastic morphological changes, considering eukaryotes managed it quite well.
"It is said that mitochondria, like bacteria, divide by fission, but the mechanisms are completely different and mitochondria use mainly components of unique eukaryotic origin."
Ever heard of intracellular parasites? An intracellular lifestyle does some weird shit in terms of intense reduction - microsporidia (fungi which shoot their cytoplasm into the host cell, where it takes over and lives off the host's resources, until forming new spores) have highly reduced genomes that have been harsh to introns due to space limitations(eg. 13 introns in an entire genome (E.cuniculi)), as well as a great purge of proteins for nucleotide+amino acid biosynthesis (Keeling & Slamovits 2005 Curr Op Genet Dev)* This makes sense - you don't have to make your own amino acids if you can just steal them from the host! So any degeneration and subsequent loss of previously essential genes is now tolerated, and thereby bound to happen.

*Ok, when you come across a paper with the following introductory paragraph, you just have to read it:
"At the bottom of the rabbit hole, Alice found a bottle labeled, ‘‘Drink Me’’. When she did, Alice shrank to a perfectly functioning, ten-inch miniature of herself. In reality, shrinking can be more difficult than simply drinking a potion, because the component parts of many systems are not themselves shrinkable, and so the system fails to function properly. In the world of eukaryotic
nuclear genomes this is probably true, despite the fact that they vary in size by factors of hundreds of thousands (Figure 1), much more than all of Alice’s many transformations combined." (Keeling & Slamovits 2005 Curr Op Genet Dev; free access)
Classical studies geek really shows here...
(I'm quite bothered by the desolate desert around Rhizaria in fig.1 =( )

Similarly, the early mitochondrion no longer desperately needed to maintain its own division machinery, which eventually became transferred over to the host or lost. In a way, it has been able to hijack the host cell to take care of its own division. (so who's 'enslaving' whom here?) Through extreme evolutionary 'laziness', some lineages have been able to lose all genomic DNA entirely, and reduce to tiny membrane bound compartments essentially for specific parts of the host's metabolism. They basically 'disolved' into the host over time! (of course, de Roos' theory would probably claim those lineages as an ancestral state, eventually increasing in complexity. Too bad phylogeny king of stands in the way. Oops.) Just because an organism isn't capable of free life now doesn't mean it ancestrally wasn't either. Again, parasites support that very well. de Roos seems to have fallen for the 'evolution aims to gain complexity' misconception, and had difficluties with it 'going backwards', as it often likes to.
"So, although we see some characteristics that are shared between mitochondria and bacteria, we see many more examples where mitochondria are actually quite different."
Yeah, shit diverges over 850my. Just because they're 'different' doesn't mean they can't share a common origin, even a fairly recent one. Again, microsporidia were considered to be very ancient due to their apparent 'absense' of mitochondria and a highly reduced structure (wiser people were a bit alarmed by the latter detail; parasitism is almost universally a secondary trait (looking back far enough, it always is; first life must have been free living, otherwise we get the chicken-and-egg problem)). Turns out, they're fungi, like the mold in your fridge. We're not well-equiped mentally to deal with such timescales, but a lot can happen in just a few million years.
Thus, as long as we do not have a clear picture of the last common ancestor and its relationship with eukaryotes, it will be difficult to interpret gene similarity as evidence for the endosymbiotic theory.
This is where parsimony helps. Sure phylogeny is fallible (again, see microsporidia), but if an endosymbiont and a free living organism share a significantly large chunk of genes, it takes a lot less explanation and hand waving to invoke endosymbiosis than to craft elaborate hypotheses of weird massive lateral gene transfer stuff. That alone doesn't make it right, but definitely much more probable. And we're really working with probabilities here to begin with.

The mitochondrial genes could be derived from transposable elements, plastids or viruses and could come from either the nuclear genome or a bacterial genome.
'Domestication' of transposons is not as easy or probably as we may like it to be. Also, much of this would have to happen between the proto-eukaryote and the last common ancestor of most eukaryotes alive today, which is an epic question mark at the moment, although it does seem like that time period may not have been that long after all ('short' paper here: Cavalier-Smith 2006 Phil Trans R Soc B; free access). Cell structure, on the other hand, seems to be more malleable than large-scale gene organisation. Also, has there been at least one case of genes randomly congregating into a de novo genome in a random compartment? That would be quite ridiculously unlikely! How did the replication and maintenance machinery get in there then?

And plastid origin of mitochondrial genes? Ok, maybe once or twice that could, in theory, happen (has it?), but we're talking about mitochondrial genes in primarily plastid-less organisms! Does this guy propose a plastid endosymbiosis as ancestral to all eukaryotic lineages with mitochondrial genomes!? He seriously needs to explore something a little outside his metazoa. He needs to take one good look at a proper tree of eukaryotes (one without the 'crown eukaryote' abomination, kthx), and read a TC-S paper or two on eukaryogenesis. Or perhaps we should cross him with Margulis, and the result would have an intermediate phenotype, and perhaps even be a decent scientist!
Intermediates exist in the form of hydrogenosomes and mitosomes from amitochondriate primitive eukaryotes.
Hey, let's pull a little prank! How about we introduce him to Blastocystis and the ciliate Nyctotherus with mitochondria-like organelles (Stechmann et al. 2008 Curr Biol)? Actually, the table in that page, if you can access it, is a powerful demonstration of the dangers of relying on a single morphological for reconstructing evolutionary history. Essentially, if you follow organelle complexity, you'll get something like: Microsporidia, Giardia, Trichomonas, Nyctotherus, Blastocystis, and us. Let's draw that as a tree, mentally (let microsporidia be basal to the rest). So far so good. Ok, let's pull out a certain tree I tend to [ab]use a lot:

(Keeling et al 2005 trends ecol evol)

(I went for quite a while without pulling that out! Did you notice? See, self-restraint works sometimes! Until it doesn't...)

Let's do a little exercise. Grab a mental marker, and let's find Microsporidia. It will be among the opisthokonts, close to chytrids and zygomycetes. Done? Great, now find Giardia. It's a Diplomonad, close to Malawimonas in the Excavates. Trichomonas is a trichomonad, close to hypermastigotes (remember Trichonympha?), again in the Excavates. Now head over to the Chromalveolates, the alveolate neibourhood, for Nyctotherus, a ciliate. And then go down to the Stramenopiles, where you'll find Blastocystis between Actinophryids ('heliozoans') and Bolidophytes. And then point at pretty much everything else. And now look at our single-trait tree, which was built keeping de Roos' hypothesis in mind.'d that go? I think someone needs to read up on basic eukaryote diversity before making shit up about the origins thereof...

See, while both de Roos and Cavalier-Smith like to make up grand hypotheses that tend to contradict the mainstream theories, Cavalier-Smith is actually good at it. He thoroughly reads astounding volumes of literature, formulates rational, testible hypothesis that make sense, and backs off his theories when evidence definitively proves them wrong (as with Archaezoa). de Roos has ways to go to even dream of such level.

And finally,
"In order for an evolutionary theory to be considered a scientific fact or a valid scientific theory, there are some basic requirements. First, it is necessary to have a reasonably detailed mechanism that explains the basic steps in the endosymbiotic scenario. [done] Second, this mechanism should be placed in the context of current Darwinian evolutionary theory and should contain no fundamental problems or falsifications[huh...?]. Third, a substantial body of empirical evidence that directly supports this scenario should be present.[nope, no evidence whatsoever... I know of a lab where people just sit around on their asses all day because there's simply no data in that field. Also, they don't publish any ridiculous number of papers, thereby making us cell biologists very jealous.] Fourth, no credible or logically sound alternatives should exist[huh? Since when is that a requirement for a valid theory?]. If these criteria are not met, the endosymbiotic theory cannot be considered to be a scientific fact that has been proven beyond reasonable doubt. Remarkably, the endosymbiotic theory fails all points." [bolded edits mine]
Yeah, to all my friends working on endosymbiosis: IT IS A LIE! OH NOES!!1!

Seriously, how can people argue that bullshit, and SOMEHOW be employed in biology?! This guy is apparently an actual biologist (although more of a biochem/bioinformatics background; As a devoted cell biologist, I have an obligation to hate them a see, the academic community has ascended far beyond the primordial practices of stone age tribalism.) After a brief search, I found another interesting abstract, although we don't have access to this paper (and I can't be bothered to ILL it):
"Current theories about the origin of the eukaryotic cell all assume that during evolution a prokaryotic cell acquired a nucleus. Here, it is shown that a scenario in which the nucleus acquired a plasma membrane is inherently less complex because existing interfaces remain intact during evolution. Using this scenario, the evolution to the first eukaryotic cell can be modeled in three steps, based on the self-assembly of cellular membranes by lipid-protein interactions. First, the inclusion of chromosomes in a nuclear membrane is mediated by interactions between laminar proteins and lipid vesicles. Second, the formation of a primitive endoplasmic reticulum, or exomembrane, is induced by the expression of intrinsic membrane proteins. Third, a plasma membrane is formed by fusion of exomembrane vesicles on the cytoskeletal protein scaffold. All three self-assembly processes occur both in vivo and in vitro. This new model provides a gradual Darwinistic evolutionary model of the origins of the eukaryotic cell and suggests an inherent ability of an ancestral, primitive genome to induce its own inclusion in a membrane." (de Roos 2006 Artificial Life; emphasis mine)
Huh?! NO! Does not compute! AAAAAH! My eyes! I can feel my brain liquifying and oozing out of all sorts of orifices! See why the computery bioinformatics folk must be kept away from any mention of an actual organism? (ok, admittedly, some can manage it well, but that doesn't mean I shouldn't stereotype for personal fun =P )

I'll fix this sometime within the coming week, and 'translate' for you a real hypothesis on eukaryotic origins.
>Psi Wavefunction casts lvl10 TC-S Attack on lvl8 Crackpot for 500 damage.
Lvl5 Crackpot sustains 500 damage; HP 130/630
>Crackpot uses Copy Attack to cast Psi's lvl10 TC-S attack.
Psi sustains 0 damage due to TC-S Immunity.
casts lvl40 HAHAPWNEDLULz! on Crackpot for 1000 damage.
>Crackpot defeated!
*cue Final Fantasy victory music
>YOU gain 2000XP
Now back to working on this week's Sunday Protist ^.^

Cavalier-Smith, T. (2006). Cell evolution and Earth history: stasis and revolution Philosophical Transactions of the Royal Society B: Biological Sciences, 361 (1470), 969-1006 DOI: 10.1098/rstb.2006.1842

KEELING, P., & SLAMOVITS, C. (2005). Causes and effects of nuclear genome reduction Current Opinion in Genetics & Development, 15 (6), 601-608 DOI: 10.1016/j.gde.2005.09.003

Lake, J. (2009). Evidence for an early prokaryotic endosymbiosis Nature, 460 (7258), 967-971 DOI: 10.1038/nature08183

STECHMANN, A., HAMBLIN, K., PEREZBROCAL, V., GASTON, D., RICHMOND, G., VANDERGIEZEN, M., CLARK, C., & ROGER, A. (2008). Organelles in Blastocystis that Blur the Distinction between Mitochondria and Hydrogenosomes Current Biology, 18 (8), 580-585 DOI: 10.1016/j.cub.2008.03.037

First lap around the sun

The blog's first anniversary today! And it's still alive! *amazement*

The initial intent wasn't so much to create 'the protist blog' (as it's headed right now), since I wasn't sure I'd be able to do much science blogging, especially from peer reviewed sources. It started out stumbling about as a place to write the occasional rants and musings, which mostly happened to be at least somewhat related to science. But my growing obsession with protists seeped into this blog, and the whole thing kind of 'evolved' into a protist blog.

Since I don't have anything 'prepared' for today, let's reflect on the past year, blog-wise:
- introductory post, some slime moulds, then fled offline for a couple weeks...

September - ranted about uninterested classmates on the first day of the protistology course; discussed fundamentalism (and why I avoid politics); fungi and slime moulds; first Sunday Protist - Tetrahymena, wherein I exhibit the very hyperadaptationist thinking I have by now come to despise >_> ; post on memetic infections(a bit too idealistic); exploding ciliate =(; and a rant on pluralism I'm still kinda proud of.

October - trippy plant epidermis micrographs; cool picture of ciliate diversity; weird protist features: kDNA, algal vision and cytotaxis.

November - reaction to the US elections (holy crap, politics! on my blog!); my own clip of Saccinobaculus motility, to my knowledge, the only publicly available one on the internet!; an introduction to the protist 'kingdom'; pictures from a moss microorganism adventure.

December - EXAMS! *shudder* ...then internetlessness...


January - Declaration of ridiculously overly ambitious plans to go aroud the Keeling et al. 2005 tree. Haha! Ha! Funny! But I never wrote any of that, shhh!; excerpts of a 'lab notebook' attempt from age 9 or 10... (I was so totally not a nerd... ok, maybe just a little bit.)

February - introduction to and brief history of protistology, was meant to be part of a series, but I really don't work well with structure; intro to my current research (stomatal development), I do intend to write more about cool secrets of their developmental biology sometime...

March - obligatory apology for slow posting; public apology to prokaryotes for calling them structurally 'simple and uninteresting', upon finding out about multicellular fungal-like Streptomyces.

April - mystery cysts (feel free to ID them! please!); my essay on ciliate genome rearrangements for protistology; squashed cockroach guts under polarised light (yumm!).

May - a reflection upon science (while running a gel); astonishment at the fact the PCRs worked despite one of my pipets having a 25% error (and photographic evidence thereof).

June - insects and jumping spiders; discussion of the state of memetics.

July - finally get my act together and start updating at a marginally acceptable rate! Post on Why should cell biologists care about evolution?; algal parasite that shoots bare nuclei into host cell cytoplasm; defending the tree concept; rant about the stupid 'gene for [X]' phrase that gets thrown around in the media.

August - Story behind 'Psi'; cute phaeodarian; termite gut microforay; Myth of evolutionary ascent; and you know the rest...

Reflection - Benefits of blogging
That probably sufficiently bored everyone. Personally, I find it interesting to see thinking change with time - while sometimes it is a bit embarassing to look back on some older ideas and thoughts, it's satisfying to know you've moved on and developed somewhere. I think that's one reason to blog - you can trace the evolutionary history of your thinking! Kinda like leaving a fossil record behind at regular intervals...

Blogging also helps think more deeply about things - being careful about what you write (and fact-checking obsessively) helps correct some of your own misconceptions, and explore topics you normally ingore. Furthermore, I found it gives me an excuse to read stuff I otherwise would never need to. As much as I'm fascinated by random obscure organisms, reading about them just for the hell of it has to go to the rock bottom of my priority list; however, if I'm reading to later relay some of the information to the public, it becomes more important and...meaningful.

I'll emphasise the importance of meaningful reading for a moment. Perhaps this is just yet another facet of my own insanity, but I find it incredibly hard to just read something without a proper context. That's not to say there's a lack of curiosity, but rather that I have problems retaining information unless I have something to do with it. Even if I'm reading for pleasure, I'll hardly remember anything unless I can apply it to some sort of real (not necessarily practical) task. Taking notes helps somewhat, but one wouldn't call notes as a real product of any kind. Having a real research project definitely accelarates the learning process by a lot, but there's a physical limitation on how many of those you can manage simultaneously. So the next best thing would be...writing about it for other people!

This, in my current view, is part of the problem with your average education techniques - your 'task' isn't genuinely necessary or interesting enough; something as blatantly artificial as a final exam is insufficient to 'seal' the information you obtain for its sake. You cram, scribble in intense mental agony for a few hours, and then the entire course simply evaporates from your mind. There's nothing controversial there. But even if you're fascinated in the subject, simply reading the textbook for the sake of learning it is not enough. Not for my particular hive of madness anyway. There's needs to be a need. And preferably, a meaningful one.

Personally, I learn a lot from writing research essays. It's weird perhaps, but those force you to explore and extract data from the literature to carefully, yet in an interesting manner, argument your thesis. This, unlike solving exam problems, is a creative activity, one demanding judgement and sound reasoning from the writer. And you have the freedom to explore the available knowledge - unlike exams, where this knowledge is artificially restricted.

As for less selfish benefits of blogging: perhaps some of my writing could could at least encourage someone, somewhere, to stop and examine topics like protistology or memetics or whatever else I blabber about here. Especially protistology. It's such a neglected, marginalised field in biology (partly due to the traditional zoology/botany dichotomy), and if I could at least convince someone to take a second look and enjoy some of its wonders, I'd be quite happy and satisfied! I don't know how well I succeed at that, but hopefully there's some positive result out there. I wish I could actually write decently...

After all, I did steal the idea for the blog title from Carl Sagan's Demon Haunted World, the chapter called "The Marriage of Skepticism and Wonder". Science (ideally) is driven by wonder, and steered by skeptical inquiry. It seems that while the public is generally low on the skepticism, science tends to lag behind in the wonder department. Especially the way it's portrayed to the public. Perhaps, eventually, the naive wonder will get beaten out of me by the harsh realities of academic life - but for now, I'll enjoy its sweet euphoria.

Someone gets it right: Cell biology -is- relevant!

I love you, Tom:
"Recent genome sequencing has fostered a simplistic
view of organisms as essentially aggregates of genes.
However, organisms are not simply a sum of their
genes nor, as some biochemists were once wont to say,
mere bags of enzymes. Genes and enzymes are both
fundamental, but play their vital roles as parts of
highly organized growing and dividing cells. Their life
depends on a mutualistic symbiosis of genes, catalysts,
membranes and cell skeleton" - TC-S 2002 Intl J Sys Evol Microbiol [emphasis mine]
=D Warm fuzzy feeling inside... an evolutionary biologist who doesn't neglect cell structure! Someone who didn't forget that there's more to life than nucleotide sequences! What we have before us here is an endangered species, a rare specimen of sanity... wait, Cavalier-Smith and sanity in one sentence? I must've fucked this up big time...

So who dares me to plow through all 70 pages of that review? It's tempting, and I have a holiday coming up... "Mom, leave me alone, can't you see I'm trying to read a TC-S paper here?!", but it's 70 pages of Tom's hypothesising. Wherein he will cite himself at least 50 times... *checks* nope, only 39 this time. It's an older paper. And holy shit, 58 own entries in his latest J Euk Microbiol paper... an entire page of references!

But it's a lot of fun to read... yes, I read TC-S papers for fun. Where do I put that on my CV?

(now if only he could go easy on the mega- and meta-, and if only he could read, absorb and obey Tufte's The Visual Display of Quantitative Information, life would be so perfect...)

And since when do I blog so frequently? Eeek...gonna set the expectations too high for the oncoming schoolyear!

4500 words...

I may be slightly insane...

Please do critique my previous post; I'd like to know exactly how badly, and in what way, I fail at science writing!

Now that this issue is out of the way, we can explore evolutionary biology further in a new light!

So much for getting real work done...

The Myth of Evolutionary Ascent

ResearchBlogging.orgMany physicists whine about the public's grotesque misunderstanding of basic concepts like centripetal force and electromagnetism. Some of those very physicists often like to consider biology to be a simple subject, delivering profound lines like "people still study evolution???". Of course, how can anyone have any problems understanding something that barely uses any formulas! Of all sciences, biology uses the smallest portion of the Greek alphabet, and hasn't even moved on to Hebrew yet. How can there be much work in a field unless Norse runes must be invoked to complete a PhD thesis without assigning multiple meanings to symbols? Life is a giant differential equation, and unless you're cracking your skull open over one you're not doing it right! Quantify and model everything!!one

But seriously, how can any one misunderstand something as simple as evolution? Let's go on a bit of a rant adventure and find out!

The Ladder to Apocalypse
There is a classical image frequently used to represent evolution. This appears on the cover of some editions of The Origin:

We really like this picture. It's polite to our fragile feelings. It dares not offend (too much) our sanctum of superiority. Fine, the abyss between Man and Animal may not be so sharp after all - we may actually be related to the beasts. Fine, we'll even let Man arise from Animal, and none other than the coarse graceless ape. But at least we can still keep our final tatter of self-importance: for while but a small chapter in the story of life, this story was written for us. We are the ultimate Species, the crown of the tree of life. How flattering seems the depiction of progress, this procession of life from the lowly ape to the fully-formed proudly-standing masterpiece of evolutionary craftsmanship!

This view is reflected in the vernacular use of 'evolution'; exposed blatantly in cases like the Russian phrase "through hard work monkeys lost their tail and became man" (although that may be just my family, who knows...) and more the familiar Japanese phenomena like this:

You may laugh, but this is a rather accurate representation of the public's (and some biologists') understanding of evolution. One may recall the oft-recited progression of life from bacteria to amoebae to sponges, fish, monkeys, and us. While preparing a talk for some compsci students, I realised Toxoplasma may have a slightly different opinion: (and almost got an aneurysm making this)

Since our good friend Toxo actually managed to parasitise most mammals and birds, it clearly must preside over the crown of our lineage. Opisthokonts(well, unikonts) are but a basal lineage to Chromalveolata, of which Toxo is a proud empress. All hail T.gondii, the fierce goddess of the crown eukaryotes!

But seriously, does anyone else get a bit tired of constantly hearing about how the stupid lowly amoebae somehow congregated together and became multicellular and wise and awsome? For the record, the sister group to animals is choanoflagellates, who are not amoebae! Our amoeboid cell types arose secondarily, since after all there isn't that much of a problem in doing both... (see Naegleria, which can switch between amoeboid and flagellate forms in <120min...) What that image does represent is an approximation of our lineage's particular path, outlined in blue here:

Homonids being basal to chimps, of course. We stopped evolving, they moved on. So how does it feel to be a basal lineage anyway? Still 'primitive'?

Furthermore, the generation span in the animal lineage tends to be much longer, and among the larger animals we have rather insanely long time periods between heritable genetic modifications (and thus material for selection to play with). This means bacteria, some of which can replicate multiple times a day, until present day have passed through many orders of magnitude more 'versions' of themselves than animals have. In some ways, one can argue bacteria are more advanced than large metazoa. And this view is quite objective, if we only use the number of generations to go by.

Now that we've established that prokaryotes rule the world, we could simply concede defeat and go home. However, there still remains a nagging thorn in the side: complexity. If we define complexity strictly as the number of components involved in a given system, one must agree metazoa do have far more components than their bacterial counterparts. That does not make us superior; however, it does raise some further points and misconceptions about directionality of evolution.

The evolutionary 'ladder' may be a valid model for one thing: the history of a single lineage, with height representing nothing more than simply the time axis. Complexity has nothing to do with it. Nor does that ladder reach anywhere but the inevitable demise of our Earth at the end of biological time.

Evolutionary Directionality
Evolutionary directionality is a myth, a massive misunderstanding of evolutionary processes. I like to call it 'evolutionary creationism', for it eerily mimics the fairy tale put forth by the 'Intelligent' Design movement, albeit devoid of a few supernatural elements. Often, 'evolutionary creationism' and religiosity can be seen to go hand-in-hand, eg. Simon Conway Morris*. Even some brilliant, quite rational thinkers like Dennett have fallen for the appeal of anthropocentrism, emphasising the rise of human 'consciousness' in the discussion of memetics and devoting an entire chapter to the importance of the intentional stance in evolutionary thinking (1995 Darwin's Dangerous Idea). Consciousness is a topic for another day, but intentionality must be used with great care.

Perhaps in some cases it may be useful to assume nature strives towards perfection and survival in order to deduce the 'function' of a certain trait (as in Dennett 1995), but even if this may help, it must be kept in mind that the concept of 'function' itself is an artefact of the human mind. We say the bird's wings are 'for' flying, but this is just a shorthand way of saying "the bird would not be capable of flying without this feature, therefore it is essential for that activity. Furthermore, it seems that flying would suffer the most in the absence of this feature, thus we shall denote this structure's purpose as 'for flying'."

This can get murky upon deeper examination. What if these structures have multiple functions? Wings help maintain balance while walking; thus we can add that an additional 'function' of the wings is exactly that. However, if you chop those wings off, the bird's circulatory system would fail. Is a function of wings to keep blood from spilling out? That sounds a bit off. Ok, let's say it never had them in the first place. Then how about escaping predators? The bird would likely fail miserably without its wings. So predator avoidance a function of the bird's wing? How about foraging? Finding mates? If the wings of male specimen have some decorative pattern, we have no problems stating they serve also 'to' attract mates; however, a bird devoid of an elaborate winged mating ritual must also have them to mate eventually! But in the latter case, we hesitate before stating mating as a 'function' of wings. Ultimately, the function of every trait is to perpetrate itself, otherwise it wouldn't be there to speak of. But this definition is even more useless.

Hopefully the above discussion seems blatantly pointless, because it is. We use whatever definition of function we find must convenient at the moment, and that's ok. Because there is no such thing as function! We made it all up! It helps us model the world around us, but just like hunches and stereotypes, it has no place in scientific explanation!

If there is no function, and therefore no purpose, how can evolution have any aim? How can there truly be any progress? We must realise that while we desperately strive to seek patterns, to find meaning in life, and therefore science, we cannot project the same features onto the world around us. (I'd go as far as arguing that our own intentionality is an epiphenomenon, an illusion, but save that for a[n even] more philosophical post...)

Life just is. Life doesn't even strive to replicate, strictly speaking. It's just that if it fails, it ceases to exist. This thereby generates an illusion of a goal (to perpetrate genes, for example). In a way, it's a ratchet - you can go in one direction, but you cannot go back (and continue existing). If you have a chemically-successful body plan capable of replication, and you maintain it, you keep replicating. If you fail, you're gone. Entire lineages can eventually fail. The only reason I'm sitting here blabbering on a blog is that a tiny fraction of lineages did manage to somehow make it this far. They didn't wish for this, it just happened.

Perhaps some other lineage could have invented computers with internet and blogs and all the rest, and the story of evolution would have a slightly different twist to it. But this wouldn't change the nature of evolution itself! It's still an aimless process, an extension of chemistry, which in turn is but a subset of the laws of physics. A subset detailing what happens if you apply certain constants and laws of the universe to certain chance conditions, of which we just happen to be part of. Of all things, I sure hope no-one would arge the universe has any intentions!

It takes discipline to avoid invoking direction and intentionality in evolutionary discussion. Our brains are adapted to a certain type of environment, and combined with a vast plethora of non-adaptive 'spandrels'**, have certain innate ways of modeling the world around us that may be less than scientific. Thus we have devised the formal Scientific Method to compensate for these biases. But it's natural to assume the intentional stance if you're a social creature. As Dennett explains, you don't make predictions about someone else's behaviour by analysing their neurology; you assume they aim for certain things, and base your predictions on that. Lacking the capacity for intentionality results in severe psychological and social problems.

Even despite my ranting here, I have, do and will make mistakes of this nature in biology. For example, in a post about Tetrahymena nearly a year ago I went on and on about how wonderful nuclear dimorphism (germline vs. somatic nucleus) is in terms of "protecting germline DNA from abuse by transcription". That was completely and utterly wrong. Upon seeing this strange phenomenon, I naturally assumed an adaptationist approach to the whole thing and blurted out this insane hypothesis. Perhaps the next section may help see how my reasoning was embarrassingly wrong in that post.

Rosie Redfield put it nicely: "[about constructive neutral evolution] Shouldn't that be our null hypothesis?" You see, we should only invoke adaptationism when simpler explanations (physics, biochemistry, molecular genetics) fail.

The Rise of Non-Adaptive Complexity
So if evolution lacks direction, how do we get such wonderful complex creations? Shouldn't everything stay at the unicellular, prokaryotic level? Well, in a way, it does. The vast majority of life on earth, by far, is unicellular. Does this mean unicellularity is better? Or does it mean very few organisms happen to 'discover' the rarer ways of being?

The answer probably involves a little bit of both. Despite fiercely disagreeing with Dennett above, I do like the 'design space' concept he tends to often use. Essentially, it's as if evolution is blindly stumbling about this design space, exploring some of the possibilities available at any given situation. Some of those options are successful, at least for some time, and lead to further possibilites. Some options are dead ends, and lead to extinction. Some options are simply never touched. Sections of this design space have repeating motifs that manifest as evolutionary convergence, for example the camera eye of mammals, cephalopods and Warnowiid dinoflagellates(Leander 2008 Trends Ecol Evol); or the morphologies of a tapeworm and Haplozoon, a similar but microbial intestinal parasite (Leander 2008 JEM).

Now how can aimlessly wandering about the corridors of design space lead to such stunning, and recurring, complexity?

The traditional explanation is positive selection. Unlike negative selection, responsible for killing things off for developing, losing or modifying certain features, positive selection 'encourages' certain traits by killing off the failing competition. While negative selection kills off the rabbits that are too slow to avoid the wolf, positive selection kills off rabbits that can't eat fast enough to compete with their rivals, to use a very crude example. This can explain some features, but opponents, as irrational as they are, do have some valid reason for being confused how this leads to the formation of new features.

Luckily, we have a powerful tool on our side. New features don't have to be selected for to arise. As long as they don't inhibit the survival of the carrier, they are free to explore design space at their whim. An additional feature is ratchets - sometimes, either due to negative selection or simply physical characteristics, once something is done, it cannot be undone. (Eg. you go to (don't!), and see things you don't really happen to savour. This is a psychological ratchet, or in the words of 4chan speak: "What has been seen cannot be unseen")

A less abstract example: Dinoflagellates like to do everything the weird way. One such oddity is the need to attach a special DNA sequence, called a splice leader(SL), onto every single mRNA transcript made in the nucleus. Without the SL, the transcript is degraded before the gene can be translated. So far so good. Now, sometimes a reverse transcriptase, which can convert RNA to DNA and insert it back to the genome, happens to do exactly that to an SL-mRNA transcript. The result is a duplication of the gene, although already containing a SL sequence. However, after transcription of this SL-containing gene, a new SL must still be reattached, otherwise the mRNA transcript degrades (the key is that the SL also contains the 5' cap, which protects the transcript from degradation. Simply containing the SL sequence is not enough).

So now we have a situation like this: 5' cap-SL-SL'-gene. Since SL' (the old splice leader) is no longer necessary, and therefore no longer conserved, it can degrade as much as it likes. In fact, so can the entire SL'-gene sequence, considering the old gene still exists. Gene duplication is a very unstable event, since either gene (but not both!) can go to hell and the organism would not feel a thing. Thus, let's assume an equal chance that either gene goes away. If the new SL'-gene sequence mutates and disappears into genomic background noise, we would never even know it happened. However, what if the old gene vanishes, leaving behind the new SL'-gene?

We get strange genes with relict degraded splice leader sequences (Slamovits & Keeling 2008 Curr Biol)! Sometimes you can even have a gene with two or more SL sequences, one more degraded than the other. Ie. SL"-SL'-gene. Because the new gene cannot easily lose the relict SL sequence, this is a perfect example of a ratchet - the genome can acquire splice-leader containing genes, but cannot lose them. One should expect that over time, the genome becomes full of genes with SL garbage at the 5' end.

There is nothing adaptive about this situation, even though arguably the complexity is increased. But this alone doesn't yet explain how seemingly functional complexity happens. What we need is an addictive personality.

Constructive Neutral Evolution
Let's say you're going about your business, and something wonderful comes up that makes your life easier. For example, here you are, happily wandering about, and suddenly come across a Blackberry or similar device. Prior to this find, you managed to organise your life quite fine - you kept your adresses neatly organised on a paper notebook, you could sit in public transit without any electronic paraphernalia, you only emailed from work and home. And the thought to complain never crossed your mind. So you find this nifty thing, and after some initial grumbling about its excessiveness and lack of real necessity, you give it a try.

Fast forward a few months later, you lose it. Suddenly, you realise how much your dependence upon this device has grown, and wonder how you've managed without for decades before. This device becomes a necessary part of your daily life, and you've even forgotten how to use a paper adressbook.

Initially, the find was neutral; you managed quite well without the device. However, after time, your other functions (eg. paper-based organisation) degraded due to excess capacity, and the electronic device became fixed and necessary for function. You have experienced a gain in complexity, although arguably the initial adaptive value of this device was minimal. (sorry, I don't worship technology as much as the media does) Of course, after you became stuck with the device, perhaps you found additional new uses for it, some of which were actually adaptive.

This type of process is not always so positive. Many patients of psychological illnesses, such as depression, become hooked on drugs and later become incapable of being happy without them. Worse yet is when a 'normal' person comes across an addictive drug they have the misfortune to enjoy. Initially, their brain could function fine on its own (one-component system). They try the drug, and enjoy it. For some time, they can quit and still revert back to the one-component state. They are in a transitional two-component situation. However, time goes by and the brain chemistry changes (degrades). Now, the drug becomes fixed in a two component system. The complexity has increased, but one probably cannot really call this adaptive or beneficial in any way.

Evolution has a rather addictive personality, largely due to an inherent system of ratchets at many points. The exploration of design space is a tricky thing, with many traps and hidden moving walkways along the way; much like some airports (eg. Heathrow).

This brings us to constructive neutral evolution, as explained in the fascinating Stoltzfus 1999 Trends Ecol Evol article (free access), which shifts too many paradigms to be well-accepted. (A follow-up is in the process of being written, however, according to reliable sources...)

The basic concept is that we have a single component system, say enzyme U that catalyses the change of molecular A to molecule B. Let's say this pathway is very important, and the organism dies without it. Say we have a mutation X that completely inhibits U's function. You would never see this mutation in action as it's lethal to its carrier.

Now, assume another protein, V, which is involved in a whole other pathway somewhere, just happens to stabilise U a little. This enhancement is insufficient to be selected for via positive evolution, and its absence reverts us back to the initial state. However, just by chance, V happens to compensate for mutation X in U! Now, if X never happens, this convenient little detail would probably never surface, and thus remain silent. We can say there is excess capacity present in this state. However, say mutation X does happen, as it's bound to eventually...

...we now have a two component system requiring both U and V for the organism's survival! The complexity has increased, although the original single-component state has done quite well on its own. Now there are two elements for evolution to tinker with, and new design space has suddenly become open for further exploration. Perhaps now some of this new design space has adaptive venues to pursue, although that is still not necessary for further gain in complexity. Hopefully this figure makes the process a little clearer:

(based on Stoltzfus 1999; any errors in this depiction are my responsibility alone)

When I first heard of this, it seemed perfectly logical and obvious, and some part of me was wondering "well, what's new here?". Then it sunk in how outright wrong my prior understanding of evolution was! I too was obsessed with hyperadaptationism, not even bothering to think that some complexity may in fact arise without any adaptive reason! My friend overheard some classmates being pissed off by this idea - they thought it was simply ridiculous! Of course, they've been taught a certain way of evolutionary thinking in all the other classes, and even wrote exams on it. Now some guy from an obscure field dares to suggest they've been taught wrong!

If undergrads feel like they must resist this idea, then what can we expect of people who've gone through entire careers thinking a certain way? Much like the tremendous psychological difficulties in abandoning one's religious views from childhood, the resistance (masked by apparent apathy) towards constructive neutral evolution plagues the bulk of evolutionary biology as a field. Thus, we will still find hyperadaptationist explanations in evolutionary research, the media and public science writing for many years to come. A wonderful example of how ideas generally become accepted not by winning over the opponents, but an entire generation growing up exposed to them! (more space for memetics-based explanations? Oh, speaking of which...! /unsubtle hint)

So are there any real physical examples that can be explained by this view?

A fairly straightforward one would be of a biochemical nature: the story of CYT18 and mitochondrial self-splicing introns of Neurospora crassa (fungus) . (Collins and Lambowitz 1985 J Mol Biol; example discussed in Stoltzfus 1999)

While we generally think of introns as requiring spliceosomal complexes to be excised (and allow the gene to be translated properly), there is a class of introns which splice out by themselves, due to the secondary RNA structure of the transcript (the assumed initial state in intron evolution, by the way). CYT18 is a mitochondrial tyrosyl-tRNA synthetase; ie it's involved in making the tRNA containing tyrosine, for protein synthesis. This is to stress it initially had nothing to do with introns. The mitochondrion also had plenty of vital genes with self-splicing introns, polite enough to remove themselves prior to translation. In doing so, the RNA structure must form a double-stranded neck. Mutations in that region result in incomplete splicing or absence thereof altogether, thereby leading to death.

CYT18 is necessary for some of those introns to splice out. One could postulate plenty of adaptive 'regulatory' reasons for this, but this turns out to be quite unparsimmonious (and therefore much less likely) when compared to the following explanation.

CYT18 initially just happened to have an affinity for the intron RNA 'neck' structure, and in doing so stabilised it a bit. Now, at that point it still wasn't necessary, nor did it actually make any difference in terms of selection (the intron was spliced out with or without). However, N.crassa is among the minority in requiring CYT18 for proper intron splicing; other fungi don't need it. This suggests an accident happened.

The 'accident' was likely a mutation in the neck region that would have otherwise been lethal, but was stabilised by CYT18 in this case. This fixed the role of CYT18 in mitochondrial intron splicing in affected lineages. That simple. No adaptive explanations required, for the N.crassa system is unlikely to be better than the regular self-splicing state. This process was constructive in that complexity has been generated; and neutral in that positive selection hadn't participated. And yeah, it's still evolution.

Interestingly, this is likely how all spliceosomes came to be! Mitochondria come from bacteria, and bacteria generally are not supposed to have introns (fuzzy territory but let's leave it at that for today). Mitochondria are not supposed to have introns, and most of introns present are self-splicing (possibly coming from a transposon, you can spread more if you politely remove yourself from interfering with the host's life). However, dependencies on random proteins like CYT18 would eventually result in arguably unnecessarily ridiculously complex structures like spliceosomes.

There's more applications of constructive neutral evolution (probably more than enough stuff for today!), and after it sinks in you become to see it more and more.

Again, as Rosie pointed out: it should be our null hypothesis.

Hopefully, I have managed to at least convince you that evolution never aspired to 'create' humanity; has neither aim, nor desire, nor direction; evolution does not strive towards complexity or progress; and that complexity can arise on its own without being called for by adaptive processes. There is no such thing as evolutionary ascent, and can we please stop desperately clinging to the last surviving strands of creationism?

*SCM visited our university a while ago, and my friends and I went to one of his talks. His talk was pretty good, although towards the end his arguments clearly began to crumble: the obsession with convergence was still tolerable, but the final note he ended on was simply insane. He actually suggested outside 'forces' guiding evolutionary processes! (I likely missed his precise argument as it was steeped in rather convoluted philosophy-speak and had little to do with actual science; but the gist of it was such.) That day, I just happened to have the Stoltzfus 1999article on me, for some inexplicable reason. So we proceeded to the front after he finished. I mentioned being quite impressed with his awareness of Paulinella (obscure Rhizarian that seems to have undergone an independent primary endosymbiosis of cyanobacteria! (=plastid)), and to give him credit, the guy does know a lot of stuff. So I brought up a rather opposite perspective on evolution to his, and showed him the paper. Interestingly, his response was along the lines of: "While this may or may not be valid, I don't care about how evolution got here; what I'm more interested about, is where evolution is going."

Now one must wonder - is it even possible, or wise of us to try to figure out the future of evolution? He does have a point there - evolutionary biology is a historical science, focusing on what happened and the mechanisms behind it, rather than predicting where things will go. He's fascinated by the more philosophical aspect. Of course, in doing so, he screams directionality. Perhaps this is his way of reconciling his religion with science; while admirable in his attempt, it seems to be driving him literally crazy. Conway Morris' religiosity has forced him to go through some intense mental gymnastics, providing yet another illustration of the disease-like properties of religion...

**While the spandrel concept is useful in biology, it may be interesting to note that the real (architectural) spandrels are not really spandrels in Gould's sense. (Dennett 1995)


Dennett, D.C. (1995). Darwin's Dangerous Idea

Collins RA, & Lambowitz AM (1985). RNA splicing in Neurospora mitochondria. Defective splicing of mitochondrial mRNA precursors in the nuclear mutant cyt18-1. Journal of molecular biology, 184 (3), 413-28 PMID: 2413216

LEANDER, B. (2008). Different modes of convergent evolution reflect phylogenetic distances: a reply to Arendt and Reznick Trends in Ecology & Evolution, 23 (9), 481-482 DOI: 10.1016/j.tree.2008.04.012

LEANDER, B. (2008). A Hierarchical View of Convergent Evolution in Microbial Eukaryotes The Journal of Eukaryotic Microbiology, 55 (2), 59-68 DOI: 10.1111/j.1550-7408.2008.00308.x

SLAMOVITS, C., & KEELING, P. (2008). Widespread recycling of processed cDNAs in dinoflagellates Current Biology, 18 (13) DOI: 10.1016/j.cub.2008.04.054

Stoltzfus, A. (1999). On the Possibility of Constructive Neutral Evolution Journal of Molecular Evolution, 49 (2), 169-181 DOI: 10.1007/PL00006540