By now, everyone must be familiar with the inside out organization of the cephalopod eye relative to ours: they have photoreceptors that face towards the light, while we have photoreceptors that are facing away from the light. There are other important differences, though, some of which came out in a recent Nature podcast with Adam Rutherford (which you can listen to here), which was prompted by a recent publication on the structure of squid rhodopsin.
Superficially, squid eyes resemble ours. Both are simple camera eyes with a lens that projects an image onto a retina, but the major details of these eyes evolved independently — the last common ancestor probably had little more than a patch of light sensitive cells with an opsin-based photopigment. The general properties of this ancient eye can still be seen in modern eyes. They detect light with a simple molecule called retinal that is capable of absorbing a photon, changing its shape from the 11-cis form to the all trans form; basically, it flips from a chain with a kink to a straight chain. Retinal is imbedded in a protein called opsin. When retinal changes shape, it changes the shape of the opsin protein, too, which can then interact with other proteins in the cell membrane.
The next protein in the sequence is called a G protein. G proteins are ubiquitous intermediates for many cellular processes; when a receptor, like opsin, is activated, it activates a G protein, which then activates other proteins, starting a signaling cascade. In the podcast, I compare this to starting an avalanche. Opsin is an agent standing on a hill; when it receives a light signal, it nudges a small boulder (the G protein), which then tumbles down setting a whole series of rocks in motion. The G protein is an intermediate which takes a small change, the initial nudge, and amplifies it into the activation of many other proteins.
So far, this is all common to both cephalopods and vertebrates. We all have retinal bound to an opsin which activates a G protein which starts a series of events that lead to a change in electrical activity in the photoreceptor cell. Now here are the differences.
We vertebrates have ciliary photoreceptors which use a variant of the opsin protein called c-opsin. The c-opsin activates a G protein called Gt, which activates an enzyme called phosphodiesterase, which decreases the concentration of a messenger molecule called cyclic GMP. This cGMP binds to sodium channels and opens them; decreasing levels turns off the electrical activity of the cell. Our photoreceptors are most active when it is dark, and when it is light, they reduce their level of electrical activity. One way to think of it is to imagine the photoreceptors being able to say only one thing to the rest of the retina and brain: “It’s dark!” When it is dark, all the photoreceptors are constantly shouting that message back; when it’s light, the photoreceptors go quiet. The retina integrates this information to put together a picture of light and dark areas in the visual field.
Cephalopods use a different pathway. They have rhabodmeric photoreceptors that use a version of opsin called r-opsin. R-opsin binds a different G protein, called Gq. Gq activates the phosphoinositol pathway, which uses diacylglycerol as a messenger, which opens ion channels in the membrane, exciting the cell. Squid photoreceptors can send the message “It’s light!”, and they shout it back when the lights are on, and go quiet when it’s dark. Logically, this is equivalent to what the vertebrate eye does, it’s just that the polarity is reversed. We have an electrical switch installed that you flip down to send a signal back, while squid have a switch that you flip up.
This difference is entirely arbitrary! We have some cells that use Gq, too, just not for photoreception; similarly, invertebrates have c-opsins and Gt proteins. Some cells even combine both kinds of pathways, which is a clever way to get double-duty out of a single cell — they can respond one way to one kind of signal, and in a diferent way to a different kind of signal. What this represents is an accident of evolution, that 600 million years ago the progenitor of the lineage that led to us settled on c-opsin/Gt for its photoreceptors, while the ancestor of squid used an r-opsin/Gq combo for the same job.
What triggered this bit of background and the Nature podcast is a new paper by Murakami and Kouyama in which they’ve worked out the structure of squid opsin. This is significant because it shows us both the similarities and differences between a c-opsin and an r-opsin, and allows us to look in more detail at the biophysics of light transduction in invertebrates. Here is that structure, with squid r-opsin overlaid in brown over blue bovine c-opsin.
Structural comparisons between squid rhodopsin and bovine rhodopsin. Squid rhodopsin is denoted by brown and magenta; bovine rhodopsin by cyan and blue.
The first thing to notice is the overall similarity: both have the same general structure, with seven helices spanning the membrane and forming an internal pocket for retinal. There are subtle differences in the conformation, with the squid opsin apparently having a slightly roomier retinal pocket, for instance, but in general the similarities are obvious. Keep in mind that these proteins are separated by over half a billion years of evolution!
The most obvious difference is at the top of the diagram, on the cytoplasmic side of the membrane, where two of the helices (V and VI) have formed a protrusion in the squid that is not present in the cow. This is the binding site for the Gq protein, and where all the specific differences in the signaling cascades triggered by the two proteins arises — one small bump.
Of course, this is all important to know for better understanding the eye of the squid, but some of the more selfish among you may be wondering what this can possibly do to benefit humankind. We don’t know. However, one possible human interest angle is that our homologous r-opsin protein is called melanopsin, which is a molecule we use for regulating our circadian rhythms. Understanding the structure of r-opsin may someday help in drug design for treating sleep disorders, for instance.
I think it’s enough to know more about cephalopods, myself.
Murakami M, Kouyama T (2008) Crystal structure of squid rhodopsin. Nature 453(7193):363-369.
Ie, some of the grant-seekers among you…
I love some of the more outlandish “human connections” you sometimes see on scientific papers. So much for “scientia gratia scientiae.”
Another good reason to learn these things is that evolution has tried out “designs” for hundreds of millions of years, and has hit on several good ones.
Artificial eyes for robots, and maybe even someday for humans, might be optimized by comparing what is good in vertebrate eyes and what is good in cephalopod eyes.
We do design by copying nature in many cases. But we almost always are able to make improvements as well, since we are not limited by past inheritances, nor by the material limitations of biology.
And since we accept the science of evolution, we can even figure out why cephalopod eyes are as they are, and why vertebrate eyes are as they are, which is due both to functionality and to the inability of evolution to think or plan ahead, or to do anything other than to modify what came beforehand.
Glen Davidson
http://tinyurl.com/2kxyc7
Nice post.
Everything about the cephalopod eye seems to me more straightforward and logical than the vertebrate eye. Photosensitive cells closer to direction of light than the nerve fibers and blood vessels, photoreceptors that turn on when stimulated by light rather than the other way around, etc.
As I understand it the vertebrate eye appeared first in the fossil record, since Haikuichthys and its relatives had them in the Cambrian, while the cephalopods as a group came later. It seems like the Intelligent Designer (TM Discovery Institute) messed up his first attempt and improved on his second try. Maybe he was still in graduate school during the Cambrian?
I love some of the more outlandish “human connections” you sometimes see on scientific papers. So much for “scientia gratia scientiae.”
just to be clear (and I’m sure you meant it this way), that’s hardly the fault of the publishing scientists, it’s directly a result of grant agencies requiring “human relevance” in their applications process.
funding for basic “non applied” science, in this country is abysmal, and getting worse.
Bear with me here, as my biochemistry is a bit rusty (OK, I don’t think I’ve ever taken any biochemistry past high school, so rusty = nonexistent). Is there an energetic difference between having photoreceptors that yell “It’s dark!” vs. “It’s light”, given the differing amounts of light and darkness in various environments? For instance, it wouldn’t be that efficient to have receptors that are most active in non-light in a benthic environment. Or are the energy costs associated with signalling pretty negligible?
Careful there, though. The logic of the squid eye — + for light — is no better the vertebrate logic — – for light. They are equivalent.
If the last common ancestor already had light sensitive patches for eyes, would it have used r-opsin or c-opsin in its eyes? A combination of both? Some other opsin that perhaps later gave rise to both r-opsin and c-opsin through gene duplication?
I read somewhere that the closest living analogs that are most similar to what we think the common ancestor might have been like had r-opsins and rhabdomeric photoreceptor cells in its eye patches and c-opsins and ciliary photoreceptors in its brain photoclock. If the common ancestor had this set-up, it makes me wonder what evolutionary quirk resulted in the vertebrate lineage going through the kluge-like process of giving up its original epithelial r-opsin eyes and re-evolving c-opsin eyes from outgrowths of its brain photo-clock, then re-commandeering r-opsins for circadian rhythm regulation, essentially ending up with the ancestral roles of c and r-opsin reversed.
Both!
When you see an eye develop over time, it just seems so…obvious. I don’t know why it gives off any irreducible complexity vibe to IDiots.
So the precambrian rabbits were an undergraduate project?
Having now derailed this thread we return you now to the interesting post…
Ever since I first started studying neuroscience in earnest during medical school I’ve always been struck by how reliant the human (and by extension the vertebrate) nervous system was on negative type signalling. Our brains are chock full of circuits where neurons are continuously firing in the null state, and are turned off by stimulation. For example, every time we make any intentional movement, our brains achieve this by turning off a continuous inhibition of our primary motor cortex.
Initially it seemed to me to be startlingly wasteful of energy, but of course that is a misunderstanding due to oversimplification. It all depends on the prevailing environment, and there may be advantages in having continuous signals that can be modulated up or down in relation to adaptability and reactivity.
Brownian, as I learned it, there is an energetic difference to consider. Specifically, it pertains to how much neurotransmitter needs to be made by the photoreceptor cell in order to shout its message. When the electrical activity of the cell is “turned on,” vesicles fuse with the cell membrane and release the neurotransmitter (NT) stored therein, thus sending the message to the next cell in the pathway.
The logical message is the same, but if you’re living most of your life in the light, it’s more energetically efficient to shout “it’s dark!” so you’re not spending as much NT to get the same message across (and vice versa).
It is possible that this difference evolved because cephalods live mainly in dark, thus the bright light means for them extraordinary change….and on the other hand, we, vertebrates are more used to the light than to the darkness?
Wait, wouldn’t turning on phophodiesterase DECREASE cGMP? Guanidine cyclase would increase cGMP. Or am I missing something?
For a fun brain twisting moment what about reversing that logic? What if the very minor amounts of extra stress ’causes vertibrates to preffer the light and cephalopods to preffer the dark?
(just having fun with logic)
#12 – I was thinking the same thing…
Ok, PZ.
“phosphodiesterase”
“phosphoinositol”
“cytoplasmic”
Those aren’t words! My spell checker even says so. You’re making this all up!
;p
But seriously, couldn’t you biologists come up with names for things that are easier to say? Don’t your tongues get tired trying to pronounce this stuff all day? As a software engineer I recognize the importance of descriptive names, but come on. “Phosphodiesterase” Really?
Maybe this is why all of the creo-fundies are so resistant to science. They see the multi-syllabic, Latin-ese concatenations which they could never hope to sound out and they cry “Witchcraft”.
A question only distantly related to the post, how does the eye of a marine creature like a squid or fish respond to changes in pressure with depth? As I remember pressure increases by about 1 bar (approx 15 pounds per squar inch) every 10m (33 feet), for any creature that changes depth would this cause significant deformation of the eye affecting the creatures vision? (Spot the engineer)
Does this mean our eyes are firing away all night when our eyelids are closed? What’s the cost of all that signaling? How often does each photoreceptor fire in normal light, anyway? Would there be an advantage to a nocturnal animal of using the squid system?
So many questions…
“As a software engineer I recognize the importance of descriptive names, but come on. “Phosphodiesterase” Really?”
The thing is, they *are* descriptive:
phospho- : from phosphorus/phosphate -inositol : that’s a type of sugar
cytoplasm : think cyto = cell
Phosphodiester- : that’s a functionnal group in organic chemistry -ase : an enzyme; so Phosphodiesterase : an enzyme that cuts phosphodiester bonds
I guess as vertebrates, we must have evolved in a photic zone that happened to receive more hours of daily sunlight then darkness. In that way, the constant protein chatter (i.e firing mechanaims) at night conserves more energy then if the chatter was during daylight hours. Either that, or perhaps I’m reading too much into it.
Another way to look at it is to imagine the energy and cost/benefit analysis represented between the LCA of vertebrates and cephalopods. Perhaps one lineage had greater photic exposure, and if the signals were constantly active in daylight, it would result in a few extra hours of wasted signaling. Conversely, perhaps the Gq lineage had greater exposure to darkness, perhaps living in deeper waters, and it was beneficial to allow signaling only in light. It may not matter what arbitrary firing occurs in vertebrates that evolved in a photic zone since there’s an equal amount of light and darkness, whereas the dark-firing mechanism for the cephalopds would have resulted in a wasteful expenditure of energy due to the greater darkness.
#18 – No wonder I can’t sleep. I know it’s dark, already! Shut the hell up!
@16:
Ok, PZ.
“phosphodiesterase”
“phosphoinositol”
“cytoplasmic”
Those aren’t words!
That is nothing! I heard two I wrote down just a week ago and am looking for the perfect moment to insert them into conversation:
Polhode and Herpolhode.
OK – so maybe they roll off the tongue a little easier than phosphodiesterase (or my favourite from “A Stress Analysis of a Strapless Evening Gown”: trapstocachumycein), but they are every bit as charming!
What? You haven’t heard of “A Stress Analysis…”? I would have assumed that “Hiawatha’s Lipid” was required reading here….
JC
@ #14
My veterinary ophtho book agrees:
“The end result of light stimulation is a decrease in cGMP levels, leading to a closure of the [Na+] ion channels. The Na+ influx stops, and the cell undergoes hyperpolarization.” Vet. Ophthalmology 3rd ed. Kirk Gelatt
#19
Ha… I see. Too descriptive maybe. But the other tendency in biochemistry is to use wretched acronyms, sometimes made up to sound like a more usual word, which make conversation between biochemists (or chemists) working on different projects quite laborious…
They may look less like witchcraft, but I’ve always found them somehow much more frightening than the descriptive names… Like the “colors” of quarks in physics… If you heard people use them (and you don’t know they’re physicists or biochemists) you’d think they’re mentally ill and enjoying a nice word salad…
These are my favorite kind of post. Thanks. Oh, and in my view, the last article in “Seed” on pufferfish was the best one so far. It’s a world of wonders.
A question only distantly related to the post, how does the eye of a marine creature like a squid or fish respond to changes in pressure with depth? As I remember pressure increases by about 1 bar (approx 15 pounds per squar inch) every 10m (33 feet), for any creature that changes depth would this cause significant deformation of the eye affecting the creatures vision? (Spot the engineer)
yes, you’re right that pressure increases by approx. 1 atmosphere per 33 feet. Eye compression would indeed be a serious issue if the eye wasn’t composed of mostly incompressible liquid.
This is why near-death experiences always include a bright light. When the retina runs out of oxygen, cGMP, which requires energy to make, cannot be resupplied. Seeing dark is an effort.
Kenny, are you listening?!?
Over a whole billion years. Half on each branch.
Haikouichthys :-)
Cytoplasmatic, indeed. <vehement nodding>
A type of sugar alcohol, actually — derivable from the sugar inose.
A phosphodiester is a molecule with two ester bonds in which a phosphate group is involved.
No, because the pressure inside the eye changes just like the pressure outside the eye does.
Oh yes. All those magic spells like Ras Raf MEK ERK…
So many questions …
Does any species have sight based on a haeme/chlorophyl chemical framework?
How does the on/off mechanism work in blind people?
Might the constant shouting of “It’s dark! It’s dark! It’s dark!” have something to do with our odd habit of dreaming?
Woo-hoo! Science post! As a philosophy grad student who’s been buried in papers and books with nary a biological ejaculation in sight, this was a refreshing break.
Thanks, PZ. I always learn so much from these posts.
#2 – “Another good reason to learn these things is that evolution has tried out “designs” for hundreds of millions of years, and has hit on several good ones.”
I think last time I saw a list of the different types it claimed 37.
One of my favourites is the eye of some shrimp that adds polarisation sensing to the suite of inputs and results in shrimpy twisting his eyes around the view axis to help aim some hunting action I can’t even remember anymore. So utterly SF-killer-droid it’s wonderful.
Bear with me here, as my biochemistry is a bit rusty (OK, I don’t think I’ve ever taken any biochemistry past high school, so rusty = nonexistent). Is there an energetic difference between having photoreceptors that yell “It’s dark!” vs. “It’s light”, given the differing amounts of light and darkness in various environments? For instance, it wouldn’t be that efficient to have receptors that are most active in non-light in a benthic environment. Or are the energy costs associated with signalling pretty negligible?
I’d like an answer to this as well; It was the first thing I thought of when I was reading about the differences between the two. Does it take significant amounts of energy to constantly send “it’s dark!” signals? Or is the energy involved in the actual signal transmission fairly minimal? Obviously being able to see at all is a huge advantage in finding food, avoiding predators, etc., so it would still be a net advantage to have eyes even if their constant signaling wastes some energy, but is this disadvantage minimized the way cephalopods do it?
PZ, #5 (and other including me) are not questioning the logical equivalence, but rather the relative energy costs to signal active=dark vs active=light.
I know eyes are old things, and it’s probably pointless to correlate nocturnal/deep-sea animals to dark/light=active, but is there a real energy cost difference here?
A thought…
In a dark environment, “it’s light!” means food.
In a light environment, “it’s dark!” means preditor.
Is the rest of the system likely to react faster to an off-to-on signal or to an on-to-off signal?
Seems to me that a system would have safeguards set up to eventually shut down or ignore a constant signal, but would be sensitive to the sudden increase in a signal. Kind of like how you get “used” to a particular smell once you have been around it for a while, but you are immediately aware of a new smell.
If given the environment the difference in on-for-dark vs. on-for-light makes a difference in the reaction times of the system then you would have an environmental pressure towards one over the other.
Make sense, or am I extrapolating too much?
The PDE error has been corrected.
No, there’s no energetic advantage to either being stimulated by light or inhibited by light — your thinking is too black and white. It doesn’t matter which way it goes, at ambient light levels the firing rate of the photoreceptors will be about the same in each case; for good sensitivity, they will be firing at an intermediate rate, and the rate will increase or decrease in response to changing light levels. It’s not as if they will be at some floor or ceiling rate of activity!
your thinking is too black and white
pun intended?
PZ, please repeat to your students: This difference is entirely arbitrary! It’s something that so many neuroscientists miss – no action potential, in general, has exactly the same information content as an action potential. All neuroscientists should take Information Theory 101.
Has anyone measured the average firing rate of photoreceptors in vertebrates and squid? I’d expect in both cases a firing rate of about 50% – it would be interesting if it’s not, in which case it wouldn’t be arbitrary which signal is on and off.
And of course, as I post PZ answers my question!
re: PZ’s #34 and related posts
And therein lies the pitfall of oversimplification via analogy. Neurons aren’t like transistors/switches with just two (on and off) states. Actually they are continuously at varying levels of “on”, unless they’re dead. I must confess it took me an embarassingly long period of time to wrap my head around this concept.
“Haikuichthys” Oops. My bad. Haikouichthys.
amphiox:
The problem is that the signal being measured (being a stochastic signal) is a set of frequencies, in different frequency ranges – it’s being run through a set of band-pass filters, and the measured frequency in that filter is a value used. So it’s not a single transistor, but an amplification system.
But still too many neuroscientists think it’s a single digital gate — primarily because too many of them haven’t actually studied sufficient engineering to recognize what the minimal metaphor must be (it may be more complicated, but it’s no simpler than an amplification system).
Of course, if they did know engineering, most would have to throw up their hands and go into a different field – those would be the sane ones!
Of course, if they did know engineering, most would have to throw up their hands and go into a different field – those would be the sane ones!
watch it!
;)
PZ, thanks, I see that at “ambient” light levels it’s efficient to be at the midpoint of a sensitivity curve, and on vs off signalling must make no difference in terms of energy efficiency.
But what if me (a female squid) spends 90% of her time deep down and seeing almost no photons most of the time? The 10% are shrimp putting on their little red light shows, a few Finding Nemo anglerfish, and some hot male squids putting on light shows.
Now we have a non-Gaussian distribution of photons (lots of darks, with some bright spots.) Are the no/yes strategies still energy equivalent in this case?
I.e. my naive questions are:
1. is high firing activity no more energy costly than low firing activity?
2. aggregate activity is approxiamtely constant even in very low photon regimes?
#27, “This is why near-death experiences always include a bright light.”
Add that to the recent Swiss(?) study about out-of-body experiences (well, IIRC the study was about perception of self but it gave results that suggested “brain-malfunction” as a cause for OBE, there was a story about it on the bbc news site), and we get more and more scientific explanations for phenomena that are often claimed to have religious implications.
#34, Thanks PZ, with that little tidbit it makes a lot more sense to me. That seems to me (as layman) to be one of those small nuggets of information that can trigger a whole lot of understanding in many neurological issues.
@ Sili (post #28): Does any species have sight based on a haeme/chlorophyl chemical framework? Chlorophyl is plants is especially senstive to red and voilet-blue light, hence plant leaves appear green. In the paper ‘Washington, I., et al., Chlorofyll derivatives as visual pigments for super vision in the red. Photochemical & Photobiological Sciences, 2007. 6: p. 775-779’ they describe the addition of chlorophyl like substance (chlorin e6) in the eyes of mice. Mice do not have an opsin sensitive to red light, but by doing this the mice eyes responded to red light with electric signaling. Also, the rodopsin of the deep-see dragonfish has a component which is similar to chorofyl and is sensitive for long light wave (~red light) as described in this paper ‘Douglas, R. H. et al. Dragon fish see using chlorophyll, Nature 393, 423-424 (1998)’.
#27: ‘This is why near-death experiences always include a bright light.’
Is this similar to the mechanism of the hypnagogic “light-show” effect?
I assume everyone gets this? How to describe it? Blue, green and purple ‘waves’, a bit like aurora that I ‘see’ when I’m falling asleep.
What a wonderful pun. And unintended to boot! Clearly the FSM has had His Noodly Appendages in this matter.
That’s probably just the after-image of what you last saw, plus your interpretation of it. After all, you can still breathe when you close your eyes!
So when squid have near-death experiences they see darkness?
“It was the safe, comforting cave of the afterlife that was calling me, I know it!”
“…some of the more selfish among you may be wondering what this can possibly do to benefit humankind”
Everything we learn about nature goes to the benefit of humanity! But if you need any other justification, the “design” of the squid eye is one in the eye for the creationists.
As the Aussies say in greeting: “Sqideye, Mate!”
So, religous squid are told to “go towards the dark?”
Icthyic:
I’ll fess up – I’m insane, so it’s only said with the greatest loving kindness.
If you knew what power the Dark Side can give you…
@#50 David Marjanovic —
Not to mention the cookies….
So when squid evolved into vertebrates, this hopeful monster the squid couple birthed had its nervous system’s polarity switched–and this all happened by random chance?
hopeful monster
Greaser’s back, letting all know how much time he’s spent reading the trashy romance novels written by Meyers.
http://www.pandasthumb.org/pt-archives/000430.html
…and it’s WAY old, moron.
don’t bring that jive ’round here, turkey.
The similarities are uncanny… makes me wonder if Horizontal Gene Transfer is involved. Could you do a post on HGT in animals, PZ? It’d be interesting to know what role it plays in convergent evolution, if any.
Squid evolved into vertebrates??!!??!!
Huh?
Methinks someone has been watching “The Future is Wild” a tad too much for his own good.
Squid evolved into vertebrates??!!??!!
that’s the greaser, for ya.
don’t encourage it, seriously. it will just shit all over the page.
#43 JNvB,
Thank you. Unfortunately my departure in disgrace from uni has left me without journal access, but I only really wanted a general idea since I recalled how absorbent porphyrin (how embarrassing of me to forget the name …) systems are so very absorbant – as seen in plants. Very interesting, though, that such an ‘intrusive’ experiment can work – does make me wonder why Nature hasn’t employed it more.
Some plants can detect light, can’t they? I mean, they can grow towards light, etc. Are they using chlorophyll or related compounds to detect the light, or is it some other mechanism?
or is it some other mechanism
Nastic movements:
http://www.tiem.utk.edu/bioed/webmodules/nasticmovements.html
Photomorphogenesis:
http://plantsinmotion.bio.indiana.edu/plantmotion/earlygrowth/photomorph/photomorph.html
(^movies!)
http://www.public.iastate.edu/~bot.512/lectures/Photo.htm
better explanation, but no movies :(
not chlorophyll, btw, but phytochromes.
It still seems inefficient to me that both the vertebrate and cephalopod phototransduction pathways go through a whole host of second messengers just to open some ion channels, when the algae Chlamydomonas reinhardtii managed to evolve an ion channel that opens all by itself in response to light – channelrhodopsin-2.
The purpose of the cascade is AMPLIFICATION. Also, more sensitive regulation.
Still temporally inefficient if you ask me, even if it does offer amplification.
One could use the amplification scheme present in the hair cells of the ear – where the potassium influx from TRPA1 channels opens voltage-gated calcium channels. So, I’d just have voltage-gated ion channels co-located with the ChR2 on the membrane, to amplify the depolarisation caused by a single open ChR2 into a full action potential.
It occurs to me that the salt and sour taste receptors also use a similar means of amplifying a signal (in that case, Na+ or H+ influx through amiloride-sensitive sodium channels) into an action potential through voltage-gated ion channels.
I’m not sure about nociception (read, I can’t remember and it’s way too late here for me to be bothered finding out), but maybe they are the same too.
@ PZ Myers:
Food for cdesign proponentsists… :-P
Holy shit that’s cool! I’d always wondered about that, why everyone sees the same bright light. I always thought that each person would see something a little different if there really was an afterlife.
What program did you use to design the above ribbon-like 2-D structure of the rhodopsin?
Thanks a lot…