Starting a lingustic foray into evolution - cray cray?

This holiday season, I've learned a new word from my nephews, and that word is 'cray-cray'*. According to my nephews, and the Urban Dictionary, cray-cray means 'really crazy'.

Researching this word has led me - yet again - to some parallels between evolution and linguistics. I want to start documenting these parallels more formally, because I think it could be important. My biology research is focused on how new traits originate during evolution, sometimes called 'evolutionary novelty'. How did eyes originate in evolution? How about hair or milk? Although I could be cray-cray, I believe this area of evolution has received less attention than other areas, and the theory and concepts are underdeveloped. Yet in linguistics, it seems novelty is a central area of theory.

Cray-cray is a new word, a novelty. Languages change so fast, with such full documentation, it seems as though linguists have a richer theory for explaining how novelties arise. One aspect of novelty in linguistics is called Word Formation, and there are several ways in which word formation occurs. I believe many of these have parallels in organic evolution, although they may not generally be differentiated or articulated. I want to explore that on future posts.

Craycray seems to be due to a particular type of word formation that is not particularly common in English, called reduplication. Actually, as I read and understand further, it seems reduplication is considered to be a change in grammar, and not as a mechanism of word formation. From this perspective, cray cray is not a new word, but is rather a grammatical change to convey a new meaning. In both evolution and linguistics, it seems challenging to think clearly and consistently about structure (word) and function (meaning) and their relationship to each other.

Reduplication is quite common in many languages, and is used in several different ways. Our cray cray example seems to be reduplication for the purpose of intensifying a noun. I don't think this is common in English. Wikipedia gives an example from Hebrew, where Gever means 'man' and 'Gever Gever' seems to mean something like a man's man or a manly man, or perhaps a macho man. A man, intensified, just as cray cray means crazy, intensified.

According to the same Wikipedia site on reduplication, there are some English examples of reduplication. We mimic baby talk, as in 'bye-bye'; use rhyming reduplication, as in super-duper; or sometimes change the vowel sounds in the reduplication, like zig-zag. An interesting example is the 'schm' reduplication - adding 'schm' to belittle something, or to indicate irony: 'craycray, schmacray - I can just say lunatic'. Schm-reduplication is said to be 'productive', because it can be used with most any word. We also use reduplication to clarify a literal meaning versus a figurative meaning. An example that comes to mind is to clarify hot - 'do you mean spicy-hot or HOT-hot'?  HOT-hot is clarifying the meaning as temperature. By the way, I think we should adopt the Spanish word picante to mean spicy-hot, a word we need in English!

Besides cray cray, I can't think of any other examples in English of intensifying reduplication. From that perspective, it might not actually be reduplication, since reduplication refers to grammar. In English, our grammar doesn't usually intensify using reduplication, so cray cray perhaps really does fit more into Word Formation. But I also cannot fit it into established modes of Word Formation, either, such as those explained on Wikipedia or a Rice site (by the way the Rice site counted zig-zag as compound word formation, not as reduplication). Instead, cray cray is part clipping - taking just part of a longer word, like ad for advertisement, or dis for disrespect - and part compounding - putting two words together, like phone booth. Crazy clipped is cray and compounded is cray cray.

My purpose here is to understand novelty in linguistics to draw parallels to evolution. For example, thinking genetically, I know that protein domains are often 'reduplicated' within the same gene. It will be interesting to think this through and research it. What types of function can protein domain reduplication provide? Are the biological-functional implications similar to linguistic-grammatical implications? I believe intensification of biological function does happen by domain reduplication (I can think of some examples, that I won't go into). But what about other parallels? That will perhaps be the subject of a future post.

I should end now before this post is so long as to be cray cray.






* I believe this is mainly a spoken word, such that the spelling is not yet standard. It could be craycray, cray-cray, or cray cray. 

Evolutionary Novelty: Get Milk?

The "Got Milk?" slogan has to be one of the most often mimicked ads of all time.  I did a quick search, and found the figure above, apparently compiled by the milk folks themselves.

So, how did animals "Get Milk" in the first place?  In other words, how did this novelty originate during evolution?

A new paper published by Lemay et al in Genome Biology has taken advantage of the recently completed genome sequence of the bovine, Bos taurus, and has begun to address this very question.

Although I am not a mammalian biologist (meaning I don't study mammals, despite being one myself), this is the third mammalian novelty I have highlighted here (see also placenta and hair).  Mammalian genome biology is ahead of other animal groups, for obvious reasons.  All my mammalian novelty posts tell a common story: the building blocks of complex biological features pre-date the origin of the integrated traits themselves.  What I wrote for hair, can also apply to milk and mammary glands:

"Just ten years ago, results ... clarifying the molecular components of trait evolution were rare, but they have become common now that genome sequences are available for many species. Before we had some idea of gene function, and before genome sequencing, scientists could only examine one level of biological organization – the trait (hair [milk] in this case). And that could only get science so far. In the case of hair [milk], it mainly got science as far as Figure 1, which leads to the inference that hair [milk] evolved a bit before the common ancestor of living mammals. But “hair [milk]” is not one thing. It is a complex of building blocks, including structural genes (like [casein]) and developmental processes. Today, scientists can decompose a trait, like hair [milk], into its components and study the evolutionary history of each part separately, tracing the parts through various genomes."

Figure 1 is here, again, replace hair with "milk".

I learned many amazing things about the genomics of milk and mammary glands from the Lamay et al paper.

• Some 6000 genes are considered "mammary related" and are found on all the bovine chromosomes.  There are 197 unique milk protein genes!
• Compared to non-mammary genes, mammary genes are more commonly present in all mammal genomes studied.  This indicates that mammary genes are evolving more slowly and may be lost less often than other genes.  This could indicate purifying selection owing to the importance of lactation for mammalian life history.
• Milk does vary a lot among species - some babies need more fat or a bigger immunity boost, depending on the lifestyle of the species.  Variation tends to be caused by variation in number of gene duplicates, but not in the sequence of the milk proteins themselves.  One explanation for milk variation could be the levels of expression of different genes (regulatory variation).
• Mammary genes are found together in the genome.  Also milk proteins are found along with mammary genes in the genome.  This could indicate that these clusters are expressed/regulated together as groups.
• The genes expressed in milk fat globule secretion have similarity with other secretory organs.

This final result suggests that mammary glands might be considered "duplicates" (paralogs in molecular evolution parlance) of other secretory organs.  It reminds us that traits do not come from nothing.  Some designer did not shoot a lightening bolt into the first mammal, imparting it with mammary glands and milk. Furthermore, natural selection did not modify lactation genes to perfection, thereby erasing their history.  These traits, like all other traits, evolved from existing building blocks, duplicating and recombining them to form something new.  The evidence for common descent is strong and it is deep.  

As the authors wrote about lactation:

"the ontogeny of the mammary gland [may have] occurred by co-opting existing structures and developmental pathways.  Lactation may be less than 200 million years old, but its biological roots are far more ancient."

Reference
Lemay, D., Lynn, D., Martin, W., Neville, M., Casey, T., Rincon, G., Kriventseva, E., Barris, W., Hinrichs, A., Molenaar, A., Pollard, K., Maqbool, N., Singh, K., Murney, R., Zdobnov, E., Tellam, R., Medrano, J., German, J., & Rijnkels, M. (2009). The bovine lactation genome: insights into the evolution of mammalian milk Genome Biology, 10 (4) DOI: 10.1186/gb-2009-10-4-r43

Evolutionary Novelties: Faves of 08

As 2008 winds down, I thought I would look back at Evolutionary Novelties and pick some of my favorite posts of the year.


The major theme of this blog is to explore how it's possible that all life has a common origin and still has diversified into the riotous diversity/complexity/disparity that we see today. New features evolve through duplication and recombination (at all levels of biological organization).

1. Box Jellies and the Red Herring of Eye Evolution is one of my favorite posts. The main thesis is that people always ask an inappropriate question "how many times did eyes evolve?". I'd thought about this idea for quite a while, and when a paper came out in PNAS that re-inforced my thesis, I incorporated the new research into the idea.

2. Coming to grips with common descent discusses the idea that during the history of evolution, people have tended to forget that everything evolves from something else. This was not conceived as a blog post, but as a chapter of a book I've toyed around with writing. In some ways, blogging satisfies my urge to write a book, so the book probably won't happen for a long time.

3. Gould: Pluralism by Monism My thesis that Gould was practicing pluralism by taking an opposing stance to the whole field of evolutionary biology. This is perhaps my favorite post of 2008 because I've never seen anyone else with this idea, and the more I think about it the more I think it explains a lot, a general theory of Gould, if you will.


The above are posts that present an idea I've had. I've also recently been writing a few posts on others' research. I find that writing about the work helps me internalize and understand the work. I'm not a rocket-science journalist, but some of the posts have been okay, I think:

4. Evolutionary Novelty: Photosynthetic Slug

5. Evolutionary Novelty: Hair


I also have a series of posts about ostracods, my ostrablogs. I haven't had time to do these for a while, but I do have one half written, so more are coming. My favorites are probably:

6. Ostrablog 5 - Three shows and a funeral retells a story that I've told many, many times in person.

7. Ostrablog 3 - How we discovered chupacabra tells about our discovery of a new ostracod species.

8. Ostra-blog 2 - to e or not to e Ostracod or ostracode?


But much of what I do is promotion of my research and papers, or posting drafts of things I'm writing:

9. Phylogeny, evolution, biodiversity and ecology discusses some research recently published in PNAS. I also noticed this was featured at NESCENT.

10. Opsins: An amazing evolutionary convergence. Slightly expanded from part of an encyclopedia article I was asked to write.



Those are 10 of my favorites from this year. Happy New Year!!

How Complexity Evolves

[Slightly altered excerpt from an invited review on the evolution of (nervous system) complexity]

The evolution of complexity is an enduring and fundamental topic in biology. Recent research is allowing new insights into the origins of complexity. Namely, scientists now have access to the components of complex structures, and their evolutionary histories. "The eye" is no longer an anonymous collection of components - Darwin may have known an eye is composed of lens retina and nerve - but he did not know what lenses or retinas were composed of, nor did he know in much detail how they functioned. We now know many of the protein components of structures like eyes and how they function, and we know that these components have evolutionary histories. Since biological entities from genes to ecosystems arise from existing entities, general patterns emerge as to where those entities came from. They either duplicate/diverge; split/diverge; or fuse in new combinations.


What is biological complexity?
Numerous definitions have been suggested for biological complexity, from mathematical and information theoretic formulas [2,3] to intuitive definitions, such as the numbers of parts or components that can be counted in a system [4,5]. In practice, a researcher’s choice of definition for complexity often boils down to his ability to measure it. In investigator-defined computer simulations [2] or circumscribed biological systems [3], information theoretic definitions using explicit mathematical formulas are tractable. However, in extensive biological systems, especially those that encompass multiple levels of biological organization with varied properties, the relationship between structure and function (e.g. genotype and phenotype) is often largely unknown, and may itself be complicated and variable. These unknowns complicate the formulation of explicit, yet general, mathematical definitions of complexity for extensive biological systems. Instead, some have argued that counting the numbers of parts of a system is an appropriate measure of complexity [4]. Although often focused on structural units, such as cell types, genes, or species, and not on the functions of those units, McShea [5] has also argued that counting structural parts should often be a good estimate of functional complexity.
Herein, we follow previous authors [4,5] and define more complex systems as those that have more parts. “Part” is used as a term that spans levels of biological organization [4]. Species are parts of ecological communities. Organs (like brains or ganglia) are parts of species. Cell types (like neuronal types) are parts of organs and of species. Proteins are parts of cells and of networks, and domains and amino acids are parts of proteins. Many other biological units are also parts [6]. For the current discussion, we are concerned less with defining or counting parts, and concerned more with how new parts originate during evolution. According to the definition of complexity that we employ, new parts (that do not come at the expense of existing parts) increase biological complexity. Therefore, those mechanisms that cause the evolution of new parts are of particular interest because those are the mechanisms that cause increases in biology complexity.

"those mechanisms that cause the evolution of new parts are of particular interest because those are the mechanisms that cause increases in biology complexity."

General patterns of increased complexity
By definition, complex systems have many parts, and the histories of those parts are varied. As such, we cannot expect a simple, one dimensional answer to the question of how complexity evolved. Nevertheless, at all levels of biological organization, conceptually similar patterns (Figure 1) have resulted from a varied array of mechanisms that historically increased complexity.



Figure 1 - Generalized patterns of increased biological complexity. The top of the figure represents an ancestral state, the bottom a descendant state. Shapes represent “parts”, a generic term for a biological feature at any level of organization. Parts can be species, genes, protein domains, pathways, brain regions, and many other biological units [see 6]. A. Copying and divergence B. Fission and divergence C. Copying and fusion. Without copying or fission, complexity does not increase because divergence (or fusion) maintains the same number of parts. Without differential divergence or fusion of parts, complexity only increases marginally.



First, parts may exhibit a pattern consistent with differential divergence of copied elements (Fig. 1a). A prime example of a specific mechanism leading to this pattern is gene duplication plus divergence. Duplicated genes are initially identical, and they gradually diverge over time, increasing genomic complexity. Second, parts may exhibit a pattern consistent with differential divergence of split elements (Fig. 1b). Here, a prime example is speciation, where populations of individual organisms, originally all of the same species, split into multiple populations that diverge to the point of becoming separate species. Splitting (fission) can also occur in an asymmetric fashion (Fig 1c), generating two uncoupled parts that together would sum to one ancestral part. Third, parts may exhibit a pattern consistent with fusion of copied parts (Fig. 1d). For example, copied protein domains often join together to generate a new gene. Another example of fusion is expression of genes in new combinations, a process termed co-option [reviewed in 7]. A primary goal of this paper is to review cases in nervous system evolution that provide specific and more detailed mechanisms that account for these patterns at different levels of biological organization.


The patterns in figure 1 are produce by a number of different mechanisms, including gene duplication, alternative splicing, retrotransposition, co-option, etc.

[The specific mechanisms leading to the general patterns is the topic of the rest of the paper from which this excerpt is taken].



References Cited
1. Striedter GF: Principles of Brain Evolution. Sunderland, MA: Sinauer; 2005.

2. Adami C, Ofria C, Collier TC: Evolution of biological complexity. Proceedings of the National Academy of Sciences of the United States of America 2000, 97:4463-4468.
3. Adamowicz SJ, Purvis A, Wills MA: Increasing morphological complexity in multiple parallel lineages of the Crustacea. Proceedings of the National Academy of Sciences of the United States of America 2008, 105:4786-4791.
4. Bonner JT: The Evolution of Complexity. Princeton: Princeton University Press; 1988.
5. McShea DW: Functional complexity in organisms: Parts as proxies. Biology & Philosophy 2000, 15:641-668.
6. McShea DW, Venit EP: What is a part? In The Character Concept in Evolutionary Biology. Edited by Wagner GP: Academic Press; 2001:259-284.
7. True JR, Carroll SB: Gene co-option in physiological and morphological evolution. Annual Review of Cell and Developmental Biology 2002, 18:53-80.

Evolutionary novelty: Photosynthetic slug

All of biology, from genes to species, is united by common descent. Therefore new biological entities – novelties – must come from the modification of existing entities. Lightening does not strike and impart new features into organisms; new features evolve from existing ones. New research in PNAS provides fascinating new insights into the evolutionary origin of a 'photosynthetic slug'.




Given new features evolve from existing ones, one way novelties originate is through duplication and divergence. Another way is through new combinations of existing biological entities. In fact, biological entities can be recombined at many levels. Protein domains fuse to form new genes, genes become expressed together in new combinations in developmental time or space, even species can merge together to form new species, as occurred at the origin of eukaryotic cells when one species merged with a bacteria that became our cells’ energy factories, the mitochondria.

Imagine if evolution happened to produce a photosynthetic animal, and ask, what are some of the ways it might happen? One likely way is to utilize existing organisms (or their genes) that already have the ability to convert light energy into chemical energy. This is exactly what has happened during the evolution of the gastropod mollusk Elysia chlorotica, a green “sea slug”. Like other types of animal including reef-building corals, E. chlorotica harbors the photosynthetic machinery of other organisms. In the case of reef corals, a symbiotic relationship with dinoflagellates provides photosynthetic ability. But in the green sea slug, only the photosynthetic machinery itself is sequestered, by ingesting an algae, and using the algae’s plastids, the photosynthetic sub-cellular structure of the algae (interestingly, the plastid joined the algal cell in an ancient novel merger of species).


This presents a puzzle. The algae’s plastid, which is being used by the green sea slug for photosynthesis, does not itself contain all of the machinery required for photosynthesis. Instead, many of the photosynthesis genes reside in the algae, only some reside in the plastid. Yet the green sea slug can photosynthesize for months using only the plastid, even in the absence of algae, and therefore in the absence of the algae’s photosynthesis machinery. How is this possible?


The authors found that at least one gene (psbO) is integrated into the genome of the green sea slug. This gene is identical in sequence to an algal gene, yet the sequence adjacent to the gene in the slug analyses make clear that the gene is in the slug’s genome and not an experimental artifact, like contamination.


As the authors indicate, this work raises many interesting questions. How does the slug’s gene target the plastids? What about all the other genes absent from the plastid that are required for photosynthesis – are those transferred to the slug, too? Or could some of the slug’s genes replace the function of the missing genes? What is the specific mechanism for horizontal transfer of genes from one species to another? Clearly, the authors are thinking about these interesting questions, and likely future research will provide us with answers.


I noticed that Carl Zimmer already posted on this article in his fine blog, The Loom


Self-promotion*

As I wrote in an article with Michael Rose called “The New Biology: Beyond the Modern Synthesis”, acceptance of biological mergers was slow, perhaps because the modern synthesis viewed genomes as sleekly functional, finely tuned to current utility. As such, moving genes from one genome to another seems like it should be suboptimal, and therefore rare. No one doubts the importance of biological mergers any more, but they are still fascinating and under-documented, in part because they were neglected for so long.


*One reason I write blog entries is to present my research interests and ideas to a potentially broader audience. As such, I like to like papers of mine when possible.











M. E. Rumpho, J. M. Worful, J. Lee, K. Kannan, M. S. Tyler, D. Bhattacharya, A. Moustafa, J. R. Manhart (2008). From the Cover: Horizontal gene transfer of the algal nuclear gene psbO to the photosynthetic sea slug Elysia chlorotica Proceedings of the National Academy of Sciences, 105 (46), 17867-17871 DOI: 10.1073/pnas.0804968105

Evolutionary origin of a light sensitive nerve

The origin of a light sensitive nerve was almost certainly an early step in the evolution of animal eyes, and this was thought to have happened only once, some 600 million years ago. But new open access research on the nematode C. elegans indicates a heretofore unknown instance where a nerve evolved light sensitivity.

One of the common, but incorrect, claims of anti-evolutionists is that the origin of complex features like eyes cannot be explained by evolutionary biology. As an example (although perhaps not written by an anti-evolutionist) see the comment on this post. For some history and a response to the incorrect anti-evolutionists claim, see this post.

It turns out that, as is often the case, the difficulty in understanding comes from trying to make a continuum into a dichotomy. An eye or even the genetic machinery for light sensitivity doesn't have to be all there or all not there. Instead, these features can build up gradually, by classical Darwinian evolution.

An early step in the evolution of complex eyes was almost certainly the origin of a light sensitive nerve. Darwin imagined that nerves might easily become light sensitive, but because of a lack of understanding of the molecular basis of photoreception, not to mention the molecular mechanisms of heredity, he could not even fathom a guess as to how nerves came to see the light. But just because Darwin didn't know how the machinery of light sensitivity could be built gradually by evolution doesn't mean it couldn't occur gradually.

Light sensitivity is a multi-step genetic process, where one protein signals to another. But all those proteins were not "turned on" all at once to suddenly allow for light sensitivity. Instead, light sensitivity evolved from existing "senses". Many signals are detected outside of a cell and they trigger proteins to send a signal inside a cell. Even yeast use proteins to sense pheromones outside their single cell and direct growth toward a potential mating partner. Many of these signaling genes are shared across all of our senses, and we can pinpoint by comparative study when a signaling gene became a light sensitive protein called opsin (again see this).

This brings us to the worm research. C. elegans has no visible eyes and its genome lacks light sensitive opsin genes. Yet it does display sensitivity to UV light!

Here is a link to a video showing light sensitivity.

How does it do this without opsin? It turns out that a different protein has become light sensitive. In this case, homologous proteins are known to be taste receptors (Gustatory receptors) in insects. Therefore, at some point in evolutionary history, the worm protein
gained light sensitivity, independently of the opsin "light switch"!

This is really fantastic work that suggests many new lines of research. For example, the mechanism of photoreception is unknown for the worm gustatory/light receptor. If this could be understood, we could get a specific idea about how a protein gained light sensitivity during evolution. Second, it is not known when light sensitivity was gained, which would require comparative study. These genes are present in insects - are the insect genes light sensitive? It would be great fun to put an insect gene in a worm to see if it could rescue the loss of light sensitivity due to a mutation.

Finally, I'll point out that this work is similar to another study published just last month . That workfocused not on the receptor, but on genes later in the cascade; especially on the gene responsible for "firing" (ie changing the concentration of the ions in) the light sensitive nerve. It turns out that that the "firing" gene is homologous to the "firing" gene used in vertebrate rod and cone cells - another example of how evolution often uses similar tools to produce parallel results.

Evolutionary Origins of Phototransduction

Below is a section of an article I am drafting on eye evolution. Does it make sense? Any parts impossible to understand? Comments are welcomed!



In The Origin of Species, Darwin hypothesized that the first step in the evolution of eyes involved the gain of photosensitivity in a nerve, writing, “…I may remark that several facts make me suspect that any sensitive nerve may be rendered sensitive to light…” Here, Darwin was making the assumption that variation leading to light sensitivity of previously non-light-sensitive nerves was abundant, and that natural selection could then act on that variation. But how did those specific variations originate? How does a nerve become light sensitive? In his notebook, Darwin suggested that it might be impossible to understand how a nerve gained light sensitivity. He wrote “to show how the first eye is formed, — how one nerve becomes sensitive to light, ...is impossible.” Since the mechanisms of heredity and the molecular mechanisms of photoreception were unknown in Darwin’s time, no specific hypothesis could even be posed about the genesis of light perception. One hundred and fifty years later, things have changed.


Today, through an understanding of the distinct evolutionary histories of the components of vision, and more specifically of phototransduction (the signaling pathway that turns light into a nerve signal), we can now pose a specific historical hypothesis for their origin: Phototransduction originated within animals by modifying an existing signaling pathway. More specifically, at some time before the divergence of jellyfish and humans, but likely after the split common ancestor of sponges and humans, the first light sensitive animal opsin protein originated. This protein did not originate from nothing, nor was it newly breathed into an ancient animal genome by a designer. Instead, opsins arose by mutation of an existing receptor to render it light sensitive. This historical hypothesis makes numerous predictions, and available data are consistent with the hypothesis. It also makes predictions that have not yet been tested, indicating promising areas for future research.






If the hypothesis that phototransduction arose within animals is valid, then some components of phototransduction should exist within animals, but should not exist (or should possess a different function) outside of animals. Such is the case for opsin, which is present as the primary photopigment gene in most animals. Recent research shows that various cnidarians, including a hydra, a sea anemone, a hydrozoan, and a box jellyfish, possess opsins (Plachetzki et al, 2007; Suga et al, 2008; Kozmik et al, 2008). At the same time, opsins are absent from sponges and non-animals (See Figure). In science, demonstrating the absence of something like a gene is difficult, because a skeptic can always invent a reason why the target was accidentally missed. In the case the opsins in question, scientists have determined the entire genome sequence of the sponge Amphimedon queenslandica, the choanoflagellate Monosiga and numerous fungi, making the presence of opsin in those organisms very unlikely. Some proteins of near-animals are in fact rather similar to opsins, but in every case the non-animal receptors lack characteristics that specifically define opsins. Therefore, although opsins might have been present at the origin of animals and lost in sponges, their absence instead strongly suggests that they originated within animals, before the split common ancestor of humans, insects, and cnidarians, all of which possess opsins.


With current knowledge that opsin is the basis of light sensitivity, Darwin’s question of how a nerve becomes light sensitive can be rephrased as, “how did animal opsins originate”? Proteins rarely originate from nowhere, and opsins are no exception. Opsins form a subfamily within a larger family of proteins called G-protein coupled receptors (GPCRs), also sometimes called serpentine proteins because they snake back and forth across cell membranes. Since serpentine proteins are present in all animals and their close relatives - including sponges, Monsiga, and fungi - this broad class of proteins long predates animals. In yeast (a fungus), these receptors are sensitive to pheromones and they even direct a signal through proteins homologous to non-opsin phototransduction proteins. As such, a signaling pathway exists outside animals, which is very similar to phototransduction, except the receptor protein detects pheromones, not light. Receptors outside animals share some characteristics with opsin, like snaking through a cell membrane seven times. It is one of these serpentine proteins that served as the progenitor of the first opsin protein, as evidenced by the similarity of opsins and other serpentine proteins.


Darwin’s question can be refined farther, to “how did a serpentine protein gain the ability to respond to light?” And since opsin’s light sensitivity is mediated by its ability to bind a light reactive chemical, called a chromophore, the question can be even further refined to ask how a GPCR must be modified to bind a chromophore. In the case of opsin, we know that a particular amino acid – a Lysine in the 7th membrane-spanning region – binds to the light reactive chemical. Presumably then, a mutation changing an amino acid in the 7th trans-membrane region of a light insensitive GPCR was involved in the acquisition of light sensitivity in animals. This fateful mutation coupled with numerous other mutations, are responsible for the origins of eyes and vision. Although science has not yet tracked down every single mutation involved in the evolution of vision, the origin of opsins clearly illustrate, in richer detail than Darwin might have imagined, the natural processes that gradually allow the evolution of complex features.