Insulin and Hydra
by MikeGene
Hydra vulgaris is a member of the phylum Cnidaria. It appears to be a relatively simple animal and has a small number of cell types (you can read more about its basic biology here). Yet, as we have seen, it turns out that cnidarians actually possess a rather complex genetic tool kit.
We have also seen that receptor tyrosine kinases (RTK) would play important roles in facilitating the evolution of multicellular life. Added to this is the recent discovery that one example of an RTK, the insulin receptor, plays an important role, along with its ligand insulin, in the development of the nervous system.
So let’s begin the process of tying this together.
Could it be possible that the protein hormone insulin, that is spread throughout the body of mammals via the circulatory system, would actually play a role in the development or life of Hydra? In 1996, Steele et al. (1) identified a gene for a receptor tyrosine kinase that was very similar to the insulin receptor in mammals, called HTK7. They found that is was expressed in ectodermal cells (the cell type that can generate nervous tissue) at both ends of Hydra’s tube.
But what is most striking of all is that they found insulin, obtained from cows, had the ability to induce both DNA replication and cell division in Hydra’s ectodermal cells.
Okay, from the perspective, there is nothing all that surprising about finding insulin receptors, and responsiveness to mammalian insulin, in cnidarians. This is just another example of deep homology that is consistent with such a system being in place with the last common ancestor of all animals.
What’s more interesting this time around is that we are talking about a hormone and its receptor. Here, the function is simple – BIND. What makes this interesting is that cows and Hydra last shared a common ancestor at least 600 million years ago. This in turn means there are 1.2 billion years of evolution that separate the Hydra insulin receptor and the bovine insulin.
Each lineage would possess an independent history of mutations in the receptor followed by secondary, suppressor mutations in the ligand. Each lineage would possess an independent history of mutations in the ligand followed by secondary, suppressor mutations in the receptor. Yet despite two separate spans of co-evolution between receptor and ligand, the ligand from cows retains the ability to function with the receptor from Hydra.
All that this indicates a fairly strong selective constraint on a seemingly simply biochemical function (BIND). So where do we go from here?
1. R. E. Steele, Pauline Lieu, Ninh H. Mai, M. Andrew Shenk and Michael P. Sarras Jr. 1996. Response to insulin and the expression pattern of a gene encoding an insulin receptor homologue suggest a role for an insulin-like molecule in regulating growth and patterning in Hydra Development Genes and Evolution 206:247-259
July 12th, 2008 at 10:13 am
OK, I'll bite. Where do we go from here?
Comment by Bilbo — July 12, 2008 @ 10:13 am
July 12th, 2008 at 10:15 am
Oh, btw, I gave up on that philsophy book…boring. I'm reading The Plausibility of Life. Fascinating.
Comment by Bilbo — July 12, 2008 @ 10:15 am
July 13th, 2008 at 10:49 am
Hi Bilbo,
I have two very busy weeks coming up, so it will at least be that long before I continue. And I'll probably do it over at the book blog.
Comment by MikeGene — July 13, 2008 @ 10:49 am
July 13th, 2008 at 5:02 pm
Looks like structure and functionality was conserved over deep time. Interestingly, the structure and functionality of sliding clamps (ring-shaped proteins aka “ringmasters” of the genome e.g. PCNA) and clamp loaders (e.g. Replication factor C) are conserved across the three domains of life with very little sequence similarity.
Wonder if chaperones have anything to do with conserving the structure and functionality of selected proteins over deep time while retaining flexibility and allowing sequence variability. Future research possibility?
Also ties in nicely with the robust Universal Optimal Code that allows for variation but also buffers against the effects of mutation.
Comment by Telicmeme — July 13, 2008 @ 5:02 pm
July 15th, 2008 at 9:32 am
Howdy all,
Where can I read more about the Universal Optimal Code? I'd like to see what is out there so I can better talk with people who think it's Darwin or nothing.
As I said in another post here, I think that the design is far more complex than we give credit to the Designer. Now when comparing our best intellects vs that of the Designer, we are like slow witted and educational deprived students being taught by a great intellect that makes our combined efforts pale when placed side by side. Like a 1st grader going into a class for PhDs in math, we can see the numbers and the patterns, but we are completely unable to fathom its depth and complexity.
Now this is not a case to not look any further. It is indeed the opposite. We can study and see how the design works or was supposed to work. We will find, I think, that the entropy that affects creation is also affecting our DNA. When we start looking into design we'll see the degrading of the DNA and perhaps we'll learn how o fix genetic disorders.
Unlike some random process looking sciences, when we learn how things are designed, it'll be much easier to fix them. If you get a wrecked car into a shop, one that had never seen a car before and doesn't believe it was ever designed, then when they try to fix it, watch out. Who knows what they'll do to "fix it". Compare that with a shop that while they've never seen it, understands the concepts of design. When they get how the car was once designed, they will be able to fix it like new.
A shop that believes in some "random process" could never do as good as a job.
Comment by lcd — July 15, 2008 @ 9:32 am
July 15th, 2008 at 2:24 pm
Icd,
You could read this essay by Mike Gene:
http://idthink.net/biot/code/index.html
Or you could buy his book, The Design Matrix.
Comment by Bilbo — July 15, 2008 @ 2:24 pm