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Biology is built on the assumption that the most fit organisms survive and past on their successful adaptations to future generations.  But adaptationism isn’t the whole story.  There are many examples of inheritable traits that persist without conferring any success to the organism.  Non-adaptationist thinking is important because it offers a nuanced understanding of evolution.  It can also explain traits we see in some organisms that can’t be explained by adaptations.  Some adaptations are vestiges of an earlier time when the trait would have been essential to that organism’s continued survival.  When conditions changed, the trait was no longer essential, but nor was it detrimental.  Far from refuting the theory of evolution by natural selection, evidence of non-adaptationism strongly vindicates the power of mutation, migration, and genetic drift to drive evolution.

Some traits are just a chance product of random mutation and while they don’t confer any selective advantage, they don’t appear to hinder an organism’s survival either.  These traits just happen to have persisted onto the present because earlier lineages never got rid of them and it propagated onward into the present purely by serendipity.  There was no clear advantage in keeping that trait around but there was no strong selection against individuals with it.  These random mutations can help scientists track the evolutionary history of a clade this these mutations are so unique to a species; any groups with that trait can almost certainly be traced to a lineage with a common ancestor.  These traits are called parochial traits because they are isolated within a one very specific lineage and haven’t popped up anywhere else.  (See convergent evolution…)  The color of red blood cells are an example of a non-adapationist trait.  Hemoglobin happens to turn red when it binds to oxygen.  The color red isn’t the trait that’s being strongly selected for in blood; it’s the ability to carry oxygen that determines how fit an organism is.  Red is merely correlative to the ability to hold oxygen.  The redder blood is, the more oxygen is binding to hemoglobin in the blood, and the more efficient respiration is in that organism.

Notothenioidei heart

As the result of genetic drift, mutations in an organism’s genome can accumulate over time.  Some genetic variation present in populations does not affect fitness one way or another, but it can be used as a marker to track the evolution of populations.  If a parochial trait gets passed on to future lineages, biologists can track its history based on fossil records and DNA evidence.  In Sean Carroll’s The Making of the Fittest, Carroll highlights a prime example of non-adaptationist thinking; the bloodless icefish of the Antarctic.  Members of the suborder Notothenioidei have transparent blood, almost entirely devoid of the red blood cells that make up 40% of the volume of human blood.    The graphic below shows that the myoglobin protein that makes heart muscle red is missing in some clades of icefish, too.  Curiously, this gene seems to have been deleted or deactivated four times in the fossil record.  Each mutation provides exactly the same effect; no myoglobin.  Where the mutation responsible for deactivating the gene that codes for Mb protein mutated doesn’t make any difference.  There is no advantage to the gene breaking in any one spot over any other.  What matters is that because this common gene to the different icefish families mutated on different occasions, we can start a family tree for the icefish by organizing each species based on whether or not they have myoglobin and if not, which mutation caused that gene to deactivate.  Notothenioidei isn’t the only clade with antifreeze glycoproteins, or AFGPs.  Eelpouts are another Antarctic fish that make use of AFGPs.  But eelpouts are separated from icefish by millions of years of evolution.  They utilize a completely different antifreeze protein to keep their blood flowing and research suggests that the eelpout’s antifreeze proteins come from a mutated sialic acid synthase gene.  Scientists are able to track the evolution of traits using molecular and genetic testing techniques in order to come up with a phylogenetic tree.

Let’s return to our example of icefish.  Exaptations are mutations that are later co-opted for a different use than how the adaptation was initially being used.  Carroll reveals that in extreme cold environments, red blood cells are a hindrance, making the more viscous blood rich in erythrocytes harder to pump.  And apparently under such frigid conditions, seawater has a much higher capacity to hold unto dissolved oxygen and the icefish can take in the oxygen directly through their plasma without the need for the hemoglobin molecule that performs that function at room temperature in red-blooded organisms.  These icefish thrive in extreme cold temperatures because their genes for the production of red blood cells were jettisoned.  Normally, if the genes responsible for the production of red blood cells mutate even by one base pair, just about any random mutation would spell disaster for the organism.  But because red blood cells aren’t as important in antarctic water (and can even be deleterious!), mutations in the genes that code for the production of red blood cells aren’t so deleterious for the icefish, and mutations can pile up until those genes are riddles with errors.

Red blood cells not only transport oxygen through the circulatory system, they also also to suppress the freezing point of blood.  If blood were just plasma, it would freeze around zero degrees Celsius and doom the organism.  Icefish have maneuvered their way around this with a curious re-purposing of an already-established adaptation.  Originally utilized to break down food in the intestines, an extra copy of a pancreatic trypsinogen gene could also serve the icefish by producing a glycoprotein in the gut that prevents ice crystals from forming in water at or below its freezing point.  Even more curiously, icefish further benefited from the extra digestive enzyme gene that manufactured antifreeze in their gut when that glycoprotein ended up in the blood by first travelling through the liver, which ultimately keeps their translucent blood from freezing over.