Cellular Machinery Redesigns Genes For Cold Temperature Operation

Really Cool

The central nervous system is constantly sending electronic impulses called action potentials which are propagated along nerve cells via the finely-tuned actions of various proteins that are located in the nerve cell’s membrane. First, there is a membrane protein that simultaneously pumps potassium ions into the cell and sodium ions out of the cell. This sets up a chemical gradient across the membrane. There is more potassium inside the cell than outside, and there is more sodium outside than inside. Also, there are more negatively charged ions inside the cell so there is a voltage drop (50-100 millivolt) across the membrane. In addition to the sodium-potassium pump, there are also sodium channels and potassium channels. These membrane proteins allow sodium and potassium, respectively, to pass through the membrane. They are normally closed, but when the action potential travels along the nerve cell tail, it causes the voltage-controlled sodium channels to open quickly. Sodium ions outside the cell then come streaming into the cell down the electro-chemical gradient. As a result the voltage drop is reversed and the decaying electronic impulse, which caused the sodium channels to open, is boosted as it continues on its way along the nerve cell tail. When the voltage goes from negative to positive inside the cell, the sodium channels slowly close and the potassium channels open. Hence the sodium channels are open only momentarily, and now with the potassium channels open, the potassium ions concentrated inside the cell come streaming out down their electro-chemical gradient. As a result the original voltage drop is reestablished. This process repeats itself until the impulse finally reaches the end of the nerve cell tail.

Not surprisingly this process is sensitive to conditions. Its sensitivity to temperature is mainly in the falling phase, when the original voltage drop is reestablished. This suggests that the potassium channels are more sensitive to temperature and researchers indeed discovered that extreme cold temperatures slows the closing of the potassium channels causing the action potential’s voltage profile to broaden and slowing the nerve cell’s capacity to transmit action potentials.

So how do organisms in extreme cold temperatures compensate? One might think that the potassium channels genes would be adapted, with the proper nucleotide substitutions that would lead to the proper modifications in the potassium channel protein.

But new research, examining octopus species in warm and cold regions, shows that the genetic differences are minor. As the paper explains:

On the basis of conventional natural selection, we hypothesized that the channels’ genes would have evolved mutations to help tune them to their respective environments. Surprisingly, the primary sequences encoded by the two genes were virtually identical, differing at only four positions.

So how do these cold temperature organisms adjust their potassium channels? As the paper concludes, by editing the RNA transcript, the so-called mRNA, of the gene:

the transcribed messenger RNAs are extensively edited, creating functional diversity. One editing site, which recodes an isoleucine to a valine in the channel’s pore, greatly accelerates gating kinetics by destabilizing the open state. This site is extensively edited in both Antarctic and Arctic species, but mostly unedited in tropical species

I just rearranged a sentence in this post. Imagine if I created a computer program to edit the text rather than me editing it manually? That is what these octopus species have, editing machinery to adjust the potassium channels genes automatically, after they are copied from the DNA and before they are translated into proteins. Wow.