Given that the membrane proteins TRPV2 and TRPM8 are used as sensors to detect “hot” and “cold,” respectively, would it be plausible that for such sensations to have been front-loaded? After all, both sensors are highly conserved in all vertebrates.
Inspector Bunny decided to take a quick look and use the mouse sequence for these proteins to BLAST away.
When the mouse sequence of TRPV2 was used to BLAST, the “vanilloid receptor-related osmotically activated chain” from Ostreococcus tauri was retrieved. It shows 44% positions with identical or very similar amino acids and had a E value of 3e-30.
Since TRPV2 is the capsaicin receptor, and capsaicin is a vanilloid, it looks like we have a genuine homolog for detecting those chili peppers.
So what is Ostreococcus tauri? It only happens to be a single-celled green algae and the smallest known free-living eukaryote.
But what about that minty, cool sensation? When the mouse sequence for TRPM8 was used to BLAST, I retrieved a significant hit from Monosiga brevicollis annotated as a hypothetical protein. It shows 43% positions with identical or very similar amino acids and had a E value of 1e-72. And you know what Monosiga is, right?
So the “hot” and “cool” sensors are both found in unicellular organisms (and AFAIK, no one else has yet to notice this). Yet the sensors don’t seem to be found in the same extant unicellular genome (thus far). Oh, and it gets more interesting when you realize the “hot” sensors may also function as pain receptors:
Annu Rev Neurosci. 2001;24:487-517.
The vanilloid receptor: a molecular gateway to the pain pathway.
Caterina MJ, Julius D.
The detection of painful stimuli occurs primarily at the peripheral terminals of specialized sensory neurons called nociceptors. These small-diameter neurons transduce signals of a chemical, mechanical, or thermal nature into action potentials and transmit this information to the central nervous system, ultimately eliciting a perception of pain or discomfort. Little is known about the proteins that detect noxious stimuli, especially those of a physical nature. Here we review recent advances in the molecular characterization of the capsaicin (vanilloid) receptor, an excitatory ion channel expressed by nociceptors, which contributes to the detection and integration of pain-producing chemical and thermal stimuli. The analysis of vanilloid receptor gene knockout mice confirms the involvement of this channel in pain sensation, as well as in hypersensitivity to noxious stimuli following tissue injury. At the same time, these studies demonstrate the existence of redundant mechanisms for the sensation of heat-evoked pain.
It would be interesting to see if the choanoflagellate or green algae protein was capable of functionally substituting for their mouse homologs.
In the meantime, it looks like we can make a reasonable case that the sensors for “hot,” “cold,” and “pain” were front-loaded into single-celled life forms hundreds of millions of years prior to the appearance of any nervous system. And given that so much of the machinery used to build a nervous system long predates nervous systems, (see The Neurotransmitter Toolkit, Front-loading and the Nervous System, ‘Fight or Flight’ Might be Ancient, The Calcium Toolkit), Inspector Bunny would like to know why we are supposed to believe that the appearance of the nervous system was just a fortuitous accident.