This is very cool. The TL;DR is buried in the middle of the article:
> The team found that within the structure of the interlocked molecules, the [odor receptor, one of a "family of proteins known as G-protein-coupled receptors (GPCRs)" - gumby] had trapped propionate within a small pocket. When they enlarged the pocket, the receptor lost much of its sensitivity to propionate and to another small molecule that normally activates it. The tweaked receptor preferred larger odor molecules, which confirmed that the size and chemistry of the binding pocket tunes the receptor to detect only a narrow set of molecules.
> The structural analysis also uncovered a small, flexible loop atop the receptor, which locks down like a lid over the pocket once an odor molecule binds inside it. The discovery suggests that this highly variable looping piece may contribute to our ability to detect diverse chemistry, according to Manglik.
I saw a Ted talk some years ago called “The science of smell” - and I think the jury was out on whether that speaker was really on to something or was a bit of a crack pot. It seemed legit to me!
I’d like to know if this research is consistent with, or invalidates the theories mentioned in that talk.
Even if his education is in physiology, most of his fame is due to his work as critic and historian of the perfume world, having written some best-seller books.
His scientific works have been heavily criticized though:
How does the receptor un-lock? What happens to the previously airborne molecule, now coupled to the cell with the receptor, to make that receptor open to receiving again?
Maybe a naive question, but could that help explain why your sense of smell adjusts? If there is a finite number of receptors and they require excitation to trigger the sense of smell, it stands to reason that saturation would dull the sense of smell.
Visit somewhere smelly like a farm and your sense of smell is blown away by what you would call pretty odiferous smells. Stay there a few days and the smell seems to lessen. I guess the receptors get blasé about these molecules to help you cope with your new environment. So I would go with the idea of saturation.
"olfactory sensory neurons do not express the gene that encodes the ACE2 receptor protein, which SARS-CoV-2 uses to enter human cells. Instead, ACE2 is expressed in cells that provide metabolic and structural support to olfactory sensory neurons"
So basically, the ACE2 receptor that covid attaches to is found on (among many other places) the cells that provide support to the olfactory cells that allow us to smell.
> The team found that within the structure of the interlocked molecules, the [odor receptor, one of a "family of proteins known as G-protein-coupled receptors (GPCRs)" - gumby] had trapped propionate within a small pocket. When they enlarged the pocket, the receptor lost much of its sensitivity to propionate and to another small molecule that normally activates it. The tweaked receptor preferred larger odor molecules, which confirmed that the size and chemistry of the binding pocket tunes the receptor to detect only a narrow set of molecules.
> The structural analysis also uncovered a small, flexible loop atop the receptor, which locks down like a lid over the pocket once an odor molecule binds inside it. The discovery suggests that this highly variable looping piece may contribute to our ability to detect diverse chemistry, according to Manglik.