See how they both respond, with and without light.Global Leadership Initiative on Malnutrition (GLIM)Ī Framework for Diagnosing Adult Malnutrition Publications So ya, we should get some retinal cells and some other neuron cell type, make them express these proteins and then do some testing. I dunno, could just be seeing things, but if true could point to an interaction between a structural element or gated channel such that it's motion could trigger neurons firing. I was looking at some of the immunofluorescent images and it sort of looked like the MagR proteins were near the membrane of the neurons. This way they have an innate magnetic field and can point in the direction of an applied field by their magnetic field aligning. They mention that it is ferrimagnetic, so I suspect that absorbing the light is 'suppressing' one set of electron spins in the FeS clusters. In the original paper they talk about the mechanism of how the protein complex is magnetic. Doesn't require a lot of light, but needs some. More importantly they mention that the magnetosensing only works during the day, specifically when the bird is exposed to blue or green light. In the paper they talk about the importance of light for at least the bird version of the protein complex. I'm trying to find evidence for it triggering neurons to fire. f-cos is part of AP-1 which controls gene expression amongst other things. So the HEK cell test would allow us to figure lots of things out at once how important is the light exposure, is the protein inherently magnetic, is it strong enough to yank cells around, will producing these proteins harm cells.ĭifferent paper that talks about the interaction between cryptochrome proteins, neurons, and this other protein called c-fos that's also expressed in the same areas. All of this assuming of course that light isn't needed to make the thing magnetic. If the proteins form in parcinian corpuscules or similair, the motion should cause them to fire. Cause if they do, then you could just make this into a plasmid with a neuron specfic promoter and then apply it locally with DMSO/lipofectamine to the area you want to be magnetic. That'd be a great indication that this works. The simplest test would be to just do this in hek cells and then stick a magnet next to the flask and see if the cells move. I worry that you'd have signal contamination though because the moving magnet would induce currents in the small wires potentially so I dunno. In magical wonderful land, you'd want to grow these in one of the petri dishes with the tiny wire traces printed on the surface of the dish so you can connect up some electrode and see if the neurons fire when you pass a magnet over it. I think the ideal way to test this under perfect circumstance would be in some neuron cell lines and ideally a retinal cell line. I'll need to double check to confirm that. So you'd need to provide the dcry4 since humans don't produce it, but we should have the MagR gene already. Only 1 version of cry and MagR actually come together to form the complex. Cause that's probably the most important part I need to read more to see how it hands off any signal it generates to the retinal cells to be interpreted as information. I suspect that the exposure to light induces a bit of charge movement in the complex which helps to align the spins of the feS clusters and potentially pull off some electrons to allow it to be intrinsically magnetic. Normally you need much much more material to maintain magnetism.

that whole protein has maybe 10 FeS clusters tops which is an absurdly small amount of magnetic material. I wonder if the reason this requires light exposure to work is because normally things aren't magnetic at such a small size. I think the photoreceptor aspect of this might be really important. Your secondary challenge would be to determine if the resultant data from the modified photoreceptors is even something the human brain can process in any meaningful way. My suggestion would be to try to induce the development of this complex in lab rats and go from there. From what I have read they're one of the most difficult types of progenitor cells to access, and I couldn't find anything on how often our retinal cells are replaced, if they ever are.

To induce the development of the complex in a human retina would require successful modification of the neural precursor cells that develop into the retina. I don't see how you could easily get the complex to express in blood within the body. The combination of photoreceptors (Cry) and magnetoreceptors (MagR), a complex that we define as the magnetosensor.This putative magnetoreceptor protein (MagR) forms a rod-like complex with Cry, and co-localizes with Cry in the pigeon retina.' However, 'Therefore, a magnetosensitive nanoscale biocompass would be assembled by

Glims define