Way to drop some knowledge on MHC. One question, how are MHC I and II evolutionarily related? And how did cross-presentation evolve?
Hopefully you applied to National Jewish/Univerity of Colorado. John Kappler would be lucky to have you (assuming you're interested in studying MHC).
Both the MHC class I and MHC class II pathways were duplicated and specialised into their respective functions from the early proto-MHC region. It is possible that the MHC I region was the first to become duplicated during the jawless/jawed vertebrate split. Adaptive immunity as we know it, involving specialised antigen presentation cells requiring the MHC II pathway possibly arose from another duplication event in the last common ancestor of jawed vertebrates.
I would like to study the evolutionary relationships of the MHC, but unfortunately I'm a lot more interested in farming and the infectious diseases of farmed animals. I take what I eat rather seriously and having the food we eat free of disease is of keen interest for me.
"Calnexin, which is required for the complete assembly of the final MHC complex by stablising the two heavy chain is already present in eukaryotic cells."
Aegeri, what makes you think Calnexin is required? Even where chaperone redundancy is minimized, it isn't required, as assembly is about 33-50% efficient without it. In mammalian knockout cells, lack of calnexin has absolutely no phenotype in class I biogenesis.
I take it you are reffering to Denzel et al., (2002): Early Postnatal Death and Motor Disorders in Mice Congenitally Deficient in Calnexin Expression. Molecular cell biology, 22:7398-7404.
Or alternatively
Prasad et al., (1998): Calnexin expression does not enhance the generation of MHC class I-peptide complexes. Journal of European Immunology, 28:907-913.
It's more a bit of sloppy language on my part rather than anything else 
It's current function is certainly to stablise MHC molecules, but it's certainly not the be all and end all of MHC I expression. If you delete it out the other chaperones can accomodate very well for the loss of that chaperone. Of course, the mutation is still lethal because this isn't the case for all subsystems that calnexin is involved with.
I suppose you could potentially call it a vestigial part of the pathway. Something that is there but doesn't currently critically function in MHC I expression as other chaperones can take over its role now. I think the text I've written is fine as it is, although the discussion here does clarify the issue. Anyone sufficiently curious can look at the references.
I think you have a problem admitting errors. Which is "nutty" in my opinion.
Not really I was already aware of the Denzel and Prasad papers when I wrote this. Is there some actual objection to my clarification you would like to bring up?
Uhh yeah Aegeri, calnexin is not required for assembly of MHC. In it's absence other chaperones can compensate, and when this type of redundancy is minimized, assembly still occurs (with lower efficiency). The statement is false, why you wouldn't correct it is beyond me, but hey it is your blog.
Actually the efficiency isn't really any different from what I gather, see the Prasad paper, which shows it doesn't have any effect on the amount of MHC or its ability to bind peptides as well. I don't think it's a particularly problem in the context of what I'm talking about (MHC evolution), but I will change some words around in the main body of the text 
I'm writing a Part IV on this series that focuses entirely on chaperones in the MHC pathway and where they came from incidentally. It will elucidate a lot more on calnexin and what role it played in the origin of adaptive immunity.
Incidentally Guts, you can call me Joseph and not Aegeri :p
"Actually the efficiency isn't really any different from what I gather, see the Prasad paper, which shows it doesn't have any effect on the amount of MHC or its ability to bind peptides as well."
The Prasad paper is referring to a different context which I already mention above, where calnexin has absolutely no phenotype in class I biogenesis. But where redundancy is minimized, even then it's not required, but the efficiency is reduced.
"I don't think it's a particularly problem in the context of what I'm talking about (MHC evolution), but I will change some words around in the main body of the text"
The statement that something is required when it isn't is simply false. Thats a problem. We all make mistakes sometimes. Just because I'm a pro-ID person doesn't mean you have to have an ego about being corrected. If this situation was in the reverse, I wouldn't mind mofiying my post.
"I'm writing a Part IV on this series that focuses entirely on chaperones in the MHC pathway and where they came from incidentally. It will elucidate a lot more on calnexin and what role it played in the origin of adaptive immunity."
I havn't really read your posts, I was just clicking around out of curiousity and I had read about calnexin several weeks ago, it caught me eye.
"Incidentally Guts, you can call me Joseph and not Aegeri :p"
Ahh thought you were a pseudoname.
that should be absence of calnexin
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