In selenoproteins, in-frame TGA (STOP) codons are translationally recoded as codons for selenocysteine (SEC), with the help of special elongation factor eEFSec and SECIS elements in the 3' UTR (in eukaryotes) of the mRNA.
In eukaryotes the nonsense-mediated mRNA decay has evolved to detect in-frame STOP codons that may arise from aberrant mRNA splicing, and rapidly degrade the mRNA. This is performed by a first round of translation where a ribosome scans the mRNA and strips off all the Exon Junction Complexes at the sites of splicing. If there are no mistakes the messenger is translated to a full-sized protein. If there is an in-frame sSTOP the ribosome stalls and it recruits the machinedry for mRNA degradation.
Does anyone know if there are studies on how the presence of an in-frame codon for Sec, which is the same as a STOP codon, in the mRNA for a selenoprotein impacts on the mechanism of nonsense-mediated mRNA decay? Is it possible that some messenger for selenoprotein is at least in part degraded because it is recognized as containing a nonsense mutation?
Article Nonsense-mediated decay factors are involved in the regulati...
...Yes? It looks like this is a fairly active field of research, to be honest. You'll probably have better searching pubmed than asking here.
Article Selenocysteine incorporation: A trump card in the game of mRNA decay
I can come up with this 2015 review but there will be more, I guess. Hope this helps.
Sorry, John Hildyard, if you took the time for an answer like yours you could have helped out a colleague in the same time as well. Have a nice day.
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