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Study provides insight into cellular defenses against genetic mutation

stop codon is labeled premature when it occurs more than 55 nucleotides upstream (toward the 5-prime end) of an exon-exon junction.

If these spatial requirements are met, CBP80 interacts with human up-frameshift proteins, factors that come together at exon-exon junction complexes to drive NMD review. The three up-frameshift proteins work together to trigger decay once an early nonsense codon is detected, most likely by recruiting enzymes that remove the tail and cap from suspect mRNAs and digest their chains. If nonsense codons are not detected, CBP80 and its partner CBP20 are replaced by another cap-binding protein that renders mRNA immune to further notice by NMD.

"NMD is an elegant process that offers a number of targets for future medical therapies," Maquat said. "Beyond its role in screening out faulty mRNAs through immediate decay, we have also learned that the NMD factor Upf1 is part of a related process that regulates the expression of many normal genes by controlling the timeframe in which their encoded mRNAs decay. Evolution often borrows a useful mechanism from one process and puts it to work in another."


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Source:University of Rochester Medical Center


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