Spermatogenesis Studies Reveal a Distinct Nonsense-Mediated mRNA Decay (NMD) Mechanism for mRNAs with Long 3'UTRs.

Oliver Mühlemann,Mihaela Zavolan

doi:10.1371/journal.pgen.1005979

Abstract

Spermatogenesis Studies Reveal a Distinct Nonsense-Mediated mRNA Decay (NMD) Mechanism for mRNAs with Long 3'UTRs.

Highlights

The term nonsense-mediated mRNA decay (NMD) was initially coined to describe the accelerated degradation observed for mRNAs with nonsense mutations that prematurely truncate the open reading frame (ORF) [6]
The three conserved core factors (UPF1, UPF2, and UPF3) and additional metazoan-specific proteins are required for NMD in mammalian cells and, the exact molecular mechanism of NMD is not known, inefficient or aberrant translation termination seems to be a key trigger for NMD
It has been empirically found that exon–exon junctions located >50 nucleotides downstream of the termination codon often trigger NMD, which is typically the case in aberrant premature translation termination codons (PTCs)-containing transcripts, and that long 30UTRs can elicit NMD, a feature found in many of the PTC-free NMD targets [8,9,10]

Summary

Introduction

The term NMD was initially coined to describe the accelerated degradation observed for mRNAs with nonsense mutations that prematurely truncate the open reading frame (ORF) [6]. Genome-wide studies uncovered that beyond degrading aberrant mRNAs harboring premature translation termination codons (PTCs), NMD targets many “normal” mRNAs encoding apparently full-length functional proteins, suggesting a broader biological function in posttranscriptional gene regulation [5,7].

Results

Conclusion