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Updated: Jun 13, 2026

Determining Genome-wide Transcript Decay Rates in Proliferating and Quiescent Human Fibroblasts
Published on: January 2, 2018
Transcripts enriched in codons that trigger P-site tRNA-mediated mRNA decay possess stable mRNA.
Rodolfo Lopes Carneiro1, Fernando Lucas Palhano1
1Programa de Biologia Estrutural, Instituto de Bioquímica Médica Leopoldo de Meis, Universidade Federal do Rio de Janeiro, Brazil.
Human P-site tRNA-mediated decay (PTMD) selectively reduces the stability of long-lived transcripts, unlike yeast mRNA decay mechanisms. This distinct process involves specific codons and CNOT3, highlighting a novel regulatory role in gene expression.
Area of Science:
- Molecular Biology
- Genetics
- Gene Regulation
Background:
- Synonymous codon usage impacts mRNA stability and decay in yeast via the CCR4-NOT complex.
- Codon-mediated mRNA decay in humans is less understood, with recent identification of P-site tRNA-mediated decay (PTMD).
Purpose of the Study:
- To investigate the characteristics of human transcripts affected by PTMD.
- To elucidate the distinct regulatory role of PTMD in human gene expression compared to yeast.
Main Methods:
- Analysis of public transcriptomic datasets.
- Identification of transcripts enriched in PTMD-associated codons (specific arginine codons at P-site).
Main Results:
- Human PTMD involves specific arginine codons (CGG, CGA, AGG) at the P site and slow A-site decoding.
- Transcripts enriched in PTMD codons were found to have longer half-lives.
- PTMD selectively targets and reduces the stability of otherwise long-lived human transcripts.
Conclusions:
- Human PTMD represents a distinct mRNA decay mechanism from yeast, focusing on stabilizing long-lived transcripts.
- PTMD, involving CNOT3, plays a regulatory role in human gene expression by modulating the stability of specific mRNA populations.
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