Sense Codon

2001 ◽  
pp. 1809
Author(s):  
J.H. Miller
Keyword(s):  
2021 ◽  
Vol 22 (4) ◽  
pp. 1876
Author(s):  
Frida Belinky ◽  
Ishan Ganguly ◽  
Eugenia Poliakov ◽  
Vyacheslav Yurchenko ◽  
Igor B. Rogozin

Nonsense mutations turn a coding (sense) codon into an in-frame stop codon that is assumed to result in a truncated protein product. Thus, nonsense substitutions are the hallmark of pseudogenes and are used to identify them. Here we show that in-frame stop codons within bacterial protein-coding genes are widespread. Their evolutionary conservation suggests that many of them are not pseudogenes, since they maintain dN/dS values (ratios of substitution rates at non-synonymous and synonymous sites) significantly lower than 1 (this is a signature of purifying selection in protein-coding regions). We also found that double substitutions in codons—where an intermediate step is a nonsense substitution—show a higher rate of evolution compared to null models, indicating that a stop codon was introduced and then changed back to sense via positive selection. This further supports the notion that nonsense substitutions in bacteria are relatively common and do not necessarily cause pseudogenization. In-frame stop codons may be an important mechanism of regulation: Such codons are likely to cause a substantial decrease of protein expression levels.


Science ◽  
2021 ◽  
Vol 372 (6546) ◽  
pp. 1057-1062
Author(s):  
Wesley E. Robertson ◽  
Louise F. H. Funke ◽  
Daniel de la Torre ◽  
Julius Fredens ◽  
Thomas S. Elliott ◽  
...  

It is widely hypothesized that removing cellular transfer RNAs (tRNAs)—making their cognate codons unreadable—might create a genetic firewall to viral infection and enable sense codon reassignment. However, it has been impossible to test these hypotheses. In this work, following synonymous codon compression and laboratory evolution in Escherichia coli, we deleted the tRNAs and release factor 1, which normally decode two sense codons and a stop codon; the resulting cells could not read the canonical genetic code and were completely resistant to a cocktail of viruses. We reassigned these codons to enable the efficient synthesis of proteins containing three distinct noncanonical amino acids. Notably, we demonstrate the facile reprogramming of our cells for the encoded translation of diverse noncanonical heteropolymers and macrocycles.


2015 ◽  
Vol 43 (16) ◽  
pp. 8111-8122 ◽  
Author(s):  
Takahito Mukai ◽  
Atsushi Yamaguchi ◽  
Kazumasa Ohtake ◽  
Mihoko Takahashi ◽  
Akiko Hayashi ◽  
...  

ChemBioChem ◽  
2013 ◽  
Vol 14 (15) ◽  
pp. 1967-1972 ◽  
Author(s):  
Radha Krishnakumar ◽  
Laure Prat ◽  
Hans-Rudolf Aerni ◽  
Jiqiang Ling ◽  
Chuck Merryman ◽  
...  
Keyword(s):  

Science ◽  
2020 ◽  
Vol 368 (6488) ◽  
pp. eaay6912 ◽  
Author(s):  
Robert Buschauer ◽  
Yoshitaka Matsuo ◽  
Takato Sugiyama ◽  
Ying-Hsin Chen ◽  
Najwa Alhusaini ◽  
...  

Control of messenger RNA (mRNA) decay rate is intimately connected to translation elongation, but the spatial coordination of these events is poorly understood. The Ccr4-Not complex initiates mRNA decay through deadenylation and activation of decapping. We used a combination of cryo–electron microscopy, ribosome profiling, and mRNA stability assays to examine the recruitment of Ccr4-Not to the ribosome via specific interaction of the Not5 subunit with the ribosomal E-site in Saccharomyces cerevisiae. This interaction occurred when the ribosome lacked accommodated A-site transfer RNA, indicative of low codon optimality. Loss of the interaction resulted in the inability of the mRNA degradation machinery to sense codon optimality. Our findings elucidate a physical link between the Ccr4-Not complex and the ribosome and provide mechanistic insight into the coupling of decoding efficiency with mRNA stability.


RNA ◽  
2003 ◽  
Vol 9 (7) ◽  
pp. 780-786 ◽  
Author(s):  
A. FRANKEL

Biochemistry ◽  
2015 ◽  
Vol 54 (50) ◽  
pp. 7355-7364 ◽  
Author(s):  
Wil Biddle ◽  
Margaret A. Schmitt ◽  
John D. Fisk

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