scholarly journals High Rate of Protein Coding Sequence Evolution and Species Diversification in the Lycaenids

Author(s):  
Loïc Pellissier ◽  
Anna Kostikova ◽  
Glenn Litsios ◽  
Nicolas Salamin ◽  
Nadir Alvarez
PLoS Genetics ◽  
2008 ◽  
Vol 4 (11) ◽  
pp. e1000250 ◽  
Author(s):  
Tobias Warnecke ◽  
Nizar N. Batada ◽  
Laurence D. Hurst

2013 ◽  
Vol 94 (7) ◽  
pp. 1486-1495 ◽  
Author(s):  
Graham J. Belsham

The foot-and-mouth disease virus (FMDV) Leader (L) protein is produced in two forms, Lab and Lb, differing only at their amino-termini, due to the use of separate initiation codons, usually 84 nt apart. It has been shown previously, and confirmed here, that precise deletion of the Lab coding sequence is lethal for the virus, whereas loss of the Lb coding sequence results in a virus that is viable in BHK cells. In addition, it is now shown that deletion of the ‘spacer’ region between these two initiation codons can be tolerated. Growth of the virus precisely lacking just the Lb coding sequence resulted in a previously undetected accumulation of frameshift mutations within the ‘spacer’ region. These mutations block the inappropriate fusion of amino acid sequences to the amino-terminus of the capsid protein precursor. Modification, by site-directed mutagenesis, of the Lab initiation codon, in the context of the virus lacking the Lb coding region, was also tolerated by the virus within BHK cells. However, precise loss of the Lb coding sequence alone blocked FMDV replication in primary bovine thyroid cells. Thus, the requirement for the Leader protein coding sequences is highly dependent on the nature and extent of the residual Leader protein sequences and on the host cell system used. FMDVs precisely lacking Lb and with the Lab initiation codon modified may represent safer seed viruses for vaccine production.


1989 ◽  
Vol 9 (12) ◽  
pp. 5484-5490
Author(s):  
T van Daalen Wetters ◽  
M Macrae ◽  
M Brabant ◽  
A Sittler ◽  
P Coffino

The activity of ornithine decarboxylase (ODC) is negatively regulated by intracellular polyamines, which thereby mediate a form of feedback inhibition of the initial enzyme in the pathway of their synthesis. This phenomenon has been believed to result, at least in part, from translational regulation. To investigate this further, we performed four series of experiments. First, we found that a chimeric protein encoded by an mRNA containing the ODC 5' leader sequence did not exhibit polyamine-dependent regulation. Second, we showed that transcripts containing the protein-coding sequence of ODC, but no other ODC-derived sequence information, exhibited regulation. Third, we found that the association of ODC mRNA with ribosomes was not altered when intracellular polyamine levels were modulated under conditions previously deemed to cause translational regulation. Last, we carried out experiments to measure the incorporation of [35S]methionine into ODC in polyamine-starved and polyamine-replete cells. Differential incorporation diminished progressively as pulse-label times were shortened; at the shortest labeling time used (4 min), the difference in favor of ODC in polyamine-starved cells was less than twofold. These findings suggest that it is necessary to reevaluate the question of whether polyamines cause alterations of translation of ODC mRNA.


eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Nicola Palmieri ◽  
Carolin Kosiol ◽  
Christian Schlötterer

Orphans are genes restricted to a single phylogenetic lineage and emerge at high rates. While this predicts an accumulation of genes, the gene number has remained remarkably constant through evolution. This paradox has not yet been resolved. Because orphan genes have been mainly analyzed over long evolutionary time scales, orphan loss has remained unexplored. Here we study the patterns of orphan turnover among close relatives in the Drosophila obscura group. We show that orphans are not only emerging at a high rate, but that they are also rapidly lost. Interestingly, recently emerged orphans are more likely to be lost than older ones. Furthermore, highly expressed orphans with a strong male-bias are more likely to be retained. Since both lost and retained orphans show similar evolutionary signatures of functional conservation, we propose that orphan loss is not driven by high rates of sequence evolution, but reflects lineage-specific functional requirements.


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