Many viruses use overprinting (alternate reading frame utilization) as a means to increase protein diversity in genomes severely constrained by size. However, the evolutionary steps that facilitate the de novo generation of a novel protein within an ancestral ORF have remained poorly characterized. Here, we describe the identification of an overprinting gene, expressed from an Alternate frame of the Large T Open reading frame (ALTO) in the early region of Merkel cell polyomavirus (MCPyV), the causative agent of most Merkel cell carcinomas. ALTO is expressed during, but not required for, replication of the MCPyV genome. Phylogenetic analysis reveals that ALTO is evolutionarily related to the middle T antigen of murine polyomavirus despite almost no sequence similarity. ALTO/MT arose de novo by overprinting of the second exon of T antigen in the common ancestor of a large clade of mammalian polyomaviruses. Taking advantage of the low evolutionary divergence and diverse sampling of polyomaviruses, we propose evolutionary transitions that likely gave birth to this protein. We suggest that two highly constrained regions of the large T antigen ORF provided a start codon and C-terminal hydrophobic motif necessary for cellular localization of ALTO. These two key features, together with stochastic erasure of intervening stop codons, resulted in a unique protein-coding capacity that has been preserved ever since its birth. Our study not only reveals a previously undefined protein encoded by several polyomaviruses including MCPyV, but also provides insight into de novo protein evolution. gene evolution | synonymous substitution | disordered motifs T he birth of new genes has fascinated biologists for decades. Although the steps required to generate a new gene by gene duplication or gene rearrangement have been characterized, less is known about the birth of new genes de novo. One particularly intriguing mechanism of de novo gene birth is via "overprinting," in which a novel overprinting gene is encoded as an alternate ORF within an ancestral "overprinted" gene (1). Overprinting results in two unrelated functional proteins encoded as overlapping ORFs within the same DNA sequence. However, the origins of such a complex evolutionary solution have remained elusive.Viruses appear to be especially adept at this form of evolutionary innovation. This frequent use of overprinting is likely the result of the severe constraints imposed on viral genome size, making gene innovation more likely to occur as overprinting rather than within a noncoding region (2). Due to the numerous examples of overprinting in single-stranded RNA viruses, a great deal of research has focused in particular on this class of viruses (3-6). However, small DNA viruses, such as adenoviruses, papillomaviruses, and polyomaviruses, have a similar requirement to maximize the coding capacity of their genomes. In this study, we have taken advantage of our identification of an overprinting gene born in the ancestor of a large clade of polyomaviruses to investigate the...

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Although retroviruses are relatively promiscuous in choice of integration sites, retrotransposons can display marked integration specificity. In yeast and slime mold, some retrotransposons are associated with tRNA genes (tDNAs). In the Saccharomyces cerevisiae genome, the long terminal repeat retrotransposon Ty3 is found at RNA polymerase III (Pol III) transcription start sites of tDNAs. Ty1, 2, and 4 elements also cluster in the upstream regions of these genes. To determine the extent to which other Pol III-transcribed genes serve as genomic targets for Ty3, a set of 10,000 Ty3 genomic retrotranspositions were mapped using high-throughput DNA sequencing. Integrations occurred at all known tDNAs, two tDNA relics (iYGR033c and ZOD1), and six non-tDNA, Pol III-transcribed types of genes (RDN5, SNR6, SNR52, RPR1, RNA170, and SCR1). Previous work in vitro demonstrated that the Pol III transcription factor (TF) IIIB is important for Ty3 targeting. However, seven loci that bind the TFIIIB loader, TFIIIC, were not targeted, underscoring the unexplained absence of TFIIIB at those sites. Ty3 integrations also occurred in two open reading frames not previously associated with Pol III transcription, suggesting the existence of a small number of additional sites in the yeast genome that interact with Pol III transcription complexes.

The freak oscillation in one-dimensional dusty plasma is studied numerically by particle-in-cell method. Using a perturbation method, the basic set of fluid equations is reduced to a nonlinear Schrödinger equation (NLSE). The rational solution of the NLSE is presented, which is proposed as an effective tool for studying the rogue waves in dusty plasma. Additionally, the application scope of the analytical solution of the rogue wave described by the NLSE is given.

The application scope of the Poincare-Lighthill-Kuo (PLK) method is suggested by using the Particle-in-cell (PIC) numerical method to study head-on collision of two solitary waves. Comparisons between the numerical results from PIC simulations and the analytical ones from the PLK method indicate that the both are in good agreement with each other. The dependence of the phase shifts after the head-on collision on both amplitudes of two solitary waves is given from our PIC method. It is found that the phase shifts depended on the amplitude of both waves. The maximum amplitude during the colliding process is approximately equal to the sum of both amplitudes for the small amplitude solitary waves.

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The head-on collision of two ion acoustic solitary waves in plasmas composed of hot electrons and cold ions has been studied by using the Poincare-Lighthill-Kuo (PLK) perturbation method and one-dimensional Particle-in-Cell (PIC) simulation. Then the phase lags of ion acoustic solitary waves (IASWs) obtained from the two approaches have been compared and discussed. It has been found that: if the amplitudes of both the colliding IASWs are small enough, the phase lags obtained from PLK method are in good agreement with those obtained from PIC simulation. As the amplitudes of IASWs increase, the phase lags from PIC simulation become smaller than the analytical ones from PLK method. Besides, the PIC simulation shows the phase lag of an IASW involved in collision depends not only on the characteristics of the wave it collides with but also on itself, which disagrees with the prediction of the PLK method. Finally, the application scopes of the PLK method in studying both the single IASW and the head-on collisions of IASWs have been studied and discussed, and the latter turns out to be more strict.

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