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Rijk, Anke van

doi:10.1023/a:1024138600624

Cited by 34 publications

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“…The mechanisms of exon shuffling include illegitimate recombination [ 192 , 193 ], retroposition [ 125 ], segmental duplication [ 45 ] and L1 retrotransposon-mediated 3′ transduction [ 125 ].…”

Section: Introductionmentioning

confidence: 99%

Expression of evolutionarily novel genes in tumors

Kozlov

2016

Infect Agents Cancer

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The evolutionarily novel genes originated through different molecular mechanisms are expressed in tumors. Sometimes the expression of evolutionarily novel genes in tumors is highly specific. Moreover positive selection of many human tumor-related genes in primate lineage suggests their involvement in the origin of new functions beneficial to organisms.It is suggested to consider the expression of evolutionarily young or novel genes in tumors as a new biological phenomenon, a phenomenon of TSEEN (tumor specifically expressed, evolutionarily novel) genes.

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Section: Introductionmentioning

confidence: 99%

Expression of evolutionarily novel genes in tumors

Kozlov

2016

Infect Agents Cancer

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“…Alternatively, recombination could also occur between exonic sequences of two different genes [16]. The two main types of recombination are non-allelic homologous recombination (NAHR) [8,17], which relies on short regions of homology, and illegitimate recombination (IR) [8,9,18], also known as non-homologous end joining, which does not require such homologous regions. In addition to these mechanisms, new protein coding sequence can be gained through: 1, deletion of the intervening sequence between two adjacent genes and subsequent exon fusion [19]; 2, exonization of previously non-coding sequence [20]; and 3, insertion of viral or transposon sequences into a gene [21].…”

Section: Introductionmentioning

confidence: 99%

Quantifying the mechanisms of domain gain in animal proteins

2010

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BackgroundProtein domains are protein regions that are shared among different proteins and are frequently functionally and structurally independent from the rest of the protein. Novel domain combinations have a major role in evolutionary innovation. However, the relative contributions of the different molecular mechanisms that underlie domain gains in animals are still unknown. By using animal gene phylogenies we were able to identify a set of high confidence domain gain events and by looking at their coding DNA investigate the causative mechanisms.ResultsHere we show that the major mechanism for gains of new domains in metazoan proteins is likely to be gene fusion through joining of exons from adjacent genes, possibly mediated by non-allelic homologous recombination. Retroposition and insertion of exons into ancestral introns through intronic recombination are, in contrast to previous expectations, only minor contributors to domain gains and have accounted for less than 1% and 10% of high confidence domain gain events, respectively. Additionally, exonization of previously non-coding regions appears to be an important mechanism for addition of disordered segments to proteins. We observe that gene duplication has preceded domain gain in at least 80% of the gain events.ConclusionsThe interplay of gene duplication and domain gain demonstrates an important mechanism for fast neofunctionalization of genes.

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“…Similarly, the phylogenetic tree of zebrafish repeats is consistent with repeats 12-15 having appeared through individual single exon duplication events. Multiple methods have been proposed to account for repeat amplification and contraction including strand slippage (Petruska et al 1998), retrotransposition (Xiao et al 2008), gene conversion (Chen et al 2007), and illegitimate recombination (either nonhomologous or unequal crossover mediated) during meiotic recombination (Van Rijk and Bloemendal 2003). Strand-slippage is primarily associated with trinucleotide repeat amplification and is thus unlikely to be relevant to Piccolo.…”

Section: Discussionmentioning

confidence: 99%

A Window into Domain Amplification Through Piccolo in Teleost Fish

Nonet

2012

G3 Genes|Genomes|Genetics

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I describe and characterize the extensive amplification of the zinc finger domain of Piccolo selectively in teleost fish. Piccolo and Bassoon are partially functionally redundant and play roles in regulating the pool of neurotransmitter-filled synaptic vesicles present at synapses. In mice, each protein contains two N-terminal zinc finger domains that have been implicated in interacting with synaptic vesicles. In all teleosts examined, both the Bassoon and Piccolo genes are duplicated. Both teleost bassoon genes and one piccolo gene show very similar domain structure and intron-exon organization to their mouse homologs. In contrast, in piccolo b a single exon that encodes a zinc finger domain is amplified 8 to 16 times in different teleost species. Analysis of the amplified exons suggests they were added and/or deleted from the gene as individual exons in rare events that are likely the result of unequal crossovers between homologous sequences. Surprisingly, the structure of the repeats from cod and zebrafish suggest that amplification of this exon has occurred independently multiple times in the teleost lineage. Based on the structure of the exons, I propose a model in which selection for high sequence similarity at the 5′ and 3′ ends of the exon drives amplification of the repeats and diversity in repeat length likely promotes the stability of the repeated exons by minimizing the likelihood of mispairing of adjacent repeat sequences. Further analysis of piccolo b in teleosts should provide a window through which to examine the process of domain amplification.

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Cited by 34 publications

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Expression of evolutionarily novel genes in tumors

Expression of evolutionarily novel genes in tumors

Quantifying the mechanisms of domain gain in animal proteins

A Window into Domain Amplification Through Piccolo in Teleost Fish

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