Conserved Functions of Yeast Genes Support the Duplication, Degeneration and Complementation Model for Gene Duplication

Hoof, Ambro van

doi:10.1534/genetics.105.044057

Cited by 89 publications

(84 citation statements)

References 40 publications

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“…In the duplication, degeneration, and complementation (DDC) model, duplicated genes each lose one of the original functions and together retain the entire set of ancestral functions (47,48), whereas in the specialization model the divergence of functions among paralogs also involves the accumulation of advantageous mutations in at least one of the duplicated genes, enabling it to outperform the ancestral gene (10,11,49,50). An earlier study investigating the nonduplicated Orc1 from Saccharomyces kluyveri concluded that Orc1 subfunctionalized through the DDC pathway, based on the ability of SkOrc1 to complement both orc1 and sir3 mutations in S. cerevisiae (34). However, we suggest that although the SIR3-ORC1 gene pair did subfunctionalize, it is more likely a case of specialization.…”

Section: Discussioncontrasting

confidence: 55%

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Transcriptional silencing functions of the yeast protein Orc1/Sir3 subfunctionalized after gene duplication

Hickman

Rusché

2010

Proc. Natl. Acad. Sci. U.S.A.

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The origin recognition complex (ORC) defines origins of replication and also interacts with heterochromatin proteins in a variety of species, but how ORC functions in heterochromatin assembly remains unclear. The largest subunit of ORC, Orc1, is particularly interesting because it contains a nucleosome-binding BAH domain and because it gave rise to Sir3, a key silencing protein in Saccharomyces cerevisiae, through gene duplication. We examined whether Orc1 possessed a Sir3-like silencing function before duplication and found that Orc1 from the yeast Kluyveromyces lactis, which diverged from S. cerevisiae before the duplication, acts in conjunction with the deacetylase Sir2 and the histone-binding protein Sir4 to generate heterochromatin at telomeres and a matingtype locus. Moreover, the ability of KlOrc1 to spread across a silenced locus depends on its nucleosome-binding BAH domain and the deacetylase Sir2. Interestingly, KlOrc1 appears to act independently of the entire ORC, as other subunits of the complex, Orc4 and Orc5, are not strongly associated with silenced domains. These findings demonstrate that Orc1 functioned in silencing before duplication and suggest that Orc1 and Sir2, both of which are broadly conserved among eukaryotes, may have an ancient history of cooperating to generate chromatin structures, with Sir2 deacetylating histones and Orc1 binding to these deacetylated nucleosomes through its BAH domain.heterochromatin | replication | SIR

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Section: Discussioncontrasting

confidence: 55%

“…Nonduplicated orthologs of Orc1 and Sir3 display more sequence similarity to ScOrc1 than to ScSir3, and this accelerated sequence divergence in Sir3 has led to the hypothesis that the silencing function of Sir3 arose through neofunctionalization (29). However, others have argued that Orc1 and Sir3 subfunctionalized (34).…”

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confidence: 99%

Transcriptional silencing functions of the yeast protein Orc1/Sir3 subfunctionalized after gene duplication

Hickman

Rusché

2010

Proc. Natl. Acad. Sci. U.S.A.

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“…This is conceptually similar to no-go decay, which is the rapid endonucleolytic cleavage of mRNAs with an internally stalled ribosome (25). Furthermore, nonstop decay and no-go decay require the paralogs SKI7 and HBS1, respectively (22,25,39). Given this similarity, we considered the possibility that Rrp44p may be the endonuclease responsible for no-go decay and that our nonstop mRNAs with stalled ribosomes at their 3′ ends were also susceptible to no-go decay.…”

Section: Either the Endo-or Exonuclease Activity Of Rrp44p Can Efficimentioning

confidence: 96%

Different nuclease requirements for exosome-mediated degradation of normal and nonstop mRNAs

Schaeffer

Hoof

2011

Proc. Natl. Acad. Sci. U.S.A.

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Two general pathways of mRNA decay have been characterized in yeast. In one pathway, the mRNA is degraded by the cytoplasmic form of the exosome. The exosome has both 3′ to 5′ exoribonuclease and endoribonuclease activity, and the available evidence suggests that the exonuclease activity is required for the degradation of mRNAs. We confirm here that this is true for normal mRNAs, but that aberrant mRNAs that lack a stop codon can be efficiently degraded in the absence of the exonuclease activity of the exosome. Specifically, we show that the endo-and exonuclease activities of the exosome are both capable of rapidly degrading nonstop mRNAs and ribozyme-cleaved mRNAs. Additionally, the endonuclease activity of the exosome is not required for endonucleolytic cleavage in no-go decay. In vitro, the endonuclease domain of the exosome is active only under nonphysiological conditions, but our findings show that the in vivo activity is sufficient for the rapid degradation of nonstop mRNAs. Thus, whereas normal mRNAs are degraded by two exonucleases (Xrn1p and Rrp44p), several endonucleases contribute to the decay of many aberrant mRNAs, including transcripts subject to nonstop and nogo decay. Our findings suggest that the nuclease requirements for general and nonstop mRNA decay are different, and describe a molecular function of the core exosome that is not disrupted by inactivating its exonuclease activity.Dis3 | Saccharomyces cerevisiae

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“…The relative probabilities of neofunctionalization and subfunctionalization remain unclear. However, growing evidence suggests subfunctionalization is common (Van Hoof 2005).…”

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confidence: 99%

Formation and Longevity of Chimeric and Duplicate Genes inDrosophila melanogaster

Rogers

Bedford²,

Hartl

2009

Genetics

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Historically, duplicate genes have been regarded as a major source of novel genetic material. However, recent work suggests that chimeric genes formed through the fusion of pieces of different genes may also contribute to the evolution of novel functions. To compare the contribution of chimeric and duplicate genes to genome evolution, we measured their prevalence and persistence within Drosophila melanogaster. We find that $80.4 duplicates form per million years, but most are rapidly eliminated from the genome, leaving only 4.1% to be preserved by natural selection. Chimeras form at a comparatively modest rate of $11.4 per million years but follow a similar pattern of decay, with ultimately only 1.4% of chimeras preserved. We propose two mechanisms of chimeric gene formation, which rely entirely on local, DNA-based mutations to explain the structure and placement of the youngest chimeric genes observed. One involves imprecise excision of an unpaired duplication during large-loop mismatch repair, while the other invokes a process akin to replication slippage to form a chimeric gene in a single event. Our results paint a dynamic picture of both chimeras and duplicate genes within the genome and suggest that chimeric genes contribute substantially to genomic novelty.

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Conserved Functions of Yeast Genes Support the Duplication, Degeneration and Complementation Model for Gene Duplication

Cited by 89 publications

References 40 publications

Transcriptional silencing functions of the yeast protein Orc1/Sir3 subfunctionalized after gene duplication

Transcriptional silencing functions of the yeast protein Orc1/Sir3 subfunctionalized after gene duplication

Different nuclease requirements for exosome-mediated degradation of normal and nonstop mRNAs

Formation and Longevity of Chimeric and Duplicate Genes inDrosophila melanogaster

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