Homologues of 26S proteasome subunits are regulators of transcription and translation

Aravind, L.; Ponting, Chris P.

doi:10.1002/pro.5560070521

Cited by 125 publications

(105 citation statements)

References 41 publications

(17 reference statements)

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“…However, several distinct pathways and complexes stand in sharp contrast to this trend, suggesting coelimination of functionally interacting sets of proteins (Table 1). A clear-cut example is the eIF3͞signalosome complex that participates in multiple protein-protein interactions mediating signaling, translation, and protein degradation (15,16). Although the majority of these proteins are conserved in animals, plants, and S. pombe (17), most of them seem to be missing in S. cerevisiae, indicating that they probably have been lost as a group (Table 1).…”

Section: Materials and Methods)mentioning

confidence: 99%

Lineage-specific loss and divergence of functionally linked genes in eukaryotes

Aravind

Watanabe

Lipman

et al. 2000

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

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269

212

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By comparing 4,344 protein sequences from fission yeast Schizosaccharomyces pombe with all available eukaryotic sequences, we identified those genes that are conserved in S. pombe and nonfungal eukaryotes but are missing or highly diverged in the baker's yeast Saccharomyces cerevisiae. Since the radiation from the common ancestor with S. pombe, S. cerevisiae appears to have lost about 300 genes, and about 300 more genes have diverged by far beyond expectation. The most notable feature of the set of genes lost in S. cerevisiae is the coelimination of functionally connected groups of proteins, such as the signalosome and the spliceosome components. We predict similar coelimination of the components of the posttranscriptional gene-silencing system that includes the recently identified RNA-dependent RNA polymerase. Because one of the functions of posttranscriptional silencing appears to be ''taming'' of retrotransposons, the loss of this system in yeast could have triggered massive retrotransposition, resulting in elimination of introns and subsequent loss of spliceosome components that become dispensable. As the genome database grows, systematic analysis of coordinated gene loss may become a general approach for predicting new components of functional systems or even defining previously unknown functional complexes.A major outcome of the recent advances in comparative genomics is the realization of the major role of horizontal gene transfer and lineage-specific gene loss in the evolution of prokaryotes (1-4). These phenomena appear to account largely for the remarkable diversity of the prokaryotic gene repertoires. The likelihood of horizontal gene transfer between eukaryotes, at least multicellular ones, is low because, for a gene to be laterally transferred, it must enter the germ line. In contrast, there is no such restriction for gene loss. The dramatic variation in the number of genes among eukaryotes, in some cases even between rather closely related species-yeast Saccharomyces cerevisiae, for example, has about 6,000 genes compared with at least 8,000-9,000 in multicellular ascomycetes such as Aspergillus (5)-suggests that, along with proliferation of gene families (6), lineage-specific gene loss could have been important in eukaryotic evolution.The two yeasts, S. cerevisiae and Schizosaccharomyces pombe, are probably the optimal current choice of genomes to compare with the aim of estimating the number of lost genes. The genome of S. cerevisiae, arguably the best-studied eukaryote in terms of gene functions (6), has been completed (7), and for S. pombe, up to 70% of the genome sequence is available. For estimating gene loss, it is critical to have assurance that (nearly) all genes in the analyzed genome have been identified; S. cerevisiae is the only eukaryotic genome for which such confidence exists, particularly because of the paucity of introns, which facilitates gene detection. The two yeast species are close enough so that direct counterparts among their genes [orthologs (8)] are readily identifiable b...

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Section: Materials and Methods)mentioning

confidence: 99%

Lineage-specific loss and divergence of functionally linked genes in eukaryotes

Aravind

Watanabe

Lipman

et al. 2000

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

Self Cite

269

212

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“…Thus, Prp8 is thought to provide a vital scaffold and catalytic function in the spliceosome of all eukaryotes. However, despite its remarkable evolutionary conservation, the only obvious motif within Prp8 is a carboxy-terminal MPN/Mov34 domain (Aravind and Ponting 1998). The function of this domain is unclear, but it is also found in proteasome regulatory subunits, eIF-3 subunits, The numbers to the right indicate the size of the euchromatic (euch.)…”

Section: Ms1096dp110mentioning

confidence: 99%

“…KD genes on a physical map of the second chromosome is shown with respect to the wg Genetic Modifiers of a Small-Wing Phenotypeand regulators of transcription factors (Aravind and Ponting 1998). Additionally, Grainger and Beggs have recently defined a putative nuclear localization sequence, an RNA recognition motif (RRM), and a third domain they call the ''39 splice site fidelity region'' on the basis of the clustering of S. cerevisiae PRP8 mutations that suppress defects in splicing pre-mRNA 39 splice site mutations (Grainger and Beggs 2005; Figure 7A).…”

Section: Ms1096dp110mentioning

confidence: 99%

A Genetic Screen for Dominant Modifiers of a Small-Wing Phenotype in Drosophila melanogaster Identifies Proteins Involved in Splicing and Translation

et al. 2005

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Studies in the fly, Drosophila melanogaster, have revealed that several signaling pathways are important for the regulation of growth. Among these, the insulin receptor/phosphoinositide 3-kinase (PI3K) pathway is remarkable in that it affects growth and final size without disturbing pattern formation. We have used a small-wing phenotype, generated by misexpression of kinase-dead PI3K, to screen for novel mutations that specifically disrupt organ growth in vivo. We identified several complementation groups that dominantly enhance this small-wing phenotype. Meiotic recombination in conjunction with visible markers and single-nucleotide polymorphisms (SNPs) was used to map five enhancers to single genes. Two of these, nucampholin and prp8, encode pre-mRNA splicing factors. The three other enhancers encode factors required for mRNA translation: pixie encodes the Drosophila ortholog of yeast RLI1, and RpL5 and RpL38 encode proteins of the large ribosomal subunit. Interestingly, mutations in several other ribosomal protein-encoding genes also enhance the small-wing phenotype used in the original screen. Our work has therefore identified mutations in five previously uncharacterized Drosophila genes and provides in vivo evidence that normal organ growth requires optimal regulation of both pre-mRNA splicing and mRNA translation.

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“…eIF3f is a member of the Mov34 family, which is involved in translation initiation, regulation of the proteasome and transcription (Aravind and Ponting, 1998). We used a yeast two-hybrid screening strategy and identified eIF3f as an interacting partner of caspase processed C-terminal kinase domain of the cyclindependent kinase 11 (CDK11 p46 ) protein kinase (Shi et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Decreased expression of eukaryotic initiation factor 3f deregulates translation and apoptosis in tumor cells

et al. 2006

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The eukaryotic initiation factor 3f (eIF3f) is the p47 subunit of the multi-subunit eIF3 complex. eIF3 plays an important role in translation initiation. In the present study, we investigate the biological function of eIF3f in translation and apoptosis in tumor cells. We demonstrated for the first time that eIF3f is downregulated in most human tumors using a cancer profiling array and confirmed by real-time reverse transcription PCR in melanoma and pancreatic cancer. Overexpression of eIF3f inhibits cell proliferation and induces apoptosis in melanoma and pancreatic cancer cells. Silencing of eIF3f protects melanoma cells from apoptosis. We further investigated the biological function of eIF3f. In vitro translation studies indicate that eIF3f is a negative regulator of translation and that the region between amino acids 170 and 248 of eIF3f is required for its translation regulatory function. Ectopic expression of eIF3f inhibits translation and overall cellular protein synthesis. Ribosome profile and ribosomal RNA (rRNA) fragmentation assays revealed that eIF3f reduces ribosomes, which may be associated with rRNA degradation. We propose that eIF3f may play a role in ribosome degradation during apoptosis. These data provide critical insights into the cellular function of eIF3f and in linking translation initiation and apoptosis.

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Homologues of 26S proteasome subunits are regulators of transcription and translation

Cited by 125 publications

References 41 publications

Lineage-specific loss and divergence of functionally linked genes in eukaryotes

Lineage-specific loss and divergence of functionally linked genes in eukaryotes

A Genetic Screen for Dominant Modifiers of a Small-Wing Phenotype in Drosophila melanogaster Identifies Proteins Involved in Splicing and Translation

Decreased expression of eukaryotic initiation factor 3f deregulates translation and apoptosis in tumor cells

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