Depletion of aDrosophila homolog of yeast Sup35p disrupts spindle assembly, chromosome segregation, and cytokinesis during male meiosis

Basu, Joydeep; Williams, Byron; Li, ZeXiao; Williams, Erika V.; Goldberg, Michael L.

doi:10.1002/(sici)1097-0169(1998)39:4<286::aid-cm4>3.0.co;2-1

Cited by 49 publications

(36 citation statements)

References 55 publications

(65 reference statements)

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“…It is interesting that the eEF1␣ is associated with the mitotic apparatus, particularly with centrosomes and other microtubule organizing centers and may play an important role in the microtubule nucleation (17,21,26). Mutation of the DSUP35 gene encoding the Drosophila homolog of the yeast eRF3 affects the meiotic spindle assembly and results in abnormal chromosome segregation during the meiotic divisions (2). With regard to the eEF1␣-like domain in the Pelo protein and accumulation of aneuploid cells in the Pelo null embryos, it is likely that the Pelo is involved in the mitotic spindle structure and function.…”

Section: Discussionmentioning

confidence: 99%

Disruption of the Pelota Gene Causes Early Embryonic Lethality and Defects in Cell Cycle Progression

Adham¹,

Sallam²,

Steding³

et al. 2003

Molecular and Cellular Biology

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Mutations in either the Drosophila melanogaster pelota or pelo gene or the Saccharomyces cerevisiae homologous gene, DOM34, cause defects of spermatogenesis and oogenesis in Drosophila, and delay of growth and failure of sporulation in yeast. These phenotypes suggest that pelota is required for normal progression of the mitotic and meiotic cell cycle. To determine the role of the pelota in mouse development and progression of cell cycle, we have established a targeted disruption of the mouse Pelo. Heterozygous animals are variable and fertile. Genotyping of the progeny of heterozygous intercrosses shows the absence of Pelo ؊/؊ pups and suggests an embryo-lethal phenotype. Histological analyses reveal that the homozygous Pelo deficient embryos fail to develop past day 7.5 of embryogenesis (E7.5). The failure of mitotic active inner cell mass of the Pelo ؊/؊ blastocysts to expand in growth after 4 days in culture and the survival of mitotic inactive trophoplast indicate that the lethality of Pelo-null embryos is due to defects in cell proliferation. Analysis of the cellular DNA content reveals the significant increase of aneuploid cells in Pelo ؊/؊ embryos at E7.5. Therefore, the percent increase of aneuploid cells at E7.5 may be directly responsible for the arrested development and suggests that Pelo is required for the maintenance of genomic stability.The Pelo gene was originally identified in a mutagenesis screen for spermatogenesis-specific genes of Drosophila melanogaster (7). Spermatogenesis in pelo mutants progresses normally during the four mitotic divisions, and the 16 spermatocytes undergo a premeiotic S-phase and duplicate their DNA content. However, spermatocytes in the mutant arrested prior to full chromosome condensation, spindle pole organization, and nuclear breakdown. Metaphase and anaphase figures of the meiotic divisions, which are clearly recognized in squashed preparations of wild-type testis, were not observed in testis of the pelo mutant. Although meiotic division arrests in pelo spermatocytes, germ cell differentiation continues, resulting in 4N spermatids with head and tail structures. These results indicate that the Pelo is required for the meiotic division during the G 2 /M transition (10). Beside the effect of the mutation on spermatogenesis, the eyes of the pelo homozygotes are up to 30% smaller than those of wild-type siblings, and the ovaries in mutants are very small. In contrast to the arrest in meiotic divisions in male germ cells, during oogenesis the mitotic divisions are affected. The mitotic zone of ovaries appears disorganized and often contains degenerating cells. Despite the apparent phenotype observed in the gametogenesis of Drosophila mutant, the pelo transcripts are not restricted to germ cells but also detected in early embryonic development.Analysis of mitotic and meiotic division in the dom34 mutant of Saccharomyces cerevisiae, which has a mutation in the pelota orthologous gene, reveals that the dom34 mutant exhibits a growth delay and fails to undergo sporulation pr...

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Section: Discussionmentioning

confidence: 99%

Disruption of the Pelota Gene Causes Early Embryonic Lethality and Defects in Cell Cycle Progression

Adham¹,

Sallam²,

Steding³

et al. 2003

Molecular and Cellular Biology

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“…In Drosophila melanogaster, partial inactivation of the SUP35 homolog by insertion of a P-element in its promoter (Basu et al, 1998) also causes cytoskeleton defects in male meiosis. Involvement of Sup35 and Sup45 proteins in cytoskeleton organizations in yeast has been studied by TerAvanasyan's group in conditions of down regulations of their synthesis in mitosis.…”

Section: Influence On Cell Cycle Related Functionsmentioning

confidence: 99%

Eukaryotic release factors (eRFs) history

Инге-Вечтомов

Zhouravleva

Maury

2003

Biology of the Cell

113

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In the present review, we describe the history of the identification of the eukaryotic translation termination factors eRF1 and eRF3. As in the case of several proteins involved in general and essential processes in all cells (e.g., DNA replication, gene expression regulation...) the strategies and methodologies used to identify these release factors were first established in prokaryotes. The genetic investigations in Saccharomyces cerevisiae have made a major contribution in the field. A large amount of data have been produced, from which it was concluded that the SUP45 and SUP35 genes were controlling translation termination but were also involved in other functions important for the cell organization and the cell cycle accomplishment. This does not seem to be restricted to yeast but is also probably the case in eukaryotes in general. The biochemical studies of the proteins encoded by the higher eukaryote homologs of SUP45 and SUP35 were efficient and permitted the identification of eRF1 as being the key protein in the termination process, eRF3 having a stimulating role. Around 25 years were needed after the identification of sup45 and sup35 mutants for the characterization of their gene products as eRF1 and eRF3, respectively. It also has to be pointed out that if the results came first from bacteria, the identification of RF3 and eRF3 was made practically at the same time. Moreover, eRF1 was the first crystal structure obtained for a class-1 release factor, the bacterial RF2 structure came later. The goal is now to understand at the molecular level the roles of both eRF1 and eRF3 in addition to their translation termination functions.

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“…Intriguingly, there is evidence to suggest that Sup35p does serve a role in eukaryotes other than that of a polypeptide release factor. For example, Sup35p has been identified as a putative cell cycle factor of S.cerevisiae (Kikuchi et al, 1988), and recently the Drosophila homologue of yeast Sup35p has been shown to mediate meiotic spindle assembly (Basu et al, 1998).…”

Section: Allosuppression Enhances Stress Tolerancementioning

confidence: 99%

Translation termination efficiency can be regulated in Saccharomyces cerevisiae by environmental stress through a prion-mediated mechanism

1999

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Depletion of aDrosophila homolog of yeast Sup35p disrupts spindle assembly, chromosome segregation, and cytokinesis during male meiosis

Cited by 49 publications

References 55 publications

Disruption of the Pelota Gene Causes Early Embryonic Lethality and Defects in Cell Cycle Progression

Disruption of the Pelota Gene Causes Early Embryonic Lethality and Defects in Cell Cycle Progression

Eukaryotic release factors (eRFs) history

Translation termination efficiency can be regulated in Saccharomyces cerevisiae by environmental stress through a prion-mediated mechanism

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