Modulation of <i>gurken</i> translation by insulin and TOR signaling in <i>Drosophila</i>

Ferguson, Scott B.; Blundon, Malachi A.; Klovstad, Martha; Schüpbach, Trudi

doi:10.1242/dev.083451

Cited by 2 publications

(3 citation statements)

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“…Wild-type and altered pim sequences were cloned into pTIGER (Ferguson et al, 2012) with N-terminal EGFP. Constructs were integrated at attP2 sites (Genetic Services).…”

Section: Drosophila Stocksmentioning

confidence: 99%

Role of Securin, Separase and Cohesins in female meiosis and polar body formation in Drosophila

Guo

Batiha

Bourouh

et al. 2016

Journal of Cell Science

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Chromosome segregation in meiosis is controlled by a conserved pathway that culminates in Separase-mediated cleavage of the α-kleisin Rec8, leading to dissolution of cohesin rings. Drosophila has no gene encoding Rec8, and the absence of a known Separase target raises the question of whether Separase and its regulator Securin (Pim in Drosophila) are important in Drosophila meiosis. Here, we investigate the role of Securin, Separase and the cohesin complex in female meiosis using fluorescence in situ hybridization against centromeric and arm-specific sequences to monitor cohesion. We show that Securin destruction and Separase activity are required for timely release of arm cohesion in anaphase I and centromere-proximal cohesion in anaphase II. They are also required for release of arm cohesion on polar body chromosomes. Cohesion on polar body chromosomes depends on the cohesin components SMC3 and the mitotic α-kleisin Rad21 (also called Vtd in Drosophila). We provide cytological evidence that SMC3 is required for arm cohesion in female meiosis, whereas Rad21, in agreement with recent findings, is not. We conclude that in Drosophila meiosis, cohesion is regulated by a conserved Securin-Separase pathway that targets a diverged Separase target, possibly within the cohesin complex.

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“…Wild-type and altered pim sequences were cloned into pTIGER (Ferguson et al, 2012) with N-terminal EGFP. Constructs were integrated at attP2 sites (Genetic Services).…”

Section: Drosophila Stocksmentioning

confidence: 99%

Role of Securin, Separase and Cohesins in female meiosis and polar body formation in Drosophila

Guo

Batiha

Bourouh

et al. 2016

Journal of Cell Science

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“…Males of the genotype st spnB BU sr e/TM6,Hu were treated with EMS according to standard procedures and mated to appropriate females to establish stocks (Ferguson et al, 2012). To find dominant suppressor mutations, males from these lines were crossed to st spnB 153 /TM3,Sb females and the eggs of the resulting *st spnB BU sr e/ st spnB 153 females were scored.…”

Section: Generation and Mapping Of Bh167mentioning

confidence: 99%

“…Analogous to the yeast model, mutations in eIF1A would diminish the amount of 43S PIC and allow more ribosomes to reinitiate translation at the start codon of grk. In support of this hypothesis, a protein-rich diet (yeast paste) often exacerbates the DV patterning defects in eggs laid by the spnB females (Ferguson et al, 2012). It would be interesting to test whether eliminating these uORFs from the grk 5′UTR has an effect on Grk translation and whether such deletions would upregulate Grk translation in the spnB mutant.…”

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confidence: 99%

Repression of Gurken translation by a meiotic checkpoint inDrosophilaoogenesis is suppressed by a reduction in the dose ofeIF1A

Klovstad

Schüpbach

2014

Development

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In Drosophila melanogaster, the anteroposterior (AP) and dorsoventral (DV) axes of the oocyte and future embryo are established through the localization and translational regulation of gurken (grk) mRNA. This process involves binding of specific factors to the RNA during transport and a dynamic remodeling of the grk-containing ribonucleoprotein (RNP) complexes once they have reached their destination within the oocyte. In ovaries of spindle-class females, an activated DNA damage checkpoint causes inefficient Grk translation and ventralization of the oocyte. In a screen for modifiers of the oocyte DV patterning defects, we identified a mutation in the eIF1A gene as a dominant suppressor. We show that reducing the function of eIF1A in spnB ovaries suppresses the ventralized eggshell phenotype by restoring Grk expression. This suppression is not the result of more efficient DNA damage repair or of disrupted checkpoint activation, but is coupled to an increase in the amount of grk mRNA associated with polysomes. In spnB ovaries, the activated meiotic checkpoint blocks Grk translation by disrupting the accumulation of grk mRNA in a translationally competent RNP complex that contains the translational activator Oo18 RNA-binding protein (Orb); this regulation involves the translational repressor Squid (Sqd). We further propose that reduction of eIF1A allows more efficient Grk translation possibly because of the presence of specific structural features in the grk 5′UTR.

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Modulation of gurken translation by insulin and TOR signaling in Drosophila

Cited by 2 publications

References 1 publication

Role of Securin, Separase and Cohesins in female meiosis and polar body formation in Drosophila

Role of Securin, Separase and Cohesins in female meiosis and polar body formation in Drosophila

Repression of Gurken translation by a meiotic checkpoint inDrosophilaoogenesis is suppressed by a reduction in the dose ofeIF1A

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