Drosophila oogenesis: Versatile spn doctors

Morris, Jason Z; Lehmann, Ruth

doi:10.1016/s0960-9822(99)80010-4

Cited by 21 publications

(15 citation statements)

References 19 publications

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“…In addition to delays in meiotic restriction, females with mutant DSB repair enzymes lay eggs with dorsalventral (DV) defects known as the spindle phenotype (Gonzalez-Reyes et al 1997;Ghabrial et al 1998;Morris and Lehmann 1999;Staeva-Vieira et al 2003). The persistence of DSBs in these mutants activates the ATR-like kinase Mei-41 and the Drosophila checkpoint protein 2 (dChk2) (Ghabrial and Schupbach 1999;Abdu et al 2002;Staeva-Vieira et al 2003).…”

Section: A S Cells Divide Checkpoints Delay the Transition Tomentioning

confidence: 99%

A Maternal Screen for Genes Regulating Drosophila Oocyte Polarity Uncovers New Steps in Meiotic Progression

2007

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Meiotic checkpoints monitor chromosome status to ensure correct homologous recombination, genomic integrity, and chromosome segregation. In Drosophila, the persistent presence of double-strand DNA breaks (DSB) activates the ATR/Mei-41 checkpoint, delays progression through meiosis, and causes defects in DNA condensation of the oocyte nucleus, the karyosome. Checkpoint activation has also been linked to decreased levels of the TGFa-like molecule Gurken, which controls normal eggshell patterning. We used this easy-toscore eggshell phenotype in a germ-line mosaic screen in Drosophila to identify new genes affecting meiotic progression, DNA condensation, and Gurken signaling. One hundred eighteen new ventralizing mutants on the second chromosome fell into 17 complementation groups. Here we describe the analysis of 8 complementation groups, including Kinesin heavy chain, the SR protein kinase cuaba, the cohesin-related gene dPds5/cohiba, and the Tudor-domain gene montecristo. Our findings challenge the hypothesis that checkpoint activation upon persistent DSBs is exclusively mediated by ATR/Mei-41 kinase and instead reveal a more complex network of interactions that link DSB formation, checkpoint activation, meiotic delay, DNA condensation, and Gurken protein synthesis.

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Section: A S Cells Divide Checkpoints Delay the Transition Tomentioning

confidence: 99%

A Maternal Screen for Genes Regulating Drosophila Oocyte Polarity Uncovers New Steps in Meiotic Progression

2007

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“…In wildtype ovaries, γ-H2Av foci begin to accumulate in region 2 of the germarium, when the Spo11 nuclease (encoded by the mei-W68 gene) initiates meiotic breaks (McKim and Hayashi-Hagihara 1998). The axis specification defects associated with repair mutations are efficiently suppressed by mei-W68 mutations (Ghabrial and Schüpbach 1999;Morris and Lehmann 1999), confirming that meiotic breaks are the source of damage. However, the axis specification defects in armi mutants are not suppressed by mei-W68 (Table 1), and γ-H2Av foci in armi, aub, and spn-E appear to arise somewhat earlier than in wild-type controls.…”

Section: Discussionmentioning

confidence: 96%

rasiRNAs, DNA Damage, and Embryonic Axis Specification

Theurkauf

Klattenhoff²,

Bratu³

et al. 2006

Cold Spring Harbor Symposia on Quantitative Biology

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Drosophila repeat-associated small interfering RNAs (rasiRNAs) have been implicated in retrotransposon and stellate locus silencing. However, mutations in the rasiRNA pathway genes armitage, spindle-E, and aubergine disrupt embryonic axis specification, triggering defects in microtubule organization and localization of osk and grk mRNAs during oogenesis. We show that mutations in mei-41 and mnk, which encode ATR and Chk2 kinases that function in DNA damage signal transduction, dramatically suppress the cytoskeletal and RNA localization defects associated with rasiRNA mutations. In contrast, stellate and retrotransposon silencing are not restored in mei-41 and mnk double mutants. We also find that armitage, aubergine, and spindle-E mutations lead to germ-line-specific accumulation of γ-H2Av foci, which form at DNA double-strand breaks, and that mutations in armi lead to Chk2-dependent phosphorylation of Vasa, an RNA helicase required for axis specification. The Drosophila rasiRNA pathway thus appears to suppress DNA damage in the germ line, and mutations in this pathway block axis specification by activating an ATR/Chk2-dependent DNA damage response that disrupts microtubule polarization and RNA localization.

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“…spindle A (spn-A) and okra (okr). The respective proteins catalyse DNA-strand exchange as part of the recombination repair process (Ghabrial et al, 1998;Morris and Lehmann, 1999;Staeva-Vieira et al, 2003). Disruption of this well-conserved DSB repair machinery initiates a meiotic checkpoint, mediated by the activities of the Mei-41 and DmChk2 kinases, the Drosophila ATR and Chk2/Mnk homologues that act in DNA damage signalling (Abdu et al, 2002;overview in Shiloh, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…The epidermal growth factor receptor is activated in the dorsal follicle cells by the ligand Gurken (Grk) which is localised to the anterodorsal side of the oocyte. If Grk is absent or mislocalised then the dorsalising signal is missing, and the egg cannot develop dorsal appendages (Schüpbach, 1987; overview in Morris and Lehmann, 1999). If the meiotic checkpoint is active, i.e.…”

Section: Introductionmentioning

confidence: 99%

“…If the meiotic checkpoint is active, i.e. from persistent or increased numbers of DSBs, the germline helicase Vasa, which acts as a translation initiation factor of grk mRNA, is modified so that the efficient translation of grk mRNA is suppressed and the correct establishment of the dorsoventral axis is impaired (Abdu et al, 2002;Ghabrial and Schüpbach, 1999; overview in Morris and Lehmann, 1999). Thus the ventralised eggshell phenotype of the spindle class mutants is a side effect of meiotic checkpoint activation.…”

Section: Introductionmentioning

confidence: 99%

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Cyclin G is involved in meiotic recombination repair inDrosophila melanogaster

Nagel

Fischer

Szawinski

et al. 2012

Journal of Cell Science

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SummaryCyclin G (CycG) belongs to the atypical cyclins, which have diverse cellular functions. The two mammalian CycG genes, CycG1 and CycG2, regulate the cell cycle in response to cell stress. Detailed analyses of the role of the single Drosophila cycG gene have been hampered by the lack of a mutant. We generated a null mutant in the Drosophila cycG gene that is female sterile and produces ventralised eggs. This phenotype is typical of the downregulation of epidermal growth factor receptor (EGFR) signalling during oogenesis. Ventralised eggs are also observed in mutants (for example, mutants of the spindle class) that are defective in meiotic DNA double-strand break repair. Double-strand breaks (DSBs) induce a meiotic checkpoint by activating Mei-41 kinase (the Drosophila ATR homologue), thereby indirectly causing dorsoventral patterning defects. We provide evidence for the role of CycG in meiotic checkpoint control. The increased incidence of DSBs in cycG mutant germaria may reflect inefficient DSB repair. Therefore, the downregulation of Mei-W68 (an endonuclease that induces meiotic DSBs), Mei-41, or Drosophila melanogaster Chk2 (a downstream kinase that initiates the meiotic checkpoint) rescues the cycG mutant eggshell phenotype. In vivo, CycG associates with Rad9 and BRCA2. These two proteins are components of the 9-1-1 complex, which is involved in sensing DSBs and in activating meiotic checkpoint control. Therefore, we propose that CycG has a role in an early step of meiotic recombination repair, thereby affecting EGFR-mediated patterning processes during oogenesis.

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Drosophila oogenesis: Versatile spn doctors

Cited by 21 publications

References 19 publications

A Maternal Screen for Genes Regulating Drosophila Oocyte Polarity Uncovers New Steps in Meiotic Progression

A Maternal Screen for Genes Regulating Drosophila Oocyte Polarity Uncovers New Steps in Meiotic Progression

rasiRNAs, DNA Damage, and Embryonic Axis Specification

Cyclin G is involved in meiotic recombination repair inDrosophila melanogaster

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