Identification of Novel Drosophila Meiotic Genes Recovered in a P-Element Screen

Sekelsky, Jeff; McKim, Kim S.; Messina, L; French, Rachael L.; Hurley, W D; Arbel, T; Chin, Gregory M.; Deneen, Benjamin; Force, S J; Hari, Kumar; Jang, Janet K.; Laurençon, Anne; Madden, LD; Matthies, H; Milliken, D B; Page, Scott L.; Ring, A D; Wayson, Sarah M.; Zimmerman, C C; Hawley, R. Scott

doi:10.1093/genetics/152.2.529

Cited by 83 publications

(10 citation statements)

References 50 publications

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“…Screens in Drosophila have recovered many mutations that cause disruption to normal meiotic chromosome behavior (Baker and Carpenter, 1972; Sandler, 1974; Sekelsky et al ., 1999; McKim et al ., 2002). They were identified based on the ability to recognize abnormal events, such as chromosome loss, non‐disjunction or a change in recombination frequency.…”

Section: Discussionmentioning

confidence: 99%

An essential role of DmRad51/SpnA in DNA repair and meiotic checkpoint control

2003

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Rad51 is a conserved protein essential for recombinational repair of double‐stranded DNA breaks (DSBs) in somatic cells and during meiosis in germ cells. Yeast Rad51 mutants are viable but show meiosis defects. In the mouse, RAD51 deletions cause early embryonic death, suggesting that in higher eukaryotes Rad51 is required for viability. Here we report the identification of SpnA as the Drosophila Rad51 gene, whose sequence among the five known Drosophila Rad51‐like genes is most closely related to the Rad51 homologs of human and yeast. DmRad51/spnA null mutants are viable but oogenesis is disrupted by the activation of a meiotic recombination checkpoint. We show that the meiotic phenotypes result from an inability to effectively repair DSBs. Our study further demonstrates that in Drosophila the Rad51‐dependent homologous recombination pathway is not essential for DNA repair in the soma, unless exposed to DNA damaging agents. We therefore propose that under normal conditions a second, Rad51‐independent, repair pathway prevents the lethal effects of DNA damage.

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Section: Discussionmentioning

confidence: 99%

An essential role of DmRad51/SpnA in DNA repair and meiotic checkpoint control

2003

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“…The y 1 cv 1 IP3K2 wy-74i f 1 stock was generated by isolating a recombinant between cv 1 and IP3K2 wy-74i from y 1 cv 1 v 1 f 1 /sc 1 ec 1 IP3K2 wy-74i f 1 females (Bloomington Drosophila Stock Center #1274). This new y 1 cv 1 IP3K2 wy-74i f 1 stock was partially isogenized by crossing the single male recombinant to FM7w females [ 29 ]. We refer to IP3K2 wy-74i as wy in the main text for clarity.…”

Section: Methodsmentioning

confidence: 99%

Heterozygous inversion breakpoints suppress meiotic crossovers by altering recombination repair outcomes

Berent

Hadjipanteli

et al. 2023

PLoS Genet

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Heterozygous chromosome inversions suppress meiotic crossover (CO) formation within an inversion, potentially because they lead to gross chromosome rearrangements that produce inviable gametes. Interestingly, COs are also severely reduced in regions nearby but outside of inversion breakpoints even though COs in these regions do not result in rearrangements. Our mechanistic understanding of why COs are suppressed outside of inversion breakpoints is limited by a lack of data on the frequency of noncrossover gene conversions (NCOGCs) in these regions. To address this critical gap, we mapped the location and frequency of rare CO and NCOGC events that occurred outside of the dl-49 chrX inversion in D. melanogaster. We created full-sibling wildtype and inversion stocks and recovered COs and NCOGCs in the syntenic regions of both stocks, allowing us to directly compare rates and distributions of recombination events. We show that COs outside of the proximal inversion breakpoint are distributed in a distance-dependent manner, with strongest suppression near the inversion breakpoint. We find that NCOGCs occur evenly throughout the chromosome and, importantly, are not suppressed near inversion breakpoints. We propose a model in which COs are suppressed by inversion breakpoints in a distance-dependent manner through mechanisms that influence DNA double-strand break repair outcome but not double-strand break formation. We suggest that subtle changes in the synaptonemal complex and chromosome pairing might lead to unstable interhomolog interactions during recombination that permits NCOGC formation but not CO formation.

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“…Consistent with a model wherein GATOR2 opposes the activity of GATOR1 and DSBs, eliminating GATOR1 or DSBs suppresses mio mutant phenotypes in flies 18,39,45 . Spo11 (SPO11 initiator of meiotic double stranded breaks) is a conserved, essential enzyme for generating meiotic DSBs [46][47][48] . In zebrafish, Spo11 is not required for viability or oocyte production in females, although mutant gametes are likely aneuploid because embryos of mutant mothers are not viable 48 .…”

Section: Mios Is Required For Oocyte Differentiation Independent Of D...mentioning

confidence: 99%

Rbpms2 promotes female fate upstream of the nutrient sensing Gator2 complex component, Mios

Marlow,

Wilson,

Romano

et al. 2024

Preprint

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Reproductive success relies on proper establishment and maintenance of biological sex. In many animals, including mammals, the primary gonad is initially ovary in character. We previously showed the RNA binding protein (RNAbp), Rbpms2, is required for ovary fate in zebrafish. Here, we identified Rbpms2 targets in oocytes (Rbpms2-bound oocyte RNAs; rboRNAs). We identify Rbpms2 as a translational regulator of rboRNAs, which include testis factors and ribosome biogenesis factors. Further, genetic analyses indicate that Rbpms2 promotes nucleolar amplification via the mTorc1 signaling pathway, specifically through the mTorc1-activating Gap activity towards Rags 2 (Gator2) component, Missing oocyte (Mios). Cumulatively, our findings indicate that early gonocytes are in a dual poised, bipotential state in which Rbpms2 acts as a binary fate-switch. Specifically, Rbpms2 represses testis factors and promotes oocyte factors to promote oocyte progression through an essential Gator2-mediated checkpoint, thereby integrating regulation of sexual differentiation factors and nutritional availability pathways in zebrafish oogenesis.

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Identification of Novel Drosophila Meiotic Genes Recovered in a P-Element Screen

Cited by 83 publications

References 50 publications

An essential role of DmRad51/SpnA in DNA repair and meiotic checkpoint control

An essential role of DmRad51/SpnA in DNA repair and meiotic checkpoint control

Heterozygous inversion breakpoints suppress meiotic crossovers by altering recombination repair outcomes

Rbpms2 promotes female fate upstream of the nutrient sensing Gator2 complex component, Mios

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