ArticlePloS one2010
Reduced cul-5 activity causes aberrant follicular morphogenesis and germ cell loss in Drosophila oogenesis.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Cul2 Is Essential for theInternational journal of molecular sciences · 2025Article
- Functional complementation of two splicing variants of Gustavus in Neocaridina denticulata sinensis during ovarian maturation.Scientific reports · 2024Article
- Oocyte competence is maintained by mCell death and differentiation · 2020Article
- The functions and properties of cullin-5, a potential therapeutic target for cancers.American journal of translational research · 2020Review
- Drosophila SOCS36E negatively regulates JAK/STAT pathway signaling via two separable mechanisms.Molecular biology of the cell · 2013Article
- Role of the insulin/Tor signaling network in starvation-induced programmed cell death in Drosophila oogenesis.Cell death and differentiation · 2012Article
- Cullin-5 and cullin-2 play a role in the development of neuromuscular junction and the female germ line of Drosophila.Journal of genetics · 2011Article
- cDNA cloning and expression analysis of gustavus gene in the oriental river prawn Macrobrachium nipponense.PloS one · 2011Article
- The cullin protein family.Genome biology · 2011Review
- Regulation of Drosophila vasa in vivo through paralogous cullin-RING E3 ligase specificity receptors.Molecular and cellular biology · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Drosophila oogenesis is especially well suited for studying stem cell biology, cellular differentiation, and morphogenesis. The small modifier protein ubiquitin regulates many cellular pathways. Ubiquitin is conjugated to target proteins by a diverse class of enzymes called ubiquitin E3 ligases. Here we characterize the requirement of Cul-5, a key component of a subgroup of Cullin-RING-type ubiquitin E3 ligases, in Drosophila oogenesis. We find that reduced cul-5 activity causes the formation of aberrant follicles that are characterized by excess germ cells. We show that germ line cells overproliferate in cul-5 mutant females, causing the formation of abnormally large germ line cysts. Also, the follicular epithelium that normally encapsulates single germ line cysts develops aberrantly in cul-5 mutant, leading to defects in cyst formation. We additionally found that Cul-5 is required for germ cell maintenance, as germ cells are depleted in a substantial fraction of cul-5 mutant ovaries. All of these cul-5 phenotypes are strongly enhanced by reduced activity of gustavus (gus), which encodes a substrate receptor of Cul-5-based ubiquitin E3 ligases. Taken together, our results implicate Cul-5/Gus ubiquitin E3 ligases in ovarian tissue morphogenesis, germ cell proliferation and maintenance of the ovarian germ cell population.
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