FB2026_03 , released September 17, 2026
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Citation
Thomalla, J.M., Giedt, M.S., White, R.P., Wipf, I.J., Shipley, A., Chen, M., Welte, M.A., Tootle, T.L. (2025). The lipid droplet protein Jabba promotes actin remodeling downstream of prostaglandin signaling during Drosophila oogenesis.  Mol. Biol. Cell 36(9): ar105.
FlyBase ID
FBrf0263122
Publication Type
Research paper
Abstract
Growing evidence supports that lipid droplets (LD) are critical for producing high-quality oocytes. However, the functions of LDs during oocyte development remain largely unknown. Using Drosophila oogenesis as a model, we previously discovered that the LD-associated Adipose Triglyceride Lipase (ATGL) promotes actin remodeling necessary for oocyte development by providing the substrate for producing lipid signals termed prostaglandins (PG). Here, we find that Jabba, a LD-associated protein best known for its role in anchoring other proteins to LDs, also promotes PG-dependent actin remodeling. Overexpression of Jabba results in thickened cortical actin and excessive actin bundles, whereas loss of Jabba results in cortical actin breakdown and severely defective actin bundle formation. We find that Jabba regulates actin remodeling in conjunction with PG signaling. However, the lack of a genetic interaction between Jabba and ATGL suggests the PG-Jabba pathway is independent of ATGL. These data are consistent with the model that there are multiple PG signaling pathways promoting actin remodeling. Overexpression of Jabba rescues the actin defects when PG signaling is lost. Together, these data lead to the model that PGs produced independently of ATGL positively regulate Jabba to promote actin remodeling necessary for follicle morphogenesis.
PubMed ID
PubMed Central ID
PMC12415609 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Mol. Biol. Cell
    Title
    Molecular Biology of the Cell
    Publication Year
    1992-
    ISBN/ISSN
    1059-1524
    Data From Reference