Format

Send to

Choose Destination
See comment in PubMed Commons below
Dev Biol. 2015 Feb 15;398(2):206-17. doi: 10.1016/j.ydbio.2014.11.021. Epub 2014 Dec 3.

Somatic insulin signaling regulates a germline starvation response in Drosophila egg chambers.

Author information

1
Department of Cell Biology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, United States.
2
Graduate School of Life and Environmental Sciences, University of Tsukuba, Seinou-tou D301, Tennoudai 1-1-1, Tsukuba,, Ibaraki 305-8572, Japan.
3
Department of Genetics, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, United States.
4
Department of Cell Biology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, United States; Department of Genetics, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, United States; Department of Molecular, Cellular and Developmental Biology, Yale University, 260 Prospect Street, New Haven, CT 06510, United States. Electronic address: lynn.cooley@yale.edu.

Abstract

Egg chambers from starved Drosophila females contain large aggregates of processing (P) bodies and cortically enriched microtubules. As this response to starvation is rapidly reversed upon re-feeding females or culturing egg chambers with exogenous bovine insulin, we examined the role of endogenous insulin signaling in mediating the starvation response. We found that systemic Drosophila insulin-like peptides (dILPs) activate the insulin pathway in follicle cells, which then regulate both microtubule and P body organization in the underlying germline cells. This organization is modulated by the motor proteins Dynein and Kinesin. Dynein activity is required for microtubule and P body organization during starvation, while Kinesin activity is required during nutrient-rich conditions. Blocking the ability of egg chambers to form P body aggregates in response to starvation correlated with reduced progeny survival. These data suggest a potential mechanism to maximize fecundity even during periods of poor nutrient availability, by mounting a protective response in immature egg chambers.

KEYWORDS:

Dynein; Insulin; Kinesin; Microtubule; Oogenesis; P body

PMID:
25481758
PMCID:
PMC4340711
DOI:
10.1016/j.ydbio.2014.11.021
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center