title: The lack of autophagy triggers precocious activation of Notch signaling during Drosophila oogenesis.
abstract: BACKGROUND
  The proper balance of autophagy, a lysosome-mediated degradation process, is indispensable for oogenesis in Drosophila. We recently demonstrated that egg development depends on autophagy in the somatic follicle cells (FC), but not in the germline cells (GCs). However, the lack of autophagy only affects oogenesis when FCs are autophagy-deficient but GCs are wild type, indicating that a dysfunctional signaling between soma and germline may be responsible for the oogenesis defects. Thus, autophagy could play an essential role in modulating signal transduction pathways during egg development.
  
  
  RESULTS
  Here, we provide further evidence for the necessity of autophagy during oogenesis and demonstrate that autophagy is especially required in subsets of FCs. Generation of autophagy-deficient FCs leads to a wide range of phenotypes that are similar to mutants with defects in the classical cell-cell signaling pathways in the ovary. Interestingly, we observe that loss of autophagy leads to a precocious activation of the Notch pathway in the FCs as monitored by the expression of Cut and Hindsight, two downstream effectors of Notch signaling.
  
  
  CONCLUSIONS
  Our findings point to an unexpected function for autophagy in the modulation of the Notch signaling pathway during Drosophila oogenesis and suggest a function for autophagy in proper receptor activation. Egg development is affected by an imbalance of autophagy between signal sending (germline) and signal receiving cell (FC), thus the lack of autophagy in the germline is likely to decrease the amount of active ligand and accordingly compensates for increased signaling in autophagy-defective follicle cells.
authors.affiliation: Institute of Molecular Systems Biology, ETH Zurich, Zurich, Switzerland.
authors.forename: Julia M I
authors.initials: JM
authors.lastname: Barth
authors.forename: Ernst
authors.initials: E
authors.lastname: Hafen
authors.forename: Katja
authors.initials: K
authors.lastname: Köhler
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D001343:Autophagy / Q000235:genetics; D029721:Drosophila Proteins / Q000096:biosynthesis; D004331:Drosophila melanogaster / Q000378:metabolism / Q000502:physiology*; D005260:Female; D018398:Homeodomain Proteins / Q000096:biosynthesis; D009687:Nuclear Proteins / Q000096:biosynthesis; D009866:Oogenesis; D006080:Ovarian Follicle / Q000166:cytology / Q000378:metabolism*; D034622:RNA Interference; D034741:RNA, Small Interfering; D051880:Receptors, Notch / Q000378:metabolism*; D015398:Signal Transduction; D014157:Transcription Factors / Q000096:biosynthesis
chemical_list: D029721:Drosophila Proteins; D018398:Homeodomain Proteins; D009687:Nuclear Proteins; D034741:RNA, Small Interfering; D051880:Receptors, Notch; D014157:Transcription Factors; C066381:ct protein, Drosophila; C106513:peb protein, Drosophila