Role of Scrib and Dlg in anterior-posterior patterning of the follicular epithelium during Drosophila oogenesis.
BACKGROUND
Proper patterning of the follicle cell epithelium over the egg chamber is essential for the Drosophila egg development. Differentiation of the epithelium into several distinct cell types along the anterior-posterior axis requires coordinated activities of multiple signaling pathways. Previously, we reported that lethal(2)giant larvae (lgl), a Drosophila tumor suppressor gene, is required in the follicle cells for the posterior follicle cell (PFC) fate induction at mid-oogenesis. Here we explore the role of another two tumor suppressor genes, scribble (scrib) and discs large (dlg), in the epithelial patterning.


RESULTS
We found that removal of scrib or dlg function from the follicle cells at posterior terminal of the egg chamber causes a complete loss of the PFC fate. Aberrant specification and differentiation of the PFCs in the mosaic clones can be ascribed to defects in coordinated activation of the EGFR, JAK and Notch signaling pathways in the multilayered cells. Meanwhile, the clonal analysis revealed that loss-of-function mutations in scrib/dlg at the anterior domains result in a partially penetrant phenotype of defective induction of the stretched and centripetal cell fate, whereas specification of the border cell fate can still occur in the most anterior region of the mutant clones. Further, we showed that scrib genetically interacts with dlg in regulating posterior patterning of the epithelium.


CONCLUSIONS
In this study we provide evidence that scrib and dlg function differentially in anterior and posterior patterning of the follicular epithelium at oogenesis. Further genetic analysis indicates that scrib and dlg act in a common pathway to regulate PFC fate induction. This study may open another window for elucidating role of scrib/dlg in controlling epithelial polarity and cell proliferation during development.
Li
Qi
Q
MoE Key Laboratory of Developmental Genetics and Neuropsychiatric Diseases, Bio-X Center, School of Life Science and Biotechnology, Shanghai Jiao Tong University, 200240 Shanghai, PR China.emc0013@sjtu.edu.cn
Shen
Ling
L
Xin
Tianchi
T
Xiang
Wenjuan
W
Chen
Wenlian
W
Gao
Yin
Y
Zhu
Mingwei
M
Yu
Lingzhu
L
Li
Mingfa
M
D000818:Animals; D019521:Body Patterning / Q000235:genetics / Q000502:physiology; D002454:Cell Differentiation / Q000235:genetics / Q000502:physiology; D004330:Drosophila; D029721:Drosophila Proteins / Q000235:genetics / Q000502:physiology*; D004848:Epithelium / Q000196:embryology* / Q000378:metabolism*; D005260:Female; D008565:Membrane Proteins / Q000235:genetics / Q000502:physiology*; D009866:Oogenesis / Q000235:genetics / Q000502:physiology*; D006080:Ovarian Follicle / Q000166:cytology / Q000196:embryology* / Q000378:metabolism*; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000502:physiology*
D029721:Drosophila Proteins; D008565:Membrane Proteins; C404683:Scrib protein, Drosophila; D025521:Tumor Suppressor Proteins; C070350:dlg1 protein, Drosophila