期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 28, 期 6, 页码 1964-1973出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.01743-07
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资金
- NCI NIH HHS [R01CA128002, P01 CA078582, R01 CA128002-04, R01 CA109860, R01 CA109860-04, P01 CA078582-080005, R01 CA128002] Funding Source: Medline
- NIGMS NIH HHS [R01 GM057843-08, R01GM57843, R01 GM057843] Funding Source: Medline
Border cell migration during Drosophila melanogaster oogenesis is a highly pliable model for studying epithelial to mesenchymal transition and directional cell migration. The process involves delamination of a group of 6 to 10 follicle cells from the epithelium followed by guided migration and invasion through the nurse cell complex toward the oocyte. The guidance cue is mainly provided by the homolog of platelet-derived growth factor/vascular endothelial growth factor family of growth factor, or Pvf, emanating from the oocyte, although Drosophila epidermal growth factor receptor signaling also plays an auxiliary role. Earlier studies implicated a stringent control of the strength of Pvf-mediated signaling since both down-regulation of Pvf and overexpression of active Pvf receptor (Pvr) resulted in stalled border cell migration. Here we show that the metastasis suppressor gene homolog Nm23/awd is a negative regulator of border cell migration. Its down-regulation allows for optimal spatial signaling from two crucial pathways, Pvr and JAK/STAT. Its overexpression in the border cells results in stalled migration and can revert the phenotype of overexpressing constitutive Pvr or dominant-negative dynamin. This is a rare example demonstrating the relevance of a metastasis suppressor gene function utilized in a developmental process involving cell invasion.
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