The fully linked HTML version of this article has now been published.
Development ePress online publication date 6 Jul 2005
doi: 10.1242/dev.01910
Research article
Requirement for JAK/STAT signaling throughout border cell migration in Drosophila
Debra L. Silver,
Erika R. Geisbrecht,
and
Denise J. Montell*
* Author for correspondence (e-mail: dmontell{at}jhmi.edu)
The evolutionarily conserved JAK/STAT signaling pathway is essential for the proliferation, survival and differentiation of many cells including cancer cells. Recent studies have implicated this transcriptional pathway in the process of cell migration in humans, mice, Drosophila and Dictyostelium. In the Drosophila ovary, JAK/STAT signaling is necessary and sufficient for the specification and migration of a group of cells called the border cells; however, it is not clear to what extent the requirement for cell fate is distinct from that for cell migration. We found that STAT protein is enriched in the migrating border cells throughout their migration and is an indicator of cells with highest JAK/STAT activity. In addition, statts mutants exhibited border cell migration defects after just 30 minutes at the non-permissive temperature, prior to any detectable change in the expression of cell fate markers. At later times, cell fate changes became evident, indicating that border cell fate is labile. JAK/STAT signaling was also required for organization of the border cell cluster. Finally, we show that both the accumulation of STAT protein and nuclear accumulation are positively regulated by JAK/STAT activity. The activity of the pathway is negatively regulated by overexpression of a SOCS protein and by blocking endocytosis. Together, our findings suggest that the requirement for STAT in border cells extends beyond the initial specification and delamination of cells from the epithelium.
This article has been cited by other articles:
|
|
|
|
 
M. Zhao, P. Szafranski, C. A. Hall, and S. Goode
Basolateral Junctions Utilize Warts Signaling to Control Epithelial-Mesenchymal Transition and Proliferation Crucial For Migration and Invasion of Drosophila Ovarian Epithelial Cells
Genetics,
April 1, 2008;
178(4):
1947 - 1971.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Nallamothu, J. A. Woolworth, V. Dammai, and T. Hsu
awd, the Homolog of Metastasis Suppressor Gene Nm23, Regulates Drosophila Epithelial Cell Invasion
Mol. Cell. Biol.,
March 15, 2008;
28(6):
1964 - 1973.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
O. Devergne, C. Ghiglione, and S. Noselli
The endocytic control of JAK/STAT signalling in Drosophila
J. Cell Sci.,
October 1, 2007;
120(19):
3457 - 3464.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Bastock and D. Strutt
The planar polarity pathway promotes coordinated cell migration during Drosophila oogenesis
Development,
September 1, 2007;
134(17):
3055 - 3064.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Furriols, G. Ventura, and J. Casanova
Two distinct but convergent groups of cells trigger Torso receptor tyrosine kinase activation by independently expressing torso-like
PNAS,
July 10, 2007;
104(28):
11660 - 11665.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Grammont
Adherens junction remodeling by the Notch pathway in Drosophila melanogaster oogenesis
J. Cell Biol.,
April 9, 2007;
177(1):
139 - 150.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Marchetti, M.-N. Monier, A. Fradagrada, K. Mitchell, F. Baychelier, P. Eid, L. Johannes, and C. Lamaze
Stat-mediated Signaling Induced by Type I and Type II Interferons (IFNs) Is Differentially Controlled through Lipid Microdomain Association and Clathrin-dependent Endocytosis of IFN Receptors
Mol. Biol. Cell,
July 1, 2006;
17(7):
2896 - 2909.
[Abstract]
[Full Text]
[PDF]
|
|
|
© The Company of Biologists Ltd 2005
