scholarly journals Understanding morphogenesis in Drosophila oogenesis: Role of insulin signaling in border cell migration

2017 ◽  
Vol 145 ◽  
pp. S21
Author(s):  
Aditi Sharma ◽  
Mohit Prasad
2011 ◽  
Vol 195 (4) ◽  
pp. 540-541
Author(s):  
Caitlin Sedwick

Montell studies Drosophila oogenesis, focusing primarily on the collective migration of border cells.


Chromosoma ◽  
2018 ◽  
Vol 127 (4) ◽  
pp. 475-487 ◽  
Author(s):  
Anna A. Ogienko ◽  
Lyubov A. Yarinich ◽  
Elena V. Fedorova ◽  
Mikhail O. Lebedev ◽  
Evgeniya N. Andreyeva ◽  
...  

2002 ◽  
Vol 111 (1-2) ◽  
pp. 115-123 ◽  
Author(s):  
Simone Beccari ◽  
Luı́s Teixeira ◽  
Pernille Rørth

2012 ◽  
Vol 2 (11) ◽  
pp. 1379-1391 ◽  
Author(s):  
George Aranjuez ◽  
Elizabeth Kudlaty ◽  
Michelle S. Longworth ◽  
Jocelyn A. McDonald

2019 ◽  
Author(s):  
Maureen C. Lamb ◽  
Kelsey K. Anliker ◽  
Tina L. Tootle

AbstractFascin is an actin bundling protein that is essential for developmental cell migrations and promotes cancer metastasis. In addition to bundling actin, Fascin has several actin-independent roles. Border cell migration during Drosophila oogenesis provides an excellent model to study Fascin’s various roles during invasive, collective cell migration. Border cell migration requires Fascin. Fascin functions not only within the migrating border cells, but also within the nurse cells, the substrate for this migration. Loss of Fascin results in increased, shorter and mislocalized protrusions during migration. Data supports the model that Fascin promotes the activity of Enabled, an actin elongating factor, to regulate migration. Additionally, loss of Fascin inhibits border cell delamination. These defects are partially due to altered E-cadherin localization in the border cells; this is predicted to be an actin-independent role of Fascin. Overall, Fascin is essential for multiple aspects of this invasive, collective cell migration, and functions in both actin-dependent and -independent manners. These findings have implications beyond Drosophila, as border cell migration has emerged as a model to study mechanisms mediating cancer metastasis.


2010 ◽  
Vol 4 (3) ◽  
pp. 391-395 ◽  
Author(s):  
Inna Djagaeva ◽  
Sergey Doronkin

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2255-2263 ◽  
Author(s):  
A.M. Murphy ◽  
T. Lee ◽  
C.M. Andrews ◽  
B.Z. Shilo ◽  
D.J. Montell

To investigate the molecular mechanisms responsible for the temporal and spatial control of cell movements during development, we have been studying the migration of a small group of follicle cells, called the border cells, in the Drosophila ovary. Timely initiation of border cell migration requires the product of the slow border cells (slbo) locus, which encodes the Drosophila homolog of the transcription factor C/EBP. Here we report evidence that one target of C/EBP in the control of border cell migration is the FGF receptor homolog encoded by the breathless (btl) locus. btl expression in the ovary was border cell-specific, beginning just prior to the migration, and this expression was reduced in slbo mutants. btl mutations dominantly enhanced the border cell migration defects found in weak slbo alleles. Furthermore, C/EBP-independent btl expression was able to rescue the migration defects of hypomorphic slbo alleles. Purified Drosophila C/EBP bound eight sites in the btl 5′ flanking region by DNAse I footprinting. Taken together these results suggest that btl is a key, direct target for C/EBP in the regulation of border cell migration.


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