scholarly journals Border Cell Migration: A Model System for Live Imaging and Genetic Analysis of Collective Cell Movement

2015 ◽  
pp. 89-97 ◽  
Author(s):  
Mohit Prasad ◽  
Xiaobo Wang ◽  
Li He ◽  
Danfeng Cai ◽  
Denise J. Montell
Keyword(s):  
Cell Migration ◽  
Genetic Analysis ◽  
Cell Movement ◽  
Live Imaging ◽  
Model System ◽  
Border Cell ◽  
Border Cell Migration

Identification of mutations that cause cell migration defects in mosaic clones

Development ◽  
1999 ◽  
Vol 126 (9) ◽  
pp. 1869-1878 ◽  
Author(s):  
Y. Liu ◽  
D.J. Montell
Keyword(s):  
Cell Migration ◽  
Cell Motility ◽  
Hedgehog Signaling ◽  
Marker Gene ◽  
Cell Movement ◽  
Border Cells ◽  
Altered Expression ◽  
Border Cell ◽  
Recessive Mutations ◽  
Border Cell Migration

Cell movement is an important feature of animal development, wound healing and tumor metastasis; however, the mechanisms underlying cell motility remain to be elucidated. To further our understanding, it would be useful to identify all of the proteins that are essential for a cell to migrate, yet such information is not currently available for any cell type. We have carried out a screen for mutations affecting border cell migration in Drosophila. Mutations that cause defects in mosaic clones were identified, so that genes that are also required for viability could be detected. From 6000 mutagenized lines, 20 mutations on chromosome 2R were isolated that cause defects in border cell position. One of the mutations was dominant while all of the recessive mutations appeared to be homozygous lethal. This lethality was used to place the mutations into 16 complementation groups. Many of the mutations failed to complement cytologically characterized deficiencies, allowing their rapid mapping. Mutations in three loci altered expression of a marker gene in the border cells, whereas the remaining mutations did not. One mutation, which caused production of supernumerary border cells, was found to disrupt the costal-2 locus, indicating a role for Hedgehog signaling in border cell development. This screen identified many new loci required for border cell migration and our results suggest that this is a useful approach for elucidating the mechanisms involved in cell motility.

scholarly journals Hypoxia response pathway in border cell migration

2010 ◽  
Vol 4 (3) ◽  
pp. 391-395 ◽  
Author(s):  
Inna Djagaeva ◽  
Sergey Doronkin
Keyword(s):  
Cell Migration ◽  
Hypoxia Response ◽  
Border Cell ◽  
Border Cell Migration

scholarly journals Regulatory mechanisms required for DE-cadherin function in cell migration and other types of adhesion

2005 ◽  
Vol 170 (5) ◽  
pp. 803-812 ◽  
Author(s):  
Anne Pacquelet ◽  
Pernille Rørth
Keyword(s):  
Cell Migration ◽  
Cell Sorting ◽  
Model System ◽  
Regulatory Mechanisms ◽  
Border Cells ◽  
Specific Function ◽  
Additional Function ◽  
Border Cell ◽  
Cell Positioning

Cadherin-mediated adhesion can be regulated at many levels, as demonstrated by detailed analysis in cell lines. We have investigated the requirements for Drosophila melanogaster epithelial (DE) cadherin regulation in vivo. Investigating D. melanogaster oogenesis as a model system allowed the dissection of DE-cadherin function in several types of adhesion: cell sorting, cell positioning, epithelial integrity, and the cadherin-dependent process of border cell migration. We generated multiple fusions between DE-cadherin and α-catenin as well as point-mutated β-catenin and analyzed their ability to support these types of adhesion. We found that (1) although linking DE-cadherin to α-catenin is essential, regulation of the link is not required in any of these types of adhesion; (2) β-catenin is required only to link DE-cadherin to α-catenin; and (3) the cytoplasmic domain of DE-cadherin has an additional specific function for the invasive migration of border cells, which is conserved to other cadherins. The nature of this additional function is discussed.

Breaking a temporal barrier: signalling crosstalk regulates the initiation of border cell migration

2009 ◽  
Vol 11 (5) ◽  
pp. 536-538 ◽  
Author(s):  
Dorothea Godt ◽  
Ulrich Tepass
Keyword(s):  
Cell Migration ◽  
Border Cell ◽  
Border Cell Migration

The breathless FGF receptor homolog, a downstream target of Drosophila C/EBP in the developmental control of cell migration

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2255-2263 ◽  
Author(s):  
A.M. Murphy ◽  
T. Lee ◽  
C.M. Andrews ◽  
B.Z. Shilo ◽  
D.J. Montell
Keyword(s):  
Cell Migration ◽  
Molecular Mechanisms ◽  
Follicle Cells ◽  
Border Cells ◽  
Timely Initiation ◽  
Fgf Receptor ◽  
Border Cell ◽  
Downstream Target ◽  
Border Cell Migration ◽  
Factor C

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.

Jing: a downstream target of slbo required for developmental control of border cell migration

Development ◽  
2001 ◽  
Vol 128 (3) ◽  
pp. 321-330 ◽  
Author(s):  
Y. Liu ◽  
D.J. Montell
Keyword(s):  
Cell Migration ◽  
Leucine Zipper ◽  
Inducible Promoter ◽  
Regulatory Sequence ◽  
Border Cells ◽  
Border Cell ◽  
Downstream Target ◽  
Border Cell Migration ◽  
Factor C ◽  
Drosophila Ovary

Epithelial to mesenchymal transitions and cell migration are important features of embryonic development and tumor metastasis. We are employing a systematic genetic approach to study the border cells in the Drosophila ovary, as a simple model for these cellular behaviors. Previously we found that expression of the basic-region/leucine zipper transcription factor, C/EBP, is required for the border cells to initiate their migration. Here we report the identification of a second nuclear factor, named JING (which means ‘still’), that is required for initiation of border cell migration. The jing locus was identified in a screen for mutations that cause border cell migration defects in mosaic clones. The jing mutant phenotype resembles that of slbo mutations, which disrupt the Drosophila C/EBP gene, but is distinct from other classes of border cell migration mutants. Expression of a jing-lacZ reporter in border cells requires C/EBP. Moreover, expression of jing from a heat-inducible promoter rescues the border cell migration defects of hypomorphic slbo mutants. The JING protein is most closely related to a mouse protein, AEBP2, which was identified on the basis of its ability to bind a small regulatory sequence within the adipocyte AP2 gene to which mammalian C/EBP also binds. We propose that the need to coordinate cell differentiation with nutritional status may be the link between mammalian adipocytes and Drosophila border cells that led to the conservation of C/EBP and AEBP2.

Sign in / Sign up

Export Citation Format

Share Document