scholarly journals Impact of carbon dioxide versus air pneumoperitoneum on peritoneal cell migration and cell fate

2006 ◽  
Vol 20 (10) ◽  
pp. 1607-1613 ◽  
Author(s):  
U. Moehrlen ◽  
U. Ziegler ◽  
E. Boneberg ◽  
E. Reichmann ◽  
C. A. Gitzelmann ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Cell Migration ◽  
Cell Fate ◽  
Peritoneal Cell

Pax6-induced alteration of cell fate: Shape changes, expression of neuronal α tubulin, postmitotic phenotype, and cell migration

2006 ◽  
Vol 66 (5) ◽  
pp. 421-436 ◽  
Author(s):  
Laetitia Cartier ◽  
Terese Laforge ◽  
Anis Feki ◽  
Serge Arnaudeau ◽  
Michel Dubois-Dauphin ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Fate ◽  
Shape Changes

scholarly journals Wnt signaling promotes proliferation and stemness regulation of spermatogonial stem/progenitor cells

Reproduction ◽  
2009 ◽  
Vol 138 (1) ◽  
pp. 151-162 ◽  
Author(s):  
Nady Golestaneh ◽  
Elspeth Beauchamp ◽  
Shannon Fallen ◽  
Maria Kokkinaki ◽  
Aykut Üren ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Growth Factors ◽  
Progenitor Cells ◽  
Cell Fate ◽  
Morphological Changes ◽  
Embryonic Stem ◽  
Large Family ◽  
Self Renewal ◽  
Fate Determination

Spermatogonial stem cells (SSCs) self-renew throughout life to produce progenitor cells that are able to differentiate into spermatozoa. However, the mechanisms underlying the cell fate determination between self-renewal and differentiation have not yet been delineated. Culture conditions and growth factors essential for self-renewal and proliferation of mouse SSCs have been investigated, but no information is available related to growth factors that affect fate determination of human spermatogonia. Wnts form a large family of secreted glycoproteins, the members of which are involved in cell proliferation, differentiation, organogenesis, and cell migration. Here, we show that Wnts and their receptors Fzs are expressed in mouse spermatogonia and in the C18-4 SSC line. We demonstrate that WNT3A induces cell proliferation, morphological changes, and cell migration in C18-4 cells. Furthermore, we show that β-catenin is activated during testis development in 21-day-old mice. In addition, our study demonstrates that WNT3A sustained adult human embryonic stem (ES)-like cells derived from human germ cells in an undifferentiated stage, expressing essential human ES cell transcription factors. These results demonstrate for the first time that Wnt/β-catenin pathways, especially WNT3A, may play an important role in the regulation of mouse and human spermatogonia.

Mutations in the Drosophila gene bullwinkle cause the formation of abnormal eggshell structures and bicaudal embryos

Development ◽  
1995 ◽  
Vol 121 (9) ◽  
pp. 3023-3033 ◽  
Author(s):  
K.R. Rittenhouse ◽  
C.A. Berg
Keyword(s):  
Cell Migration ◽  
Cell Fate ◽  
Germ Line ◽  
Follicle Cell ◽  
Posterior Pole ◽  
Mirror Image ◽  
Follicle Cells ◽  
Anterior Pole ◽  
Posterior Group ◽  
General Transport

Subcellular localization of gene products and cell migration are both critical for pattern formation during development. The bullwinkle gene is required in Drosophila for disparate aspects of these processes. In females mutant at the bullwinkle locus, the follicle cells that synthesize the dorsal eggshell filaments do not migrate properly, creating short, broad structures. Mosaic analyses demonstrate that wild-type BULLWINKLE function is required in the germ line for these migrations. Since the mRNA for gurken, the putative ligand that signals dorsal follicle cell fate, is correctly localized in bullwinkle mutants, we conclude that our bullwinkle alleles do not affect the dorsoventral polarity of the oocyte and thus must be affecting the follicle cell migrations in some other way. In addition, the embryos that develop from bullwinkle mothers are bicaudal. A KINESIN:beta-GALACTOSIDASE fusion protein is correctly localized to the posterior pole of bullwinkle oocytes during stage 9. Thus, the microtubule structure of the oocyte and general transport along it do not appear to be disrupted prior to cytoplasmic streaming. Unlike other bicaudal mutants, oskar mRNA is localized correctly to the posterior pole of the oocyte at stage 10. By early embryogenesis, however, some oskar mRNA is mislocalized to the anterior pole. Consistent with the mislocalization of oskar mRNA, a fraction of the VASA protein and nanos mRNA are also mislocalized to the anterior pole of bullwinkle embryos. Mislocalization of nanos mRNA to the anterior is dependent on functional VASA protein. Although the mirror-image segmentation defects appear to result from the action of the posterior group genes, germ cells are not formed at the anterior pole. The bicaudal phenotype is also germ-line dependent for bullwinkle. We suspect that BULLWINKLE interacts with the cytoskeleton and extracellular matrix and is necessary for gene product localization and cell migration during oogenesis after stage 10a.

scholarly journals Tousled-like kinase regulates cytokine-mediated communication between cooperating cell types during collective border cell migration

2016 ◽  
Vol 27 (1) ◽  
pp. 12-19 ◽  
Author(s):  
Wenjuan Xiang ◽  
Dabing Zhang ◽  
Denise J. Montell
Keyword(s):  
Cell Migration ◽  
Cell Fate ◽  
Molecular Mechanisms ◽  
Metastatic Cancer ◽  
Cell Types ◽  
Collective Cell Migration ◽  
Border Cells ◽  
Border Cell ◽  
Stat Signaling ◽  
Border Cell Migration

Collective cell migration is emerging as a major contributor to normal development and disease. Collective movement of border cells in the Drosophila ovary requires cooperation between two distinct cell types: four to six migratory cells surrounding two immotile cells called polar cells. Polar cells secrete a cytokine, Unpaired (Upd), which activates JAK/STAT signaling in neighboring cells, stimulating their motility. Without Upd, migration fails, causing sterility. Ectopic Upd expression is sufficient to stimulate motility in otherwise immobile cells. Thus regulation of Upd is key. Here we report a limited RNAi screen for nuclear proteins required for border cell migration, which revealed that the gene encoding Tousled-like kinase (Tlk) is required in polar cells for Upd expression without affecting polar cell fate. In the absence of Tlk, fewer border cells are recruited and motility is impaired, similar to inhibition of JAK/STAT signaling. We further show that Tlk in polar cells is required for JAK/STAT activation in border cells. Genetic interactions further confirmed Tlk as a new regulator of Upd/JAK/STAT signaling. These findings shed light on the molecular mechanisms regulating the cooperation of motile and nonmotile cells during collective invasion, a phenomenon that may also drive metastatic cancer.

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