scholarly journals Tetraspanin Cd9b and Cxcl12a/Cxcr4b have a synergistic effect on the control of collective cell migration

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0260372
Author(s):  
Katherine S. Marsay ◽  
Sarah Greaves ◽  
Harsha Mahabaleshwar ◽  
Charmaine Min Ho ◽  
Henry Roehl ◽  
...  

Collective cell migration is essential for embryonic development and homeostatic processes. During zebrafish development, the posterior lateral line primordium (pLLP) navigates along the embryo flank by collective cell migration. The chemokine receptors, Cxcr4b and Cxcr7b, as well as their cognate ligand, Cxcl12a, are essential for this process. We corroborate that knockdown of the zebrafish cd9 tetraspanin orthologue, cd9b, results in mild pLL abnormalities. Through generation of CRISPR and TALEN mutants, we show that cd9a and cd9b function partially redundantly in pLLP migration, which is delayed in the cd9b single and cd9a; cd9b double mutants. This delay led to a transient reduction in neuromast numbers. Loss of both Cd9a and Cd9b sensitized embryos to reduced Cxcr4b and Cxcl12a levels. Together these results provide evidence that Cd9 modulates collective cell migration of the pLLP during zebrafish development. One interpretation of these observations is that Cd9 contributes to more effective chemokine signalling.

2021 ◽  
Author(s):  
Katherine S Marsay ◽  
Sarah Greaves ◽  
Henry Roehl ◽  
Peter N Monk ◽  
Thomas J Carney ◽  
...  

Collective cell migration is essential for embryonic development and homeostatic processes. During zebrafish development, the posterior lateral line primordium (pLLP) navigates along the embryo flank by collective cell migration. The chemokine receptors, CXCR4b and CXCR7b, as well as their cognate ligand, CXCL12a, are essential for this process. Knockdown of the zebrafish CD9 tetraspanin orthologue, cd9b, displayed mild pLL abnormalities. Through generation of CRISPR mutants, we show that cd9a and cd9b function partially redundantly in pLLP migration, which is delayed in the cd9b single and cd9a; cd9b double mutants. This delay led to a transient reduction in neuromast numbers. Loss of both CD9a and CD9b sensitized embryos to reduced CXCR4b and CXCL12a levels. Together these results provide evidence that CD9 modulates collective cell migration of the pLLP through promoting CXCR4b signalling.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Akihiro Urasaki ◽  
Seiya Morishita ◽  
Kosuke Naka ◽  
Minato Uozumi ◽  
Kouki Abe ◽  
...  

2021 ◽  
Author(s):  
Jerónimo R. Miranda-Rodríguez ◽  
Augusto Borges ◽  
Filipe Pinto-Teixeira ◽  
Indra Wibowo ◽  
Hans-Martin Pogoda ◽  
...  

SUMMARYTissue remodeling presents an enormous challenge to the stability of intercellular signaling domains. Here we investigate this issue during the development of the posterior lateral line in zebrafish. We find that the transcriptional co-activator and phosphatase Eya1, mutated in the branchio-oto-renal syndrome in humans, is essential for the homeostasis of the Wnt/β-catenin and FGF morphogenetic domains during the collective migration of lateral-line primordial cells. Loss of Eya1 strongly diminishes the expression of Dkk1, expanding Wnt/β-catenin activity in the primordium, which in turn abrogates FGFR1 expression. Deficits in Eya1 also abolishes the expression of the chemokine receptor CXCR7b, disrupting primordium migration. These results reinforce the concept that morphogenetic domains in dynamically remodeling tissues are formed by cellular states maintained by continuous signaling.


2014 ◽  
Vol 385 (2) ◽  
pp. 316-327 ◽  
Author(s):  
Hui Xu ◽  
Ding Ye ◽  
Martine Behra ◽  
Shawn Burgess ◽  
Songhai Chen ◽  
...  

2016 ◽  
Vol 419 (2) ◽  
pp. 321-335 ◽  
Author(s):  
Marina Venero Galanternik ◽  
Mark E. Lush ◽  
Tatjana Piotrowski

Author(s):  
Ramona Dries ◽  
Annemarie Lange ◽  
Sebastian Heiny ◽  
Katja I. Berghaus ◽  
Martin Bastmeyer ◽  
...  

The posterior lateral line system (pLLS) of aquatic animals comprises small clustered mechanosensory organs along the side of the animal. They develop from proneuromasts, which are deposited from a migratory primordium on its way to the tip of the tail. We here show, that the Neural Cell Adhesion Molecule Ncam1b is an integral part of the pathways initiating and regulating the development of the pLLS in zebrafish. We find that morpholino-knockdowns of ncam1b (i) reduce cell proliferation within the primordium, (ii) reduce the expression of Fgf target gene erm, (iii) severely affect proneuromast formation, and (iv) affect primordium migration. Ncam1b directly interacts with Fgf receptor Fgfr1a, and a knockdown of fgfr1a causes similar phenotypic changes as observed in ncam1b-morphants. We conclude that Ncam1b is involved in activating proliferation by triggering the expression of erm. In addition, we demonstrate that Ncam1b is required for the expression of chemokine receptor Cxcr7b, which is crucial for directed primordial migration. Finally, we show that the knockdown of ncam1b destabilizes proneuromasts, suggesting a further function of Ncam1b in strengthening the cohesion of proneuromast cells.


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