scholarly journals Estudio del papel de p73 en la ciliogénesis y el establecimiento de la polaridad celular planar en células ependimarias = Role of P73 in ependymal cell ciliogenesis and planar cell polarity establishment

2017 ◽  
Author(s):  
Sandra Fuertes Álvarez
2015 ◽  
Vol 1615 ◽  
pp. 22-30 ◽  
Author(s):  
Xiao-yu Yang ◽  
Kai Jin ◽  
Rui Ma ◽  
Juan-mei Yang ◽  
Wen-wei Luo ◽  
...  

2013 ◽  
Vol 14 (8) ◽  
pp. 525-535 ◽  
Author(s):  
Fadel Tissir ◽  
André M. Goffinet

2015 ◽  
Vol 93 (4) ◽  
pp. 396-404 ◽  
Author(s):  
Candace Elaine Rapchak ◽  
Neeraj Patel ◽  
John Hudson ◽  
Michael Crawford

The polo-like kinases are a family of conserved serine/threonine kinases that play multiple roles in regulation of the cell cycle. Unlike its four other family members, the role of Plk4 in embryonic development has not been well characterized. In mice, Plk4−/− embryos arrest at E7.5, just prior to the initiation of somitogenesis. This has led to the hypothesis that Plk4 expression may be essential to somitogenesis. Recently characterized human mutations lead to Seckel Syndrome. Riboprobe in situ hybridization revealed that plk4 is ubiquitously expressed during early stages of development of Xenopus and Danio; in later stages, expression in frogs restricts to somites as well as eye, otic vesicle, and branchial arch, and brain. Expression patterns in fish remain ubiquitous. Both somite and eye development require planar cell polarity, and disruption of plk4 function in frog by means of morpholino-mediated translational knockdown yields orientational disorganization of both these structures. These results provide the first steps in defining a new role for plk4 in organogenesis and implies a role in planar cell polarity, segmentation, and in recently described PLK4 mutations in human.


PLoS Genetics ◽  
2018 ◽  
Vol 14 (5) ◽  
pp. e1007391 ◽  
Author(s):  
Giovanna M. Collu ◽  
Andreas Jenny ◽  
Konstantin Gaengel ◽  
Ivana Mirkovic ◽  
Mei-ling Chin ◽  
...  

2013 ◽  
Vol 457 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Roberto Mayor ◽  
Eric Theveneau

The neural crest is an embryonic stem cell population whose migratory behaviour has been likened to malignant invasion. The neural crest, as does cancer, undergoes an epithelial-to-mesenchymal transition and migrates to colonize almost all the tissues of the embryo. Neural crest cells exhibit collective cell migration, moving in streams of high directionality. The migratory neural crest streams are kept in shape by the presence of negative signals in their vicinity. The directionality of the migrating neural crest is achieved by contact-dependent cell polarization, in a phenomenon called contact inhibition of locomotion. Two cells experiencing contact inhibition of locomotion move away from each other after collision. However, if the cell density is high only cells exposed to a free edge can migrate away from the cluster leading to the directional migration of the whole group. Recent work performed in chicks, zebrafish and frogs has shown that the non-canonical Wnt–PCP (planar cell polarity) pathway plays a major role in neural crest migration. PCP signalling controls contact inhibition of locomotion between neural crest cells by localizing different PCP proteins at the site of cell contact during collision and locally regulating the activity of Rho GTPases. Upon collision RhoA (ras homologue family member A) is activated, whereas Rac1 is inhibited at the contact between two migrating neural crest cells, leading to the collapse of protrusions and the migration of cells away from one another. The present review summarizes the mechanisms that control neural crest migration and focuses on the role of non-canonical Wnt or PCP signalling in this process.


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