scholarly journals Ras-Mediated FGF Signaling Is Required for the Formation of Posterior but Not Anterior Neural Tissue in Xenopus laevis

2000 ◽  
Vol 227 (1) ◽  
pp. 183-196 ◽  
Author(s):  
Stephen Ribisi ◽  
Francesca V. Mariani ◽  
Emil Aamar ◽  
Teresa M. Lamb ◽  
Dale Frank ◽  
...  
2000 ◽  
Vol 222 (2) ◽  
pp. 405-419 ◽  
Author(s):  
C.F. Strong ◽  
M.W. Barnett ◽  
D. Hartman ◽  
E.A. Jones ◽  
D. Stott
Keyword(s):  

1994 ◽  
Vol 127 (2) ◽  
pp. 521-535 ◽  
Author(s):  
S Dufour ◽  
J P Saint-Jeannet ◽  
F Broders ◽  
D Wedlich ◽  
J P Thiery

Cadherins, a family of Ca-dependent adhesion molecules, have been proposed to act as regulators of morphogenetic processes and to be major effectors in the maintenance of tissue integrity. In this study, we have compared the effects of the expression of two truncated cadherins during early neurogenesis in Xenopus laevis. mRNA encoding deleted forms of XB- and N-cadherin lacking most of the extracellular domain were injected into the four animal dorsal blastomeres of 32-cell stage Xenopus embryos. These truncated cadherins altered the cohesion of cells derived from the injected blastomeres and induced morphogenetic defects in the anterior neural tissue to which they chiefly contributed. Truncated XB-cadherin was more efficient than N-cadherin in inducing these perturbations. Moreover, the coexpression of both truncated cadherins had additive perturbation effects on neural development. The two truncated cadherins can interact with the three known catenins, but with distinct affinities. These results suggest that the adhesive signal mediated by cadherins can be perturbed by overexpressing their cytoplasmic domains by competing with different affinity with catenins and/or a common anchor structure. Therefore, the correct regulation of cadherin function through the cytoplasmic domain appears to be a crucial step in the formation of the neural tissue.


2006 ◽  
Vol 295 (1) ◽  
pp. 435
Author(s):  
Steve Jean ◽  
Michel Tremblay ◽  
Tom Moss
Keyword(s):  

1993 ◽  
Vol 155 (1) ◽  
pp. 46-57 ◽  
Author(s):  
S.L. Wolda ◽  
C.J. Moody ◽  
R.T. Moon

2011 ◽  
Vol 221 (1) ◽  
pp. 137-145 ◽  
Author(s):  
Lisa Fukui ◽  
Jonathan J. Henry

Development ◽  
2002 ◽  
Vol 129 (22) ◽  
pp. 5103-5115 ◽  
Author(s):  
Sophie Bel-Vialar ◽  
Nobue Itasaki ◽  
Robb Krumlauf

Initiation of Hox genes requires interactions between numerous factors and signaling pathways in order to establish their precise domain boundaries in the developing nervous system. There are distinct differences in the expression and regulation of members of Hox genes within a complex suggesting that multiple competing mechanisms are used to initiate their expression domains in early embryogenesis. In this study, by analyzing the response ofHoxB genes to both RA and FGF signaling in neural tissue during early chick embryogenesis (HH stages 7-15), we have defined two distinct groups of Hox genes based on their reciprocal sensitivity to RA or FGF during this developmental period. We found that the expression domain of 5′ members from the HoxB complex (Hoxb6-Hoxb9) can be expanded anteriorly in the chick neural tube up to the level of the otic vesicle following FGF treatment and that these same genes are refractory to RA treatment at these stages. Furthermore, we showed that the chickcaudal-related genes, cdxA and cdxB, are also responsive to FGF signaling in neural tissue and that their anterior expansion is also limited to the level of the otic vesicle. Using a dominant negative form of a Xenopus Cdx gene (XcadEnR) we found that the effect of FGF treatment on 5′ HoxB genes is mediated in part through the activation and function of CDX activity. Conversely, the 3′HoxB genes (Hoxb1 and Hoxb3-Hoxb5) are sensitive to RA but not FGF treatments at these stages. We demonstrated by in ovo electroporation of a dominant negative retinoid receptor construct(dnRAR) that retinoid signaling is required to initiate expression. Elevating CDX activity by ectopic expression of an activated form of aXenopus Cdx gene (XcadVP16) in the hindbrain ectopically activates and anteriorly expands Hoxb4 expression. In a similar manner, when ectopic expression of XcadVP16 is combined with FGF treatment, we found that Hoxb9 expression expands anteriorly into the hindbrain region. Our findings suggest a model whereby, over the window of early development we examined, all HoxB genes are actually competent to interpret an FGF signal via a CDX-dependent pathway. However, mechanisms that axially restrict the Cdx domains of expression, serve to prevent 3′ genes from responding to FGF signaling in the hindbrain. FGF may have a dual role in both modulating the accessibility of the HoxB complex along the axis and in activating the expression of Cdx genes. The position of the shift in RA or FGF responsiveness of Hox genes may be time dependent. Hence, the specific Hox genes in each of these complementary groups may vary in later stages of development or other tissues. These results highlight the key role of Cdx genes in integrating the input of multiple signaling pathways, such as FGFs and RA, in controlling initiation of Hox expression during development and the importance of understanding regulatory events/mechanisms that modulate Cdx expression.


2019 ◽  
Vol 42 ◽  
Author(s):  
Charles R. Gallistel

Abstract Shannon's theory lays the foundation for understanding the flow of information from world into brain: There must be a set of possible messages. Brain structure determines what they are. Many messages convey quantitative facts (distances, directions, durations, etc.). It is impossible to consider how neural tissue processes these numbers without first considering how it encodes them.


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