Sall4 isoforms act during proximal-distal and anterior-posterior axis formation in the mouse embryo

genesis ◽  
2008 ◽  
Vol 46 (9) ◽  
pp. 463-477 ◽  
Author(s):  
Nikolas Uez ◽  
Heiko Lickert ◽  
Jürgen Kohlhase ◽  
Martin Hrabe de Angelis ◽  
Ralf Kühn ◽  
...  
Keyword(s):  
Mouse Embryo ◽  
Axis Formation ◽  
Anterior Posterior ◽  
Anterior Posterior Axis

scholarly journals Dynamics of anterior–posterior axis formation in the developing mouse embryo

2012 ◽  
Vol 3 (1) ◽  
Author(s):  
Samantha A. Morris ◽  
Seema Grewal ◽  
Florencia Barrios ◽  
Sameer N. Patankar ◽  
Bernhard Strauss ◽  
...  
Keyword(s):  
Mouse Embryo ◽  
Axis Formation ◽  
Anterior Posterior ◽  
Anterior Posterior Axis

Patterning of the follicle cell epithelium along the anterior-posterior axis during Drosophila oogenesis

Development ◽  
1998 ◽  
Vol 125 (15) ◽  
pp. 2837-2846 ◽  
Author(s):  
A. Gonzalez-Reyes ◽  
D. St Johnston
Keyword(s):  
Follicle Cell ◽  
Cell Types ◽  
Follicle Cells ◽  
Follicular Epithelium ◽  
Axis Formation ◽  
Main Body ◽  
Drosophila Oogenesis ◽  
Egfr Mutant ◽  
Anterior Posterior ◽  
Anterior Posterior Axis

Gurken signals from the oocyte to the adjacent follicle cells twice during Drosophila oogenesis; first to induce posterior fate, thereby polarising the anterior-posterior axis of the future embryo and then to induce dorsal fate and polarise the dorsal-ventral axis. Here we show that Gurken induces two different follicle cell fates because the follicle cells at the termini of the egg chamber differ in their competence to respond to Gurken from the main-body follicle cells in between. By removing the putative Gurken receptor, Egfr, in clones of cells, we show that Gurken signals directly to induce posterior fate in about 200 cells, defining a terminal competence domain that extends 10–11 cell diameters from the pole. Furthermore, small clones of Egfr mutant cells at the posterior interpret their position with respect to the pole and differentiate as the appropriate anterior cell type. Thus, the two terminal follicle cell populations contain a symmetric prepattern that is independent of Gurken signalling. These results suggest a three-step model for the anterior-posterior patterning of the follicular epithelium that subdivides this axis into at least five distinct cell types. Finally, we show that Notch plays a role in both the specification and patterning of the terminal follicle cells, providing a possible explanation for the defect in anterior-posterior axis formation caused by Notch and Delta mutants.

A role for Drosophila LKB1 in anterior–posterior axis formation and epithelial polarity

Nature ◽  
2003 ◽  
Vol 421 (6921) ◽  
pp. 379-384 ◽  
Author(s):  
Sophie G. Martin ◽  
Daniel St Johnston
Keyword(s):  
Axis Formation ◽  
Epithelial Polarity ◽  
Anterior Posterior ◽  
Anterior Posterior Axis

scholarly journals The Drosophila anterior-posterior axis is polarized by asymmetric myosin activation

2021 ◽  
Author(s):  
Helene Doerflinger ◽  
Vitaly Zimyanin ◽  
Daniel St Johnston
Keyword(s):  
Light Chain ◽  
Kinase Inhibitor ◽  
Germ Line ◽  
Follicle Cell ◽  
Follicle Cells ◽  
Axis Formation ◽  
Posterior Cortex ◽  
Cortical Tension ◽  
Anterior Posterior ◽  
Anterior Posterior Axis

The Drosophila anterior-posterior (AP) axis is specified at mid-oogenesis when Par-1 kinase is recruited to the posterior cortex of the oocyte, where it polarises the microtubule cytoskeleton to define where the axis determinants, bicoid and oskar mRNAs localise. This polarity is established in response to an unknown signal from the follicle cells, but how this occurs is unclear. Here we show that the myosin chaperone, Unc-45 and Non-Muscle Myosin II (MyoII) are required in the germ line upstream of Par-1 in polarity establishment. Furthermore, the Myosin regulatory Light Chain (MRLC) is di-phosphorylated at the oocyte posterior in response to the follicle cell signal, inducing longer pulses of myosin contractility at the posterior and increased cortical tension. Over-expression of MRLC-T21A that cannot be di-phosphorylated or acute treatment with the Myosin light chain kinase inhibitor ML-7 abolish Par-1 localisation, indicating that posterior of MRLC di-phosphorylation is essential for polarity. Thus, asymmetric myosin activation polarizes the anterior-posterior axis by recruiting and maintaining Par-1 at the posterior cortex. This raises an intriguing parallel with AP axis formation in C. elegans where MyoII is also required to establish polarity, but functions to localize the anterior PAR proteins rather than PAR-1.

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