Rozario, T and DeSimone, D., 2009. The extracellular matrix in development and morphogenesis: A dynamic view.
Rozario, T, et. al. and DeSimone, D. 2009. The physical state of fibronectin matrix differentiatlly regulates morphogenic movements in vivo. Developmental Biology 327: 386-398.
Briefly tell us a bit about yourselves, your career paths over the years, and specifically what led you to begin working on Gastrulation in Xenopus.
How does FN undergo stretch-sensitive changes in conformation that potentially regulate ECM assembly and cell adhesion?
What other networks, besides FN networks, are there that work inconjunction with FN to send out mechanical signals to the ECM? Are FN networks doing it alone?
Why do you think it is that Convergent extension proceeds in the absence of FN fibrils even though past studies have shown through morpholino studies that an absence of FN, expression of dominant negative β1 Integrins, and antibody perturbations of integrin and FN adhesions lead to an inhibition in convergent extension?
What crucial aspect of intermedial intercalation is the Wnt/PCP signaling pathway contributing that cannot be provided by FN alone?
Is using 70 kD really an appropriate loss of function or does this create an artificial context, some kind of gain of function of an artificial FN matrix due to the dimer created? Could there be another way to have a clean loss of function of FN fibrils at a specific time and place without introducing anything novel to the system?
You say that there is no difference in the amount of FN in the blastoceol or expressed by the wt and 70kd inj. How can these both be considering that the addition of the 70kd FN seems to (assuming from the figure) decrease the number of FN on the surface of the BCR. Where is the excess going if it was expressed at the same rate in both systems. Moreover: if there is fibronectin floating in the blastoceol fluid is there ever a chance a cell might attach to those FN and then not follow its path to the BCR?
If cadherin (like E-Cadherin) had been up-regulated in the embryos at the same time fibrillogensis was inhibited by 70 kD FN, would the up-regulated cadherins have been able to maintain tissue tension in the BCR and ectoderm to allow for radial intercalation to proceed?
Loss of FN function in Xenopus caused defects in mesendodermal derivatives but not in embryos lacking the FN fibrils function, how would you evaluate what role the fibrils play in the formation of the mesendodermal derivatives? And does this have any connection to the accelerated closure of the mesendodermal mantle?