Development and Control of Tissue Separation at Gastrulation in Xenopus

Abstract

During Xenopus gastrulation, the internalizing mesendodermal cell mass is brought into contact with the multilayered blastocoel roof. The two tissues do not fuse, but remain separated by the cleft of Brachet. This maintenance of a stable interface is a precondition for the movement of the two tissues past each other. We show that separation behavior, i.e., the property of internalized cells to remain on the surface of the blastocoel roof substratum, spreads before and during gastrulation from the vegetal endoderm into the anterior and eventually the posterior mesoderm, roughly in parallel to internalization movement. Correspondingly, the blastocoel roof develops differential repulsion behavior, i.e., the ability to specifically repell cells showing separation behavior. From the effects of overexpressing wild-type or dominant negative XB/U or EP/C cadherins we conclude that separation behavior may require modulation of cadherin function. Further, we show that the paired-class homeodomain transcription factors Mix.1 and gsc are involved in the control of separation behavior in the anterior mesoderm. We present evidence that in this function, Mix.1 and gsc may cooperate to repress transcription.

Control of gastrula cell motility by the Goosecoid/Mix.1/ Siamois network: Basic patterns and paradoxical effects

“…This gene was included in our study for its known cooperation with Gsc in the control of motility-related properties (Wacker et al, 1998(Wacker et al, , 2000. We showed that Mix.1 acts as a com- Kreyszig, 1973; as in Fig.…”

“…2D), suggesting that Mix.1 is also necessary for rapid migration, and functions in this context as a repressor. Collaboration of Gsc and Mix.1 as repressors has previously been shown for the control of tissue separation in the HM (Wacker et al, 2000).…”

PDGF-A controls mesoderm cell orientation and radial intercalation duringXenopusgastrulation

“…The ability of the cells to migrate across adjacent cells towards a sf-PDGF-A source was directly demonstrated in vitro. The PCM is separated from the ectodermal BCR by Brachet's cleft, a tissue boundary maintained by cycles of attachment and repulsion between ectoderm and mesoderm cells (Wacker et al, 2000) (N. Rohani, L. Canty, O. Luu, F. Fagotto and R.W., unpublished). The resulting dynamic adhesion between germ layers ensures that while the PCM cells can move across the BCR, they cannot penetrate into it despite being attracted by sf-PDGF-A.…”

Shield formation at the onset of zebrafish gastrulation

“…During Xenopus and zebrafish gastrulation, the over or underexpression of paraxial protocadherin (papc) leads to defects in convergence and extension of the forming embryonic body axis (Hukriede et al, 2003;Kim et al, 1998;Yamamoto et al, 1998). Furthermore, when XB/U-or EP/C-Cadherin function is blocked at the onset of Xenopus gastrulation, both mesodermal progenitor cell involution and migration, as well as germ layer separation, are affected (Kuhl et al, 1996;Lee and Gumbiner, 1995;Wacker et al, 2000). Finally, inactivating E-Cadherin in Xenopus and zebrafish embryos causes variable defects before and during gastrulation, including impaired prechordal plate formation and migration in zebrafish and ectodermal lesions in Xenopus (Babb and Marrs, 2004;Levine et al, 1994).…”