The role of slb/wnt11 in regulating convergent extension movements during zebrafish gastrulation
1. We are analysing in detail the movements and morphologies of single cells within different regions of the gastrula using recently developed cell-tracking software (Concha and Adams, 1998). To follow single cells during the course of gastrulation we are taking high-magnification time-lapse movies of groups of cells within the different germ layers. These movies are then processed by either tracking single cells and subsequently analysing their movements using cell-tracking software or by capturing their morphology at different time points and analysing morphological changes using appropriate software. Initially, we are focussing on wild-type embryos but will subsequently extend these studies to mutant embryos exhibiting defective gastrulation movements such as slb, trilobite (tri) and knypek (kny) (Hammerschmidt et al., 1996; Solnica-Krezel et al., 1996; Heisenberg et al., 1996; Marlow et al., 1998). Eventually, this will allow us to determine how cell movements differ along the anterior-posterior and medial-lateral axis of the gastrula and between the different germ layers (mesendodermal, ectodermal and yolk syncytial cell layers). In the long term, we would like to understand how the regional patterns of cell movements generate global tissue morphogenesis during gastrulation and how these results compare to existing models for cell movements during gastrulation (Keller, 1986).
figure: (A) low magnification image of a shield stage zebrafish embryo showing the region used for image analysis (red square). (B) high magnification timelapse movie (13,1 MB) of paraxial mesodermal cells within the region high lightened in A between 60% and 80% epiboly.
2. We are performing a genetic screen with the aim to identify loci/genes modifying the slb mutant phenotype. By searching for modifiers of the slb mutant phenotype we intend to isolate genes interacting directly or indirectly with the Wnt11 signal transduction pathway. All existing and potential new mutants will be phenotypically analysed as described above (1.). We will also test if the enhancers/suppressors exhibit any phenotype on their own by analysing both potential dominant and recessive phenotypes of the induced mutation in the presence or absence of the slb mutation. Double (and possible triple) mutant embryos between the slb enhancers/suppressors and other known loci involved in convergent extension such as tri and kny will be raised and the mutant phenotype characterised to reveal any potential interaction between these genes.
* Concha, M. L., and Adams, R. J. (1998)
* Hammerschmidt, M., Pelegri, F., Mullins, M. C., Kane, D. A., Brand, M., van Eeden, F. J., Furutani-Seiki, M., Granato, M., Haffter, P., Heisenberg, C. P., Jiang, Y. J., Kelsh, R. N., Odenthal, J., Warga, R. M., and Nusslein-Volhard, C. (1996)
* Heisenberg, C. P., Brand, M., Jiang, Y. J., Warga, R. M., Beuchle, D., van Eeden, F. J., Furutani-Seiki, M., Granato, M., Haffter, P., Hammerschmidt, M., Kane, D. A., Kelsh, R. N., Mullins, M. C., Odenthal, J., and Nusslein-Volhard, C. (1996)
* Heisenberg, C. P., and Nusslein-Volhard, C. (1997)
* Heisenberg, C. P., Tada, M., Rauch, G. J., Saude, L., Concha, M. L., Geisler, R., Stemple, D. L., Smith, J. C., and Wilson, S. W. (2000)
* Keller, R. E. (1986)
* Marlow, F., Zwartkruis, F., Malicki, J., Neuhauss, S. C., Abbas, L., Weaver, M., Driever, W., and Solnica-Krezel, L. (1998)
* Solnica-Krezel, L., Stemple, D. L., Mountcastle-Shah, E., Rangini, Z., Neuhauss, S. C., Malicki, J., Schier, A. F., Stainier, D. Y., Zwartkruis, F., Abdelilah, S., and Driever, W. (1996)
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