Cellular mechanisms underlying posterior segmentation in Tribolium


Meeting Abstract

60.5  Sunday, Jan. 5 14:30  Cellular mechanisms underlying posterior segmentation in Tribolium NAKAMOTO, A.*; HESTER, S.; BLAINE, W.; IKPATT, J.; KHAHIL, S.; MATEI, M.; PACE, R.M.; TEWKSBURY, A.; NAGY, L.; WILLIAMS, T.; Univ. of Arizona; Univ. of Arizona; Trinity College ; Univ. of Arizona; Trinity College ; Univ. of Arizona; Univ. of Arizona; Trinity College ; Univ. of Arizona; Trinity College monaka@email.arizona.edu

The perceived view of Tribolium segmentation is that it proceeds from a posterior growth zone, regulated by interactions of WNT-CAD and an ODD oscillator. While such oscillators are thought to add segments in a clock-like manner, we measured the actual timing of segment addition throughout germband elongation. We use a lineage tracer to fate map small clusters of blastoderm cells. We find a direct relationship between location of a clone along the A/P egg axis and its fate in the embryo. We observe similar low rates of division between anterior and posterior blastoderm clones during axial elongation. The behavior of the clones is consistent with a model of cell rearrangement, rather than posterior growth, driving sequential segmentation in Tribolium. We develop a computational model that confirms that a realistic rate of elongation can be achieved in the absence of cell division through cells that have random, generic motility plus some directed cell movement. Embryonic injections of eveRNAi demonstrate that in the absence of Eve cells divide normally, but fail to initiate wildtype cell movements.

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