Abstract

The mouse transcription factor Noto is expressed in the notochord and involved in its development. Noto mouse mutants, Noto<sup>tc/tc</sup>(truncate) and Noto<sup>GFP/GFP</sup> (Noto null mutant), exhibit a segmental lack of the notochord in the caudal part of the embryo and subsequent tail truncation in adult animals. In order to address the relationship between the tail bud (the undifferentiated mesenchymal cells in the tip of the embryo tail) and the caudal notochord, Noto<sup>GFP/GFP</sup>, a loss- of-function mutant, was analyzed. Taking advantage of Noto<sup>GFP/+</sup> heterozygotes, we could track Noto-GFP-expressing cells from the tail bud over the tail cord to the caudal notochord, and confirm a morphological continuum from the tail bud mesenchyme to the caudal notochord. Loss of Noto affected tail bud morphogenesis: Noto-GFP-expressing cells were scattered in the tail bud mesenchyme. They segregated in the notochord-like structure within the medullary cord instead at the tail cord, which subsequently disappeared. In the tail cord, instead of the notochord, additional lumen of the tail gut was formed. These findings suggest that Noto is involved in both rearrangement and morphogenesis of the tail bud during notochord formation.

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