GENETIC PATTERNING OF THE DEVELOPING MOUSE TAIL AT THE TIME OF POSTERIOR NEUROPORE CLOSURE

Posterior neuropore (PNP) closure coincides with the end of gastrulati on, marking the end of primary neurulation and primary body axis forma tion. Secondary neurulation and axis formation involve differentiation of the tail bud mesenchyme. Genetic control of the primary-secondary transition is not understood. We report a detailed analysis of gene ex pression in the caudal region of day 10 mouse embryos during primary n europore closure. Embryos were collected at the 27-32 somite stage, fi xed, processed for whole mount in situ hybridisation, and subsequently sectioned for a more detailed analysis. Genes selected for study incl ude those involved in the key events of gastrulation and neurulation a t earlier stages and more cranial levels. Patterns of expression withi n the tail bud, neural plate, recently closed neural tube, notochord, hindgut, mesoderm, and surface ectoderm are illustrated and described. Specifically, we report continuity of expression of the genes Wnt5a, Wnt5b, Evx1, Fgf8, RAR gamma, Brachyury, and Hoxb1 from primitive stre ak and node into subpopulations of the tail bud and caudal axial struc tures. Within the caudal notochord, developing floorplate, and hindgut , HNF3 alpha, HNF3 beta, Shh, and Brachyury expression domains correla te directly with known genetic roles and predicted tissue interdepende nce during induction and differentiation of these structures. The patt erns of expression of Wnt5a, Hoxb1, Brachyury, RAR gamma, and Evx1, to gether with observations on proliferation, reveal that the caudal meso derm is organised at a molecular level into distinct domains delineate d by longitudinal and transverse borders before histological different iation. Expression of Wnt5a in the ventral ectodermal ridge supports p revious evidence that this structure is involved in epithelial-mesench ymal interaction. These results provide a foundation for understanding the mechanisms facilitating transition from primary to secondary body axis formation, as well as the factors involved in defective spinal n eurulation. (C) 1997 Wiley-Liss, Inc.