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Published May 21, 1998 | Supplemental Material
Journal Article Open

Fate mapping of the mouse midbrain–hindbrain constriction using a site-specific recombination system


The mouse midbrain–hindbrain constriction is centrally involved in patterning of the midbrain and anterior hindbrain (cerebellum), as revealed by recent genetic studies using mice and embryological studies in chick (reviewed in [1] and [2]). This region can act as an organizer region to induce midbrain and cerebellar development. Genes such as Engrailed-1, Pax-2 and Pax-5, which are expressed in the embryonic cells that will form the midbrain and the cerebellum, are required for development of these regions. Fate-mapping experiments at early somite stages in chick have revealed that the cerebellar primordium is located both anterior and posterior to the midbrain–hindbrain constriction, whereas midbrain precursors lie more anteriorly. Fate mapping in mice has been complicated by the inaccessibility of the postimplantation embryo. Here, we report the use of a new in vivo approach involving the Cre–loxP site-specific recombination system [3] to map the fate of cells in the mouse midbrain–hindbrain constriction. We show that cells originating in the mouse dorsal midbrain–hindbrain constriction during embryonic days 9–12 contribute significantly to the medial cerebellum and colliculi. Our data demonstrate the feasibility of using a recombinase-based lineage-tracing system for fate mapping in the mouse.

Additional Information

© 1998 Current Biology Ltd. Received: 26 January 1998. Revised: 6 April 1998. Accepted: 6 April 1998. Published: 11 May 1998. We thank Margosia Kownaka and Anna Auerbach for technical assistance with embryonic stem cell work, and C.C. Hui for providing lab space, advice and support to D.L.Z. during some of these studies. We thank members of the Joyner lab for their advice and suggestions, especially Sandrine Millet for making comments on the manuscript. We thank Brian Sauer for gifts of plasmids and advice, and Richard Behringer for mouse β-actin genomic clones. D.L.Z. was supported by a NSERC of Canada Scholarship, an Ontario Graduate Scholarship and an HSC RESTRACOM Studentship. E.H.M. was supported by a Damon Runyan–Walter Winchell postdoctoral fellowship. This work was funded by grants from the Canadian MRC, NINDS and HFSP to A.L.J., and by NIH/NAIMS grant 1PO1 AR 42671 (to P.I., B. Wold) to D.J.A.; A.L.J. and D.J.A. are investigators of the Howard Hughes Medical Institute.

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