Dorsoventral patterning in the Drosophila central nervous system: the intermediate neuroblasts defective homeobox gene specifies intermediate column identity
- Joseph B. Weiss1,6,
- Tonia Von Ohlen3,6,7,
- Dervla M. Mellerick4,
- Gregory Dressler5,
- Chris Q. Doe2,3,7,8, and
- Matthew P. Scott1,8
- 1Departments of Developmental Biology and Genetics, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305-5329 USA; 2Department of Cell and Structural Biology, University of Illinois/HHMI, Urbana, Illinois 61801 USA; 3Institute of Neuroscience, University of Oregon, Eugene, Oregon 97403 USA; Departments of 4Pediatric Neurology and 5Pathology, University of Michigan Medical Center, Ann Arbor, Michigan 48109 USA
Abstract
One of the first steps in neurogenesis is the diversification of cells along the dorsoventral axis. In Drosophila the central nervous system develops from three longitudinal columns of cells: ventral cells that express the vnd/nk2 homeobox gene, intermediate cells, and dorsal cells that express the mshhomeobox gene. Here we describe a new Drosophila homeobox gene,intermediate neuroblasts defective (ind), which is expressed specifically in the intermediate column cells. ind is essential for intermediate column development: Null mutants have a transformation of intermediate to dorsal column neuroectoderm fate, and only 10% of the intermediate column neuroblasts develop. The establishment of dorsoventral column identity involves negative regulation: Vnd represses ind in the ventral column, whereas ind represses msh in the intermediate column. Vertebrate genes closely related to vnd (Nkx2.1 andNkx2.2), ind (Gsh1 and Gsh2), andmsh (Msx1 and Msx3) are expressed in corresponding ventral, intermediate, and dorsal domains during vertebrate neurogenesis, raising the possibility that dorsoventral patterning within the central nervous system is evolutionarily conserved.
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Footnotes
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↵6 These authors contributed equally to this paper.
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↵7 Present address: Institutes of Neuroscience, University of Oregon, Eugene, Oregon 97403 USA.
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↵8 Corresponding authors.
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E-MAIL scott{at}cmgm.stanford.edu; FAX (650) 723-9878.
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E-MAIL cdoe{at}uoneuro.uoregon.edu; FAX (541) 346-4736.
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- Received August 10, 1998.
- Accepted September 29, 1998.
- Cold Spring Harbor Laboratory Press
