Send to

Choose Destination
Dev Biol. 1995 Oct;171(2):306-16.

Dorsal-ventral patterning genes restrict NK-2 homeobox gene expression to the ventral half of the central nervous system of Drosophila embryos.

Author information

Laboratory of Biochemical Genetics, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.


Genes that affect the expression of the NK-2 homeobox gene were identified by comparing the patterns of NK-2 mRNA in wild-type Drosophila embryos with patterns in mutant embryos that have defects in genes that are required to establish the ventral-dorsal pattern of primordia in the early embryo. The NK-2 gene was shown to be activated by dorsal in the ventral half of the embryo during the syncytial blastoderm stage of development. However, expression of the NK-2 gene is restricted to the ventral half of the ventrolateral neurogenic anlagen and part of the procephalic region. The NK-2 gene is not expressed in the mesodermal anlage due to repression by snail, in mesectodermal cells due to repression by single-minded, or in the lateral neuroectodermal and/or dorsal epidermal anlagen due to repression mediated indirectly by decapentaplegic. Twist activates the NK-2 gene in the posterior portion of the embryo or is a coactivator with dorsal. The stripes of medial neuroectodermal cells that synthesize NK-2 mRNA are converted into clusters of neuroectodermal cells that contain NK-2 mRNA by segmentally repeated decreases in NK-2 mRNA. Medial neuroblasts, neuroblasts in the posterior portion of segments, and some ganglion mother cells and neurons express the NK-2 gene. These results suggest that the NK-2 gene receives and integrates information from ventral-dorsal and anterior-posterior gradients of gene regulators and that ventral, dorsal, anterior, and posterior boundaries of each cluster of neuroectodermal cells that express NK-2 are determined independently.

[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center