Retinal morphogenesis in Drosophila: hints from an eye-specific decapentaplegic allele

decapentaplegic (dpp) regulates many aspects of imaginal disc growth and patterning in Drosophila. We have analyzed the phenotype of an eye-specific dpp allele, dppblk, which causes a reduction in the size of the retina due to a loss of ventral ommatidia. Prior to the onset of differentiation, dppbl...

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Bibliographic Details
Published in:Developmental genetics 1997, Vol.20 (3), p.197-207
Main Authors: Chanut, F. (University of California, San Francisco.), Heberlein, U
Format: Article
Language:English
Subjects:
ANIMAL TRANSGENIQUE
ANIMALES TRANSGENICOS
Animals
BETA GALACTOSIDASA
BETA GALACTOSIDASE
COMPOUND EYES
dpp
DPP ALLELE
Drosophila
Drosophila - embryology
Drosophila - genetics
Drosophila - metabolism
DROSOPHILA MELANOGASTER
Drosophila Proteins
eye development
EYE DISCS
EYES
FACTEUR DE CROISSANCE TRANSFORMANT
FACTOR DE CRECIMIENTO TRANSFORMANTE
FENOTIPOS
GENE
GENES
HISTOENZYMOLOGY
Insect Proteins - genetics
Insect Proteins - physiology
MORFOGENESIS
MORPHOGENESE
MORPHOGENESIS
morphogenetic furrow
MUTACION
MUTATION
OEIL
OJOS
patched
PHENOTYPE
PHENOTYPES
Photoreceptor Cells, Invertebrate - embryology
Photoreceptor Cells, Invertebrate - metabolism
REPORTER GENES
Retina - embryology
Retina - metabolism
TRANSFORMING GROWTH FACTOR
TRANSGENIC ANIMALS
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Description
Summary:decapentaplegic (dpp) regulates many aspects of imaginal disc growth and patterning in Drosophila. We have analyzed the phenotype of an eye-specific dpp allele, dppblk, which causes a reduction in the size of the retina due to a loss of ventral ommatidia. Prior to the onset of differentiation, dppblk eye discs are normal regarding size, shape, and ability to express dorsal and ventral markers. However, expression of a dpp-lacZ reporter is reduced at the ventral margin. Additional dorsoventral asymmetry appears during retinal differentiation: the morphogenetic furrow (MF) initiates normally at the posterior tip of the disc, but fails to propagate into the ventral epithelium. This defect can be rescued by increasing dpp expression along the ventral margin by local removal of patched function. We propose that the primary defect in dppblk is an inability to activate dpp expression properly at the ventral margin. This has two consequences: it prevents initiation from the ventral margin, and it renders the ventral epithelium unresponsive to differentiation signals emanating from the MF
ISSN:0192-253X
1520-6408
DOI:10.1002/(SICI)1520-6408(1997)20:3<197::AID-DVG3>3.0.CO;2-2