{Models}
Symbol:
- Classification - novel signaling protein
- Mad mutations can be placed in an allelic series based on the relative
severity of the maternal effect enhancement of weak dpp alleles, thus
explaining the name Mothers against dpp.
{Links}
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Flybase ID: {Flybase_ID} |
| Synonyms: {Name}
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{GadFly} |
| Function: {Short_Function} |
{LocusLink} |
| Keywords: {Keywords} |
{Interactive_Fly} |
{Summary}
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- TGF beta signal transduction
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- Found in a search for elements in the dpp signaling pathway (Raftery,
1995)
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- Cytoplasmic
- To date there is no indication that the Drosophila MAD protein is
nuclear: antibody staining experiments indicate a cytoplasmic localization.
Neverless there is clear indication that a human MAD homolog enters
the nucleus upon BMP2 signaling (Hoodless, 1996).
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- Mutations in Mad, when interacting with limiting DPP levels, produce
a defective amnioserosa, the extra-embryonic membrane comprising the
dorsal-most cells in early embryos (Raftery, 1995).
- Mad mutants produce a further reduction in wing blade size, a slight
reduction in the eye, and loss of tarsal claws
- Homozygous Mad mutant larvae also show midgut defects and a greatly
reduced gastric caecae
- DPP signaling from visceral mesoderm to midgut endoderm is required
for proper extension of the gastric caecae in parasegment 4 and for
the induction of the homeotic gene labial in the adjacent endoderm of
parasegment 7. Homozygous Mad mutant embryos lack labial expression
and have defects in midgut constriction engendered by labial expression.
Other imaginal disc derived structural defects are evident in homozygous
Mad mutants, including heldout wings, split notum, loss of distal leg
segments, duplications of the third antennal segment and defects in
female genitalia (Sekelsky, 1995).
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