{Models}
| Symbol: Ap
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Flybase ID: FBgn0000099 |
| Synonyms: {Name}
|
{GadFly} |
| Function: {Short_Function} |
{LocusLink} |
| Keywords: {Keywords} |
{Interactive_Fly} |
- a LIM-homeodomain protein (Cohen et al. 1992)
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- a LIM-homeodomain protein (Cohen et al. 1992) that is expressed in
dorsal cells and acts as a selector gene to divide the disc into dorsal
and ventral compartments (Diaz-Benjumea and Cohen, 1993; Blair, 1994)
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- Flybase
list of genetic interactions
- Regulation of Notch ligands by Ap leads to Notch signaling at the
DV boundary and the formation of an organizer for wing outgrowth and
expression of the wing-specific transcription factor vg (Kim et al.
1996; Irvine 1999).
- Vn/EGFR signaling regulates Ap expression in a cell autonomous fashion
only early in wing development
- ap expression partially overlaps that of vn in the
second instar (Fig 4I) (Wang,
2000)
- ap can be induced ectopically in ventral clones misexpressing
an activated form of the receptor, EGFRlambdatop4.2
(Fig. 4J) (Wang,
2000)
- Egfrtsla mutant clones generated in the first
instar show autonomous loss of ap expression (Fig. 4K), whereas
clones generated in the second instar express ap normally
(data not shown) (Wang,
2000)
- loss of EGFR activity in whole discs from mid-first to mid-second
instar (with a temperature-sensitive allele) results in complete
loss of ap expression, whereas ap is still expressed
in discs from larvae given a temperature shift slightly later during
the second instar (Fig. 4L–N). (Wang,
2000)
- Ap expression is completely absent in second instar vn muant discs
(Fig. 4E&F) (Wang,
2000). This is probably why there is no wing in vn mutants. This
is supported by the demonstration that ectopic ap was capable of rescuing
wing development in vn mutants (Fig. 4G,H). (Wang,
2000)
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