{Models}
| Symbol: {Name}{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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- Gli1 expression in posterior compartment activated ptc transcription
in smo+/–; posterior-compartment cells, but not in neighboring
smo–/–; cells (Fig 2), indicating that Gli1 possesses
potent activator activity that is strictly dependent on Hh signal transduction.
No effects is observed on hh transcription in posterior smo–/–;
cells, indicating that, unlike Ci, Gli1 does not acquire repressor activity
in the absence of Hh signal transduction. Gli1 functions as a Hh-regulated
activator. (von Mering, 1999)
- Gli3 expression in posterior compartment possesses moderate repressor
activity even in the presence of Hh signalling, and hh transcription
was nearly abolished in smo–/–. This indicates that
Gli3 repressor activity is maximal in the absence of, and is therefore
negatively controlled by, Hh signalling. Gli3 functions as a Hh-regulated
repressor. (von Mering, 1999)
- Gli1 can rescue a ci null mutant animal to late larval stages
when expressed from a tubulin alpha1-GLI1 transgene (Fig 3).
Therefore, Gli1 is sufficient to mediate essential aspects of Hh signalling
in embryos, however the repressor form is required to repress dpp
and hh expression (von Mering, 1999)
- proper regulation of Hh target gene expression was restored if cinull
mutant animals were rescued by ubiquitously expressed Gli1 and Gli3
(Fig 3) (von Mering, 1999)
- expressing both ptc and Gli3 in the posterior compartment had
a synergistic effect. Wings were significantly reduced in size and resembled
those produced by expression of Ci-76 in the posterior compartment.
This suggests that Gli3R represses Hh expression, and the
presence of ptc produces more Gli3R. (Aza-Blanc,
2000)
- the absence of Fu kinase activity in fuI mutant wings partially
suppresses Gli-induced overgrowth, while the 3-4 intervein region defect
(in fu mutants) is partially rescued by the presence of Gli1.
(Fig 6) (Aza-Blanc,
2000)
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- processing of Glis in Drosophila
- Gli1- single band ~175kDa, no evidence of a smaller form. (Fig
2A) (Aza-Blanc,
2000)
- Gli2- full-length form ~180-200kDa, smaller form ~90kDa, Hh didn't
seem to have an affect (Fig 2A) (Aza-Blanc,
2000)
- Gli3- full-length form ~180-200kDa, smaller form ~100kDa, more
proteolysis in the absence of Hh (Fig 2A) (Aza-Blanc,
2000)
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- Ubiquitous expression (tubulin alpha 1 or C765)
- Gli1- interruption of cubital vein 4, closely resembling the effect
of ubiquitous ci expression (Fig 1). Activated ptc transcription
and had no effect on hh expression. (von Mering, 1999)
- Gli3- small wings and the loss of L3/L4 intervein tissue (Fig
1). Repressed hh transcription (von Mering, 1999)
- ptc-GAL4
- en-GAL4
- Gli1 - alterations of vein morphology and overgrowth of P compartment.
Portions of vein 4 were frequently missing, but proximal vein 4,
usually visible, was never fused with vein 3 (Fig 1B). Activated
ptc to high levels and dpp-lacZ to low levels(Fig 3); this activation
is dependent on Hh (Fig 4). It appears as if Gli1 levels increase
slightly in the absence of Hh. (Fig 4) (Aza-Blanc,
2000)
- Gli2 - alterations of vein morphology and overgrowth of P compartment.
Proximal veins 3 & 4 were invariably fused (Fig 1C) Activated
dpp-lacZ to high levels and ptc to low levels (Fig 3); this activation
is dependent on Hh (Fig 4). The level of ptc expression in
wing discs was inversely related to the level of Gli2 expression.
(Aza-Blanc,
2000)
- Gli3 - no major alteration of vein morphology or growth. Intervein
between 3 & 4 was narrowed and veins were slightly fused (Fig
1D) (Aza-Blanc,
2000)
- suggests that Gli3 does not have any Ci-like inductive functions
in imaginal discs. Rather, Gli3 reduces hh expression in P cells,
consistent with its role in vertebrates and its efficient conversion
to a processed form. (Aza-Blanc,
2000)
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