PKAc

PKAc

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{Models}

Symbol: PKAc {Links}	Flybase ID: {Flybase_ID}
Synonyms: {Name}	{GadFly}
Function: {Short_Function}	{LocusLink}
Keywords: {Keywords}	{Interactive_Fly}

{Summary}

Function/Pathway

PKA has 2 separable roles (Wang, 1999)
- 1) it blocks the activity of Ci-155
- 2) it targets Ci-155 for Slimb-mediated proteolysis to generate Ci-75

Genetic interactions

Sense ectopic expression of PKI(1-31) [see PKAr for PKI info] is not able to induce Hh target gene expression may indicate that active free PKAc is not present at a level sufficient to promote Ci-155 proteolysis. (Kiger, 2001)
Slimb is downstream of PKA activity with regards to Ci processing (Wang, 1999)
Ci is more active in PKA clones than in slimb clones (Wang, 1999)
PKA mutant cells express dpplacZ and ptclacZ at levels similar to AP boundary (Wang, 1999) and low en expression (Ohlmeyer, 1998). Slmb mutant clones express dpplacZ at low levels and don’t express ptc or en. Slmb mutant clones with R* (see PKAr) still ectopically express ptc, indicating that PKA is involved in turning Ci into an inactive species. PKA inhibits an uncleavable form of Ci, CiU. This shows that PKA negatively regulates the transcriptional activity of the full-length Ci independent of Ci cleavage (Wang, 1999)
PKA inhibits Ci activity in slimb Su(fu) double mutant cells (Wang, 1999)
in Pka-C1 mutants in the anterior compartment Col, Ptc, and En are up regulated but only at some distance away from the DV boundary (Figs. 3A-3C) (Glise, 2002)
- did not observe any modulation of dpp-lacZ staining along the DV axis, possible do to perdurance of B-galactosidase (Glise, 2002)
- In contrast to Pka-C1 clones, clones of cells lacking Ptc activated Col in all cells within the clones except for cells along the prospective wing margin (Fig 3D) (Glise, 2002)
Col and En expression is up-regulated in pka-C1 and wg double mutants both at a distance from and close to the DV boundary (Fig 4A & 4C), however, Col (but not En) up-regulation is never observed in the prospective wing margin (Fig 4A) (Glise, 2002)
- This indicates that Wg is responsible for the repression at a distance from the DV boundary but not at the wing margin itself (Glise, 2002)

Physical interactions

{Physical interactions}

Transcriptional Regulation

{Regulation}

Structure

{Structure}

Location (protein and transcript)

{Location}

Protein Modifications and Regulation

{Modifications}

Related to

{Related to}

Mutations

PKAcA75, a catalytically impaired mutant, activates Hh target genes
This might indicate that PKAc is in a complex with Ci (Kiger, 2001)
PKAcA75, might be able to bind to an inhibitory protein in the complex sense it is not completely inactive (Kiger, 2001)
PKAc*, a constitutively active mutant mouse catalytic subunit impaired in interaction with PKAr
When expressed at low levels appears to not affect normal Hh signalling (Jiang, 1995; Li, 1995; Ohlmeyer, 1997). Higher levels override Hh signaling and promote Ci-155 proteolysis (Li, 1995, Wang, 1999)
The requirement for high level expression of PKAc* to phosphorylate Ci-155 indicates that normally the complex itself is required to facilitate phosphorylation, supporting the idea that active free PKAc is not present at a level sufficient to promote Ci-155 prteolysis.
PKA mutant cells express dpplacZ and ptclacZ at levels similar to AP boundary (Wang, 1999) and low en expression (Ohlmeyer, 1998).

Overexpression / Ectopic expression

{Overexpression}

Reagents

{Reagents}