PKA

Protein kinase A

Add Correction Suggestion

Symbol: AKA: cAMP-dependent protein kinase 1, DC0 {Links}	Flybase ID: {Flybase_ID}
Synonyms: {Name}	{GadFly}
Function: {Short_Function}	{LocusLink}
Keywords: {Keywords}	{Interactive_Fly}

{Summary}

Function/Pathway

A serine/threonine kinase involved in signal transduction
Mediated phosphorylation of Ci promotes its proteolysis (Chen,, 1998)
PKA catalytic subunit increased proteolytic processing (Chen,, 1998)
PKI, PKA inhibitor, blocks processing (Chen,, 1998)
When all Ci’s PKA sites are mutated Ci is not processed (Chen,, 1998)
Ci that cannot be phosphorylated by PKA (site mut) have increased transcriptional activity (Chen,, 1998)
Exogenous PKA can increase further the transcriptional activity of the ci PKA mut (Chen,, 1998)
Some results suggest that it is acting in a different pathway (Jiang, 1995, Li, 1995)

Genetic interactions

loss of PKA function activates Hh-target genes in the absence of a functional Hh signal regardless of Ptc concentrations, whereas loss of Ptc function is unable to activate Hh-target genes at high levels of constitutive PKA activity (Li et al., 1995). These findings imply, first, that the ability of Ptc to inhibit activation of Hh-target genes depends on PKA and second, that PKA does not act on Ptc but on a component down-stream of Ptc (Figure 8). Recent results show that high PKA activity cannot counteract the phosphorylation of Fu that depends on the Hh signal but can be inhibited by Ptc, suggesting that Fu indeed acts downstream of Hh and Ptc (Therond, 1996). It further follows that PKA does not act on a component between Ptc and Fu. It is unclear, however, whether PKA acts through Fu or a component downstream of Fu (taken from Alcedo, 1996)
role of PKA in Hh signal transduction (Jiang, 1995; Johnson et al., 1995; Lepage et al., 1995; Li et al., 1995; Pan and Rubin, 1995; Strutt et al.,1995).
Reduced PKA activity in anterior imaginal disc cells leads to cell-autonomous induction of dpp, wg, and ptc transcription that is independent of hh gene activity (Li, 1995)
Over-expression of PKA can counteract transcriptional induction of ptc by hh in cells close to the posterior compartment (Li, 1995)
PKA inhibition leads to increase C-term Ci staining (Hh & Smo independent) and Hh target gene expression (Smo dependent and somewhat Hh dependent) (Ohlmeyer, 1997)
Increase PKA activity can induce ectopic Hh target gene expression in a manner that requires Smo and Ci activities but does not involve changes in Ci protein concentrations (Ohlmeyer, 1997)
Hh signaling in embryos does not depend on cAMP-dependent regulation of PKA activity (Ohlmeyer, 1997)
PKA might act on Smo perhaps to uncouple it from the inhibition of Ptc (Ohlmeyer, 1997)
PKA antagonizes the Hh signal response (Lepage et al., 1995; Pan and Rubin, 1995, Li, 1995, Jiang, 1995)
Hh does not induce dpp and wg transcription by down-regulating PKA activity (Jiang, 1995)
PKA represses dpp expression in appendage and eye discs and not needed for dpp reporter activity (Pan and Rubin, 1995)
Restricts the expression of dpp, wg, & ptc in imaginal discs (Li, 1995)
Expressing a dominant-negative form of PKA in the dorsal compartment (UAS-R*/ap-Gal4) results in ectopic Ci-155 and ectopic expression of dpp, but no change in col expression (data not shown) (Vervoort, 1999). These results indicate that the presence of Ci-155 is not sufficient to activate col expression in the anterior compartment, in conditions where it activates dpp and ptc (Capdevila, 1994; Chen, 1996; Hepker, 1997; Li, 1995).

Physical interactions

{Physical interactions}

Transcriptional Regulation

{Regulation}

Structure

{Structure}

Location (protein and transcript)

{Location}

Protein Modifications and Regulation

{Modifications}

Related to

{Related to}

Mutations

Constitutively activated PKA catalytic subunit prevents inappropriate dpp and wg expression but does not suppress Hh signalling (Jiang, 1995) IN CONTRAST TO: hyperactivation of PKA could inhibit the normal induction of ptc by hh at the AP border (Li, 1995)
Levels of Ci protein appear to be elevated in clones of cells that lack PKA function
PKA(DN) ectopically activates A-P border genes and is a suppressor of partial-loss-of-fxn hh mutations (Pan and Rubin, 1995)
The absence of PKA function results in similar phenotypes as those caused by hh ectopic expression, both of them due to dpp and wg derepression
Pka clones in the anterior margin transform into bristles corresponding to the region anterior to vein 3 (Jiang, 1995) whereas ptc clones in similar regions transform into posterior cells (Tabata, T., 1995). Therefore pka probably does not induce ectopic en expression, as the absence of ptc, or the ectopic expression of hh, do. (taken from Sanchez-Herrero, 1996)

Overexpression / Ectopic expression

{Overexpression}

Reagents

{Reagents}