Mutant/mutation
The mutant expresses a GFP-tagged (C-terminal) form of PKG (cGMP-dependent protein kinase).

Protein (function)
Cyclic GMP-dependent protein kinases (PKGs) are the major mediators of the cGMP signal transduction pathway and regulate a variety of physiological effects

Phenotype
Expression of PKG-GFP in blood stages, gametocytes and ookinetes. Attempts to disrupt the pkg gene were unsuccessful (RMgm-325, RMgm-544), suggesting an essential role of PKG in asexual blood stages.

Additional information
In the paper it is shown that a selective inhibitor of apicomplexan PKG, the ATP analog Compound 1, potently blocked ookinete motility.

In the paper evidence is presented that in ookinetes GCß is the main source for cGMP and that a cyclic GMP signalling module exists that regulates gliding motility of ookinetes. This evidence is partly based on the analysis of mutants lacking expression PDEδ (RMgm-308) and GCβ (RMgm-307) and a mutant  lacking expression of both GCβ and PDEδ (RMgm-309). These analyses indicate that PDEδ is the relevant cGMP degrading enzyme. Signalling via a cGMP-dependent protein kinase (PKG; PF14_0346; PB000726.02.0) may regulate ookinete differentiation and motility.

It the same paper it is reported that repeated attempts were made to disrupt the pkg gene (cGMP-dependent protein kinase: PB000726.02.0, PB300651.00.0; PF14_0346). These attempts were unsuccessful (see RMgm-325), suggesting its essential role in the blood stage parasites (no information is provided on the construct used to disrupt pkg and the sequence of primers used to amplify the target regions).

(Gene models for PKG PB000726.02.0; PB300651.00.0)

Other mutants
RMgm-357: A ‘conditional knock-out mutant’ lacking expression of PKG in liver stages. The Flp/FRT site-specific recombination (SSR) system of yeast has been used to silence PKG expression specifically in liver stages.
RMgm-544: Unsuccessful attempts to disrupt the pkg gene
RMgm-325: Unsuccessful attempts to disrupt the pkg gene