GAPCp2 is integral to plastidial glycolysis and metabolic regulation. Key insights include:
GAPDH isoforms, including GAPCp2, negatively regulate plant immune responses:
Enhanced Disease Resistance: gapcp1gapcp2 knockout (KO) lines showed reduced bacterial titers of Pseudomonas syringae pv. tomato (Pst DC3000) and accelerated hypersensitive response (HR) .
ROS and Autophagy Modulation: GAPCp2 influences reactive oxygen species (ROS) accumulation and autophagy, critical for pathogen defense .
Priming Effects: Basal upregulation of pathogenesis-related genes (e.g., PR1) in GAPDH KO lines suggests constitutive immune priming .
Non-Phosphorylating Pathway: GAPCp2 participates in chloroplast glycolysis, bypassing ATP production to optimize carbon flux .
ATP/ADP Dynamics: Loss of plastidial GAPDH (GAPCp1/GAPCp2) alters ATP/ADP ratios, impacting redox balance and glycolytic flux .
Plastid Localization: Confocal microscopy confirms GAPCp2 presence in leaf epidermal cell plastids, critical for serine synthesis and starch metabolism .
Tissue Expression: Strong expression in photosynthetic tissues (e.g., leaves) and roots, with minimal activity in non-photosynthetic organs .
The antibody is widely used in plant biology research:
GAPCp2 differs significantly from cytosolic isoforms (GAPC1/GAPC2) and other plastidial forms (GAPCp1):
| Feature | GAPCp2 | GAPC1/GAPC2 | GAPCp1 |
|---|---|---|---|
| Localization | Chloroplast/plastid | Cytosol | Chloroplast/plastid |
| Function | Non-phosphorylating glycolysis, serine synthesis | Phosphorylating glycolysis, ATP production | Similar to GAPCp2 |
| Immune Role | Negative regulator of HR and ROS accumulation | Negative regulator of HR, autophagy | Overlapping with GAPCp2 |
| Expression | High in leaves, roots; low in non-photosynthetic tissues | Ubiquitous, stress-responsive | Similar to GAPCp2 |
GAPCp1/GAPCp2 Double KO:
Cytosolic vs. Plastidial KO: