Function: DGK5 phosphorylates diacylglycerol (DAG) to produce phosphatidic acid (PA), a lipid messenger critical for reactive oxygen species (ROS) production and pathogen resistance .
Mutant Phenotypes:
Localization: GFP-DGK5 fusion proteins localize to the plasma membrane, colocalizing with RBOHD and PLC2 .
Immune Modulation: DGKζ regulates T-cell responses by dampening DAG signaling, thereby suppressing excessive immune activation. Inhibition of DGKζ enhances T-cell receptor (TCR) signaling and antitumor responses .
Disease Links: Alterations in DGKζ activity are implicated in immune disorders, including asthma and cancer .
Western Blot: Detects DGKζ at ~124 kDa in HeLa and 293T lysates .
Immunohistochemistry: Strong staining in human breast carcinoma tissues, highlighting its utility in cancer research .
No DGK5-specific antibody is explicitly mentioned in the provided sources. Studies on Arabidopsis DGK5 rely on genetic mutants (e.g., dgk5.1) or tagged constructs (e.g., GFP-DGK5) . PA quantification and ROS assays are used to infer DGK5 activity .
| Feature | DGK5 (Plant) | DGKζ (Mammalian) |
|---|---|---|
| Subcellular Localization | Plasma membrane | Cytoplasm, nucleus |
| Primary Role | ROS production, pathogen resistance | T-cell regulation, immune suppression |
| Key Binding Partners | RBOHD, PLC2 | TCR signaling proteins |
| Disease Relevance | Enhanced pathogen susceptibility | Cancer, autoimmune disorders |
DGK5 in Dual Immunity:
DGK5 regulates both pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) in plants. Phosphorylation by BIK1 (a kinase) activates DGK5, while MPK4 phosphorylates it to suppress PA production, fine-tuning immune responses .
Exogenous PA rescues ROS defects in dgk5 mutants, confirming its role in RBOHD stabilization .
DGKζ as a Therapeutic Target: