| Component | Type/Function | Position in Pathway | Role |
|---|---|---|---|
| DCAR-1 | GPCR; DAMP receptor activated by HPLA | Receptor / pathway entry point | Binds the endogenous tyrosine-metabolite ligand 4-hydroxyphenyllactic acid (HPLA) generated during epidermal damage, fungal infection, or wounding; initiates epidermal innate immune signaling to AMP genes (pqac-00000000, pqac-00000001, pqac-00000004, pqac-00000012) |
| GPA-12 | Gα signaling subunit | Immediately downstream of DCAR-1 | Transduces the activated GPCR signal toward PKC-dependent immune signaling required for AMP induction after fungal infection or wounding (pqac-00000004, pqac-00000010, pqac-00000013, pqac-00000015) |
| RACK-1 | Gβ-associated signaling component / scaffold | Parallel to GPA-12 downstream of DCAR-1 | Cooperates with GPA-12 in GPCR signaling upstream of TPA-1 to promote epidermal antimicrobial gene expression (pqac-00000001, pqac-00000004, pqac-00000010, pqac-00000014) |
| EGL-8/PLC-3 | Phospholipase C enzymes | Upstream of DAG production | Convert PIP2 into DAG, providing the second messenger input needed to activate TPA-1/PKC in the epidermal immune pathway (pqac-00000010) |
| DAG | Lipid second messenger | Between PLCs and TPA-1 | Activates TPA-1, coupling upstream GPCR/G-protein signaling to the kinase cascade that drives AMP expression (pqac-00000004, pqac-00000010, pqac-00000011) |
| TPA-1 | Protein kinase C (PKC) | Downstream of GPA-12/RACK-1 and DAG | Central kinase transmitting the DCAR-1 signal toward TIR-1 and the p38 MAPK cascade in response to epidermal infection or injury (pqac-00000001, pqac-00000004, pqac-00000010, pqac-00000011) |
| TIR-1 | TIR-domain adaptor / scaffold | Upstream of MAP3K NSY-1 | Links PKC-dependent signaling to the conserved p38 MAPK module that controls antimicrobial peptide induction (pqac-00000004, pqac-00000010, pqac-00000013, pqac-00000020) |
| NSY-1 | MAP kinase kinase kinase (MAP3K) | First kinase in p38 MAPK cascade | Receives input from TIR-1 and activates downstream SEK-1 as part of the canonical epidermal innate immune cascade (pqac-00000004, pqac-00000010) |
| SEK-1 | MAP kinase kinase (MAP2K) | Middle kinase in p38 MAPK cascade | Relays the signal from NSY-1 to PMK-1 to support transcriptional activation of AMP genes (pqac-00000004, pqac-00000010) |
| PMK-1 | p38 MAP kinase | Terminal kinase in core MAPK cascade | Executes the p38 MAPK immune response downstream of DCAR-1, promoting AMP induction and antifungal defense in the epidermis (pqac-00000000, pqac-00000004, pqac-00000010, pqac-00000012) |
| STA-2 | STAT-like transcription factor | Downstream nuclear effector of PMK-1 pathway | Required for transcriptional activation of nlp genes and contributes to AMP expression after fungal infection, wounding, and damage sensing (pqac-00000002, pqac-00000010, pqac-00000011, pqac-00000022) |
| ELT-3 | GATA transcription factor | Co-regulator with STA-2 downstream of signaling cascade | Works with STA-2 to promote epidermal AMP gene transcription in response to DCAR-1 pathway activation (pqac-00000004, pqac-00000010) |
| nlp-29/cnc (target genes) | Antimicrobial peptide genes / transcriptional outputs | Terminal output | Encode epidermally induced antimicrobial effectors. nlp-29 is a canonical DCAR-1–p38 MAPK target; cnc genes can also be induced in related epidermal defense programs, with some regulation occurring through a non-canonical DBL-1/TGF-β branch depending on stimulus context (pqac-00000003, pqac-00000010, pqac-00000013, pqac-00000014) |


*Table: This table summarizes the experimentally supported DCAR-1 epidermal signaling pathway in C. elegans, from HPLA sensing at the receptor to antimicrobial peptide gene induction. It is useful for tracing how damage-associated signaling is converted into antifungal and wound-response outputs.*