| Component | Type/Function | Role in *nlp-29* regulation | Specificity (infection/wounding/osmotic stress) |
|---|---|---|---|
| HPLA | Endogenous damage-associated ligand (4-hydroxyphenyllactic acid) | Activates the upstream receptor DCAR-1 to trigger epidermal innate immune signaling leading to AMP induction including *nlp-29* (pqac-00000000, pqac-00000005) | Infection and wounding; not established as the osmotic-stress signal for *nlp-29* (pqac-00000000, pqac-00000005) |
| DCAR-1 | GPCR receptor | Functions at the top of the epidermal AMP pathway; acts upstream of GPA-12/RACK-1 and TPA-1 to induce *nlp-29* after fungal infection or epidermal injury (pqac-00000005, pqac-00000008) | Infection and wounding; not implicated in the p38-independent osmotic-stress branch (pqac-00000005, pqac-00000008) |
| GPA-12 | Gα protein | Acts downstream of DCAR-1 and upstream of TPA-1/TIR-1-p38 MAPK; epidermal activation is sufficient to promote *nlp-29* expression (pqac-00000005, pqac-00000006) | Infection and wounding; no evidence here for osmotic-stress-specific control (pqac-00000005, pqac-00000006) |
| RACK-1 | Scaffolding/signaling adaptor | Acts with/near GPA-12 upstream of TPA-1 in the epidermal signaling cascade that induces *nlp* AMP genes including *nlp-29* (pqac-00000005) | Infection and wounding; osmotic-stress role not defined in the cited evidence (pqac-00000005) |
| TPA-1 | PKCδ family protein kinase | Key upstream kinase required to relay GPCR/G protein signaling to the TIR-1–NSY-1–SEK-1–PMK-1 cascade for *nlp-29* induction (pqac-00000005, pqac-00000006) | Infection and wounding; not part of the known p38-independent osmotic branch (pqac-00000005, pqac-00000006) |
| NIPI-3 | Tribbles-like kinase/regulator | Infection-specific regulator acting upstream of both TPA-1 and the p38 MAPK cassette; required for full *nlp-29* induction after fungal infection but dispensable for wound-induced expression (pqac-00000005, pqac-00000007, pqac-00000010) | Infection-specific; not required for wounding response; no osmotic-stress role established here (pqac-00000005, pqac-00000007, pqac-00000010) |
| TIR-1 | TIR-domain adaptor protein | Adaptor upstream of NSY-1/SEK-1/PMK-1; essential for epidermal innate immune induction of *nlp-29* after infection and wounding (pqac-00000006, pqac-00000009, pqac-00000010) | Infection and wounding; not required for the p38-independent osmotic response (by inference from pathway separation) (pqac-00000006, pqac-00000009) |
| NSY-1 | MAP3K | MAP kinase kinase kinase in the core p38 cascade downstream of TIR-1; required for *nlp-29* induction (pqac-00000005, pqac-00000009) | Infection and wounding; not part of the osmotic-stress branch (pqac-00000005, pqac-00000009) |
| SEK-1 | MAP2K | MAP kinase kinase in the p38 pathway; acts cell-autonomously in the epidermis and is sufficient there to restore *nlp-29* reporter induction in mutants (pqac-00000007, pqac-00000010) | Infection and wounding; no evidence for osmotic-stress dependence (pqac-00000007, pqac-00000010) |
| PMK-1 | p38 MAPK | Terminal MAPK of the core innate immune cascade; required for infection- and wound-induced *nlp-29* expression, and high constitutive *nlp-29* in epidermal damage backgrounds is largely PMK-1-dependent (pqac-00000001, pqac-00000006, pqac-00000009) | Infection and wounding; notably dispensable for osmotic-stress-induced *nlp-29* expression (pqac-00000001, pqac-00000006) |
| STA-2 | STAT-like transcription factor | Essential transcriptional effector downstream of/with PMK-1 for *nlp-29* expression; also mediates AMP induction after structural epidermal damage and can be regulated at apical attachment structures (pqac-00000005, pqac-00000006, pqac-00000027) | Infection and wounding/structural damage; no specific osmotic-stress role established in the cited evidence (pqac-00000005, pqac-00000027) |
| ELT-3 | GATA transcription factor | Required transcription factor for *nlp* AMP transcription, including *nlp-29*; notably shared between fungus-induced and osmotic-stress-induced regulation, even though the latter is PMK-1-independent (pqac-00000005, pqac-00000001) | Infection and osmotic stress; likely contributes to wound-responsive epidermal AMP transcription as a shared epidermal regulator (pqac-00000005, pqac-00000001) |


*Table: This table summarizes the best-supported epidermal signaling cascade controlling *nlp-29* expression in *C. elegans*, from upstream ligand/receptor inputs to downstream transcription factors. It also distinguishes which components are specific to fungal infection or wounding versus the separate osmotic-stress branch.*