| Function | Description | Key Evidence | References |
|---|---|---|---|
| Antimicrobial defense | NLP-29 is an epidermally induced antimicrobial peptide (AMP) in the nlp-29 cluster that contributes to antifungal defense, especially against the natural pathogen *Drechmeria coniospora*. The primary function supported by genetics is host defense after epidermal infection. | The nlp-29 cluster is strongly induced by fungal infection; transgenic worms carrying a cosmid spanning the nlp-29 locus showed significantly increased resistance to *D. coniospora* infection in vivo. Reviews of nematode AMPs classify NLP-29 as a bona fide AMP in epidermal innate immunity. | (pqac-00000001, pqac-00000002, pqac-00000011) |
| Dendrite degeneration regulation | Beyond host defense, secreted epidermal NLP-29 functions as a neuroimmune signal that promotes age- and infection-associated degeneration of PVD sensory dendrites by acting on the neuronal receptor NPR-12. | Epidermis-specific knockdown of *nlp-29* delayed PVD dendrite degeneration, whereas epidermal expression restored the phenotype. Exogenous or overexpressed NLP-29 induced degeneration through NPR-12 and downstream autophagy-related mechanisms in neurons. | (pqac-00000004, pqac-00000012, pqac-00000013) |
| Sleep promotion | NLP-29 also acts as a somnogenic immune signal: epidermally produced NLP-29 promotes movement quiescence/sleep by signaling through NPR-12 in neurons upstream of the RIS sleep neuron. | Overexpression of *nlp-29* increased movement quiescence, and loss of *npr-12* substantially suppressed this effect. Immune activation and wounding induce AMP expression, including *nlp-29*, and animals lacking AMP genes show reduced sleep and reduced survival after injury. | (pqac-00000019, pqac-00000020, pqac-00000021, pqac-00000024) |
| Wound response | *nlp-29* is rapidly induced in the epidermis after sterile epidermal injury, making it part of the acute wound-response program as well as the infection response. | A *pnlp-29::GFP* reporter is induced within about 1 hour after epidermal wounding and remains elevated for several hours. The wound-induced response occurs in epidermal cells/hyp7 and depends on the epidermal p38 MAPK immune pathway. | (pqac-00000014, pqac-00000016, pqac-00000017) |
| Osmotic stress response | *nlp-29* is also activated by osmotic stress and epidermal damage states, showing that it is a broader epidermal stress-response effector, not only an infection marker. This osmotic-stress induction is largely independent of the canonical PMK-1/p38 infection pathway but still requires epidermal transcriptional control. | The nlp-29 cluster is induced under high osmolarity conditions; this induction differs from fungus-induced expression because it does not require the p38 MAPK cascade, while shared epidermal regulators such as ELT-3 remain important. *nlp-28* and *nlp-29* are specifically highlighted as strongly osmotic-stress inducible members of the cluster. | (pqac-00000002, pqac-00000005, pqac-00000033) |


*Table: This table summarizes the major experimentally supported biological functions of NLP-29 in *C. elegans*, spanning innate immunity, neuroimmune signaling, wound responses, and stress responses. It is useful for distinguishing NLP-29's primary antimicrobial role from its later-discovered signaling functions.*