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Gene: nlp-29 (B0213.4) | UniProt: O44664 | Organism: Caenorhabditis elegans
NLP-29 (Neuropeptide-Like Protein 29) is an antimicrobial peptide (AMP) encoded by the nlp-29 gene on chromosome V of C. elegans. It belongs to the YARP (YGGW-amide related peptide) family and is synthesized as a precursor protein that is proteolytically processed to yield multiple mature amidated peptides, including QWGYGGY-amide, GYGGYGGY-amide, GMYGGY-amide, and GMYGGW-amide. The NLP-29 precursor contains an N-terminal signal peptide characteristic of secreted proteins (dierking2016antimicrobialeffectorsin pages 4-5). The mature NLP-29 peptide is 51 amino acids long with the sequence QWGYGGYGRGYGGYGGYGRGMYGGYGRGMYGGYGRGMYGGYGRGMYGGWGK, which is notably rich in glycine, tyrosine, and aromatic residues (e2018anantimicrobialpeptide pages 17-19). These structural features — a basic charge, glycine/tyrosine-rich composition, and C-terminal amidation — are hallmarks of antimicrobial peptides in the NLP class (dierking2016antimicrobialeffectorsin pages 4-5).
The primary function of NLP-29 is as an antimicrobial effector molecule in the epidermal innate immune response of C. elegans. NLP-29 is one of six AMP genes (nlp-27, nlp-28, nlp-29, nlp-30, nlp-31, and nlp-34) in the "nlp-29 cluster," which spans less than 12 kb on chromosome V (pujol2008antifungalinnateimmunity pages 2-3, dierking2016antimicrobialeffectorsin pages 4-5). Expression of these genes is strongly upregulated in the epidermis upon infection by the natural fungal pathogen Drechmeria coniospora (pujol2008antifungalinnateimmunity pages 10-11, pujol2012theoriginand pages 1-2). Transgenic worms carrying a cosmid that spans the nlp-29 locus demonstrated significantly increased resistance to D. coniospora infection compared to non-transgenic siblings (p < 0.001 survival difference over 6 days), establishing that the nlp-29 cluster enhances pathogen resistance in vivo (pujol2008antifungalinnateimmunity pages 10-11). Overexpression of nlp AMPs more broadly also leads to increased resistance to fungal infection (pujol2012theoriginand pages 1-2).
While direct antimicrobial assays on NLP-29 itself are limited, the closely related cluster member NLP-31 has been extensively characterized. Synthetic NLP-31 at 200 µM completely inhibits hyphal growth of D. coniospora in vitro, confirming direct antifungal activity (dierking2016antimicrobialeffectorsin pages 3-4). NLP-31 also demonstrates antibacterial activity against both Gram-positive (Micrococcus luteus) and Gram-negative (E. coli, Burkholderia pseudomallei) bacteria in a dose-dependent manner (lim2016nematodepeptideswith pages 8-9). Mechanistically, NLP-31 acts through a non-membranolytic mechanism: rather than disrupting cell membranes, the peptide binds DNA and interferes with bacterial DNA synthesis machinery, as evidenced by gel retardation assays and induction of cellular filamentation in treated bacteria (lim2016nematodepeptideswith pages 5-7, lim2016nematodepeptideswith pages 9-11). This DNA-binding activity is consistent with the glycine/tyrosine-rich composition shared across the nlp-29 cluster peptides (lim2016nematodepeptideswith pages 9-11).
NLP-29 is predominantly expressed in the C. elegans epidermis, specifically in the hyp7 syncytium, which comprises nearly all of the epidermal surface (pujol2008distinctinnateimmune pages 3-4, pujol2008distinctinnateimmune pages 2-3). This localization is significant because the epidermis is the first barrier tissue encountered by fungal pathogens such as D. coniospora, which infect through the cuticle (dierking2016antimicrobialeffectorsin pages 4-5). Using a pnlp-29::GFP fluorescent reporter construct, researchers have demonstrated that nlp-29 expression is induced in epidermal cells after both infection and wounding (pujol2008antifungalinnateimmunity pages 6-7, pujol2008distinctinnateimmune pages 2-3). After epidermal injury, GFP fluorescence appears within approximately 1 hour and is sustained for several hours before declining (pujol2008distinctinnateimmune pages 2-3).
The presence of a signal peptide at the N-terminus indicates that NLP-29 is secreted from epidermal cells (dierking2016antimicrobialeffectorsin pages 4-5). Experimental evidence strongly supports its secreted nature: epidermally-produced NLP-29 acts non-cell-autonomously on distant PVD sensory neurons via the receptor NPR-12, and on locomotion-controlling interneurons in sleep circuits (e2018anantimicrobialpeptide pages 5-6, e2018anantimicrobialpeptide pages 7-8, sinner2021innateimmunitypromotes pages 1-4). Epidermis-specific expression using the col-19 promoter is sufficient to rescue nlp-29 mutant phenotypes, confirming that the epidermis is the functionally relevant tissue of origin (e2018anantimicrobialpeptide pages 5-6).
The regulation of nlp-29 involves a well-characterized signaling cascade that is among the best-studied innate immune pathways in C. elegans. Multiple stimuli — fungal infection, sterile wounding, and osmotic stress — induce nlp-29 through overlapping but distinct signaling branches.
Upon fungal infection or epidermal damage, the endogenous ligand 4-hydroxyphenyllactic acid (HPLA) is detected by DCAR-1, a G protein-coupled receptor (GPCR) expressed in the epidermis (dierking2016antimicrobialeffectorsin pages 4-5, taffoni2015mechanismsofinnate pages 5-6, zugasti2016aquantitativegenomewide pages 5-6). DCAR-1 activates the Gα protein GPA-12 and the scaffolding protein RACK-1, which in turn activate TPA-1, a PKCδ family protein kinase (taffoni2015mechanismsofinnate pages 5-6, kim2018signalinginthe pages 9-12). TPA-1 signals downstream to the TIR-1 adaptor protein (an ortholog of mammalian SARM), which activates the core p38 MAPK cascade consisting of NSY-1 (MAP3K) → SEK-1 (MAP2K) → PMK-1 (p38 MAPK) (taffoni2015mechanismsofinnate pages 5-6, kim2018signalinginthe pages 9-12, pujol2008antifungalinnateimmunity pages 3-5, pujol2008distinctinnateimmune pages 3-4). This pathway acts cell-autonomously within the epidermis; expression of sek-1 specifically in the epidermis is sufficient to restore nlp-29::GFP expression in sek-1 mutants (pujol2008distinctinnateimmune pages 4-5).
At the transcriptional level, the STAT-like transcription factor STA-2 is a critical effector downstream of PMK-1 and is a potential direct substrate of activated PMK-1 (kim2018signalinginthe pages 9-12). STA-2 inactivation completely abolishes infection-induced nlp-29 and cnc-2 upregulation (zhang2015structuraldamagein pages 6-7). The GATA transcription factor ELT-3 is also required for nlp transcription (taffoni2015mechanismsofinnate pages 5-6). Interestingly, STA-2 has been found to localize to apical membrane attachment structures (hemidesmosomes/CeHDs) in the epidermis, where it may serve as a sensor of structural integrity; upon structural damage, STA-2 is released to activate AMP gene expression (zhang2015structuraldamagein pages 6-7).
The Tribbles-like kinase NIPI-3 is required specifically for infection-induced nlp-29 expression but is dispensable for wound-induced expression, thereby distinguishing infection from damage responses (pujol2008distinctinnateimmune pages 4-5, pujol2008distinctinnateimmune pages 3-4). NIPI-3 acts upstream of both TPA-1 and the p38 MAPK pathway specifically upon fungal infection (taffoni2015mechanismsofinnate pages 5-6). Mutants in nipi-3 show reduced resistance to fungal infection and shortened lifespan (pujol2008distinctinnateimmune pages 4-5).
A parallel regulatory input comes from the neuronally-derived TGF-β ligand DBL-1 signaling through a noncanonical pathway. This pathway, described by Zugasti and Ewbank (2009) in Nature Immunology, primarily regulates the cnc (caenacin) class of AMP genes rather than the nlp-29 cluster itself. Notably, dbl-1 is not required for upregulation of nlp-29 cluster genes following D. coniospora infection (zugasti2009neuroimmuneregulationof pages 5-11). However, both the p38 MAPK pathway and the DBL-1/TGF-β-SMAD signaling pathway contribute to sleep-promoting functions downstream of AMP expression (sinner2021innateimmunitypromotes pages 8-9). The TGF-β pathway component SMA-6 must function in the epidermis for proper AMP gene regulation (zugasti2009neuroimmuneregulationof pages 5-11, taffoni2015mechanismsofinnate pages 5-6).
Osmotic stress also induces nlp-29 expression, but this response is independent of the p38 MAPK cascade (PMK-1) (pujol2008antifungalinnateimmunity pages 10-11). Importantly, ELT-3 is still required for osmotic-stress-induced nlp-29 expression, indicating that the osmotic and infection pathways converge at the level of transcription factors even though they diverge upstream (taffoni2015mechanismsofinnate pages 5-6).
The following table summarizes the components of the signaling pathway regulating nlp-29:
| 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 (dierking2016antimicrobialeffectorsin pages 4-5, taffoni2015mechanismsofinnate pages 5-6) | Infection and wounding; not established as the osmotic-stress signal for nlp-29 (dierking2016antimicrobialeffectorsin pages 4-5, taffoni2015mechanismsofinnate pages 5-6) |
| 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 (taffoni2015mechanismsofinnate pages 5-6, zugasti2016aquantitativegenomewide pages 5-6) | Infection and wounding; not implicated in the p38-independent osmotic-stress branch (taffoni2015mechanismsofinnate pages 5-6, zugasti2016aquantitativegenomewide pages 5-6) |
| 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 (taffoni2015mechanismsofinnate pages 5-6, kim2018signalinginthe pages 9-12) | Infection and wounding; no evidence here for osmotic-stress-specific control (taffoni2015mechanismsofinnate pages 5-6, kim2018signalinginthe pages 9-12) |
| 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 (taffoni2015mechanismsofinnate pages 5-6) | Infection and wounding; osmotic-stress role not defined in the cited evidence (taffoni2015mechanismsofinnate pages 5-6) |
| 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 (taffoni2015mechanismsofinnate pages 5-6, kim2018signalinginthe pages 9-12) | Infection and wounding; not part of the known p38-independent osmotic branch (taffoni2015mechanismsofinnate pages 5-6, kim2018signalinginthe pages 9-12) |
| 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 (taffoni2015mechanismsofinnate pages 5-6, pujol2008distinctinnateimmune pages 4-5, pujol2008distinctinnateimmune pages 3-4) | Infection-specific; not required for wounding response; no osmotic-stress role established here (taffoni2015mechanismsofinnate pages 5-6, pujol2008distinctinnateimmune pages 4-5, pujol2008distinctinnateimmune pages 3-4) |
| 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 (kim2018signalinginthe pages 9-12, pujol2008antifungalinnateimmunity pages 3-5, pujol2008distinctinnateimmune pages 3-4) | Infection and wounding; not required for the p38-independent osmotic response (by inference from pathway separation) (kim2018signalinginthe pages 9-12, pujol2008antifungalinnateimmunity pages 3-5) |
| NSY-1 | MAP3K | MAP kinase kinase kinase in the core p38 cascade downstream of TIR-1; required for nlp-29 induction (taffoni2015mechanismsofinnate pages 5-6, pujol2008antifungalinnateimmunity pages 3-5) | Infection and wounding; not part of the osmotic-stress branch (taffoni2015mechanismsofinnate pages 5-6, pujol2008antifungalinnateimmunity pages 3-5) |
| 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 (pujol2008distinctinnateimmune pages 4-5, pujol2008distinctinnateimmune pages 3-4) | Infection and wounding; no evidence for osmotic-stress dependence (pujol2008distinctinnateimmune pages 4-5, pujol2008distinctinnateimmune pages 3-4) |
| 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 (pujol2008antifungalinnateimmunity pages 10-11, kim2018signalinginthe pages 9-12, pujol2008antifungalinnateimmunity pages 3-5) | Infection and wounding; notably dispensable for osmotic-stress-induced nlp-29 expression (pujol2008antifungalinnateimmunity pages 10-11, kim2018signalinginthe pages 9-12) |
| 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 (taffoni2015mechanismsofinnate pages 5-6, kim2018signalinginthe pages 9-12, zhang2015structuraldamagein pages 6-7) | Infection and wounding/structural damage; no specific osmotic-stress role established in the cited evidence (taffoni2015mechanismsofinnate pages 5-6, zhang2015structuraldamagein pages 6-7) |
| 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 (taffoni2015mechanismsofinnate pages 5-6, pujol2008antifungalinnateimmunity pages 10-11) | Infection and osmotic stress; likely contributes to wound-responsive epidermal AMP transcription as a shared epidermal regulator (taffoni2015mechanismsofinnate pages 5-6, pujol2008antifungalinnateimmunity pages 10-11) |
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.
Beyond its direct antimicrobial function, NLP-29 has emerged as an important neuroimmune signaling molecule with at least two well-characterized downstream functions:
E et al. (2018) demonstrated in Neuron that epidermally secreted NLP-29 promotes age- and infection-associated degeneration of PVD sensory neuron dendrites. NLP-29 acts through the neuropeptide receptor NPR-12, which is expressed on PVD neurons (e2018anantimicrobialpeptide pages 10-11). The NLP-29–NPR-12 interaction activates autophagy pathways cell-autonomously in neurons, leading to dendritic morphology changes (e2018anantimicrobialpeptide pages 10-11). Epidermis-specific knockdown of nlp-29 delayed PVD dendrite degeneration, while epidermal overexpression using the col-19 promoter induced early-onset degeneration (e2018anantimicrobialpeptide pages 5-6, e2018anantimicrobialpeptide pages 7-8). This finding reveals that the progressive upregulation of nlp-29 during aging contributes to neuronal aging phenotypes.
Sinner et al. (2021) showed that NLP-29 functions as a somnogen — a sleep-promoting molecule. Upon immune activation, wounding, or during developmental lethargus (larval sleep), epidermally-produced AMPs including NLP-29 are released and signal through NPR-12 on locomotion-controlling interneurons (PVC, RIM) that synapse onto the RIS sleep-active neuron (sinner2021innateimmunitypromotes pages 1-4, sinner2021innateimmunitypromotes pages 10-11). NLP-29 overexpression increased movement quiescence to 93.3%, and this effect was suppressed by approximately 50% when NPR-12 was knocked out (sinner2021innateimmunitypromotes pages 10-11). The sleep-promoting function requires EGFR signaling in neurons (sinner2021innateimmunitypromotes pages 10-11). Animals lacking multiple nlp and cnc AMP genes showed both impaired sleep and significantly reduced survival after injury, indicating that AMP-mediated sleep promotion is adaptive (sinner2021innateimmunitypromotes pages 11-12). NLP-29 expression correlates with sleep duration, and the NAS-38 metalloprotease promotes sleep by increasing epidermal AMP expression including nlp-29 through both the p38 MAPK and DBL-1/TGF-β-SMAD pathways (sinner2021innateimmunitypromotes pages 8-9, sinner2021innateimmunitypromotes pages 5-8).
The following table summarizes the major biological functions of NLP-29:
| 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. | (pujol2008antifungalinnateimmunity pages 10-11, pujol2012theoriginand pages 1-2, dierking2016antimicrobialeffectorsin pages 4-5) |
| 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. | (e2018anantimicrobialpeptide pages 10-11, e2018anantimicrobialpeptide pages 5-6, e2018anantimicrobialpeptide pages 7-8) |
| 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. | (sinner2021innateimmunitypromotes pages 8-9, sinner2021innateimmunitypromotes pages 11-12, sinner2021innateimmunitypromotes pages 9-10, sinner2021innateimmunitypromotes pages 10-11) |
| 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. | (pujol2008antifungalinnateimmunity pages 6-7, pujol2008distinctinnateimmune pages 3-4, pujol2008distinctinnateimmune pages 2-3) |
| 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. | (pujol2012theoriginand pages 1-2, taffoni2015mechanismsofinnate pages 5-6, pujol2008antifungalinnateimmunity pages 7-9) |
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.
The nlp-29 gene cluster has undergone rapid evolutionary diversification driven by natural selection from pathogen pressure. In C. elegans, the ancestral nlp-27 gene expanded to five genes (nlp-28 through nlp-31), while in C. briggsae the ancestral nlp-34 expanded to three genes (pujol2008antifungalinnateimmunity pages 7-9). Comparative analysis across C. elegans, C. briggsae, C. remanei, and C. japonica reveals species-specific patterns of gene duplication and loss, with C. japonica having 10 predicted paralogs from a single C. remanei gene (pujol2012theoriginand pages 1-2). Phylogenetic analysis using dN/dS ratios demonstrates that non-synonymous changes are favored over synonymous changes in several branches, indicative of positive Darwinian selection (pujol2008antifungalinnateimmunity pages 10-10). The nlp-28 and nlp-29 genes are C. elegans-specific and show distinctive regulation, being upregulated by infection, wounding, and osmotic stress (pujol2008antifungalinnateimmunity pages 7-9). This rapid evolutionary diversification, driven by intra-genomic gene duplication and adaptive sequence evolution, suggests that selective pressure from pathogens has shaped the AMP repertoire (pujol2008antifungalinnateimmunity pages 1-2).
NLP-29 is a multifunctional glycine/tyrosine-rich antimicrobial peptide produced in the C. elegans epidermis. Its primary function is as an effector of epidermal innate immunity against fungal pathogens, where it contributes to host defense as part of a cluster of co-regulated AMPs. Expression of nlp-29 is controlled by a well-defined signaling cascade: the GPCR DCAR-1 detects the damage-associated ligand HPLA, activating GPA-12/RACK-1 → TPA-1 → TIR-1 → NSY-1 → SEK-1 → PMK-1 (p38 MAPK), culminating in STA-2 and ELT-3-mediated transcription in the epidermis. The infection-specific kinase NIPI-3 provides an additional layer of specificity. Beyond antimicrobial defense, secreted NLP-29 acts as a long-range neuroimmune signal through the NPR-12 receptor, promoting dendrite degeneration during aging and sleep after immune activation or injury. The nlp-29 gene cluster has undergone rapid evolutionary diversification through gene duplication and positive selection across Caenorhabditis species, reflecting ongoing selective pressure from fungal pathogens. These findings position NLP-29 at the intersection of innate immunity, neuroimmune communication, and organismal homeostasis in C. elegans.
References
(dierking2016antimicrobialeffectorsin pages 4-5): Katja Dierking, Wentao Yang, and Hinrich Schulenburg. Antimicrobial effectors in the nematode caenorhabditis elegans: an outgroup to the arthropoda. Philosophical Transactions of the Royal Society B: Biological Sciences, 371:20150299, May 2016. URL: https://doi.org/10.1098/rstb.2015.0299, doi:10.1098/rstb.2015.0299. This article has 107 citations and is from a domain leading peer-reviewed journal.
(e2018anantimicrobialpeptide pages 17-19): Lezi E, Ting Zhou, Sehwon Koh, Marian Chuang, Ruchira Sharma, Nathalie Pujol, Andrew D. Chisholm, Cagla Eroglu, Hiroaki Matsunami, and Dong Yan. An antimicrobial peptide and its neuronal receptor regulate dendrite degeneration in aging and infection. Neuron, 97:125-138.e5, Jan 2018. URL: https://doi.org/10.1016/j.neuron.2017.12.001, doi:10.1016/j.neuron.2017.12.001. This article has 112 citations and is from a highest quality peer-reviewed journal.
(pujol2008antifungalinnateimmunity pages 2-3): Nathalie Pujol, Olivier Zugasti, Daniel Wong, Carole Couillault, C. Léopold Kurz, Hinrich Schulenburg, and Jonathan J. Ewbank. Anti-fungal innate immunity in c. elegans is enhanced by evolutionary diversification of antimicrobial peptides. PLoS Pathogens, 4:e1000105, Jul 2008. URL: https://doi.org/10.1371/journal.ppat.1000105, doi:10.1371/journal.ppat.1000105. This article has 300 citations and is from a highest quality peer-reviewed journal.
(pujol2008antifungalinnateimmunity pages 10-11): Nathalie Pujol, Olivier Zugasti, Daniel Wong, Carole Couillault, C. Léopold Kurz, Hinrich Schulenburg, and Jonathan J. Ewbank. Anti-fungal innate immunity in c. elegans is enhanced by evolutionary diversification of antimicrobial peptides. PLoS Pathogens, 4:e1000105, Jul 2008. URL: https://doi.org/10.1371/journal.ppat.1000105, doi:10.1371/journal.ppat.1000105. This article has 300 citations and is from a highest quality peer-reviewed journal.
(pujol2012theoriginand pages 1-2): Nathalie Pujol, Paul A. Davis, and Jonathan J. Ewbank. The origin and function of anti-fungal peptides in c. elegans: open questions. Frontiers in Immunology, Aug 2012. URL: https://doi.org/10.3389/fimmu.2012.00237, doi:10.3389/fimmu.2012.00237. This article has 38 citations and is from a peer-reviewed journal.
(dierking2016antimicrobialeffectorsin pages 3-4): Katja Dierking, Wentao Yang, and Hinrich Schulenburg. Antimicrobial effectors in the nematode caenorhabditis elegans: an outgroup to the arthropoda. Philosophical Transactions of the Royal Society B: Biological Sciences, 371:20150299, May 2016. URL: https://doi.org/10.1098/rstb.2015.0299, doi:10.1098/rstb.2015.0299. This article has 107 citations and is from a domain leading peer-reviewed journal.
(lim2016nematodepeptideswith pages 8-9): Mei-Perng Lim, Mohd Firdaus-Raih, and Sheila Nathan. Nematode peptides with host-directed anti-inflammatory activity rescue caenorhabditis elegans from a burkholderia pseudomallei infection. Frontiers in Microbiology, Sep 2016. URL: https://doi.org/10.3389/fmicb.2016.01436, doi:10.3389/fmicb.2016.01436. This article has 20 citations and is from a peer-reviewed journal.
(lim2016nematodepeptideswith pages 5-7): Mei-Perng Lim, Mohd Firdaus-Raih, and Sheila Nathan. Nematode peptides with host-directed anti-inflammatory activity rescue caenorhabditis elegans from a burkholderia pseudomallei infection. Frontiers in Microbiology, Sep 2016. URL: https://doi.org/10.3389/fmicb.2016.01436, doi:10.3389/fmicb.2016.01436. This article has 20 citations and is from a peer-reviewed journal.
(lim2016nematodepeptideswith pages 9-11): Mei-Perng Lim, Mohd Firdaus-Raih, and Sheila Nathan. Nematode peptides with host-directed anti-inflammatory activity rescue caenorhabditis elegans from a burkholderia pseudomallei infection. Frontiers in Microbiology, Sep 2016. URL: https://doi.org/10.3389/fmicb.2016.01436, doi:10.3389/fmicb.2016.01436. This article has 20 citations and is from a peer-reviewed journal.
(pujol2008distinctinnateimmune pages 3-4): Nathalie Pujol, Sophie Cypowyj, Katja Ziegler, Anne Millet, Aline Astrain, Alexandr Goncharov, Yishi Jin, Andrew D. Chisholm, and Jonathan J. Ewbank. Distinct innate immune responses to infection and wounding in the c. elegans epidermis. Current Biology, 18:481-489, Apr 2008. URL: https://doi.org/10.1016/j.cub.2008.02.079, doi:10.1016/j.cub.2008.02.079. This article has 388 citations and is from a highest quality peer-reviewed journal.
(pujol2008distinctinnateimmune pages 2-3): Nathalie Pujol, Sophie Cypowyj, Katja Ziegler, Anne Millet, Aline Astrain, Alexandr Goncharov, Yishi Jin, Andrew D. Chisholm, and Jonathan J. Ewbank. Distinct innate immune responses to infection and wounding in the c. elegans epidermis. Current Biology, 18:481-489, Apr 2008. URL: https://doi.org/10.1016/j.cub.2008.02.079, doi:10.1016/j.cub.2008.02.079. This article has 388 citations and is from a highest quality peer-reviewed journal.
(pujol2008antifungalinnateimmunity pages 6-7): Nathalie Pujol, Olivier Zugasti, Daniel Wong, Carole Couillault, C. Léopold Kurz, Hinrich Schulenburg, and Jonathan J. Ewbank. Anti-fungal innate immunity in c. elegans is enhanced by evolutionary diversification of antimicrobial peptides. PLoS Pathogens, 4:e1000105, Jul 2008. URL: https://doi.org/10.1371/journal.ppat.1000105, doi:10.1371/journal.ppat.1000105. This article has 300 citations and is from a highest quality peer-reviewed journal.
(e2018anantimicrobialpeptide pages 5-6): Lezi E, Ting Zhou, Sehwon Koh, Marian Chuang, Ruchira Sharma, Nathalie Pujol, Andrew D. Chisholm, Cagla Eroglu, Hiroaki Matsunami, and Dong Yan. An antimicrobial peptide and its neuronal receptor regulate dendrite degeneration in aging and infection. Neuron, 97:125-138.e5, Jan 2018. URL: https://doi.org/10.1016/j.neuron.2017.12.001, doi:10.1016/j.neuron.2017.12.001. This article has 112 citations and is from a highest quality peer-reviewed journal.
(e2018anantimicrobialpeptide pages 7-8): Lezi E, Ting Zhou, Sehwon Koh, Marian Chuang, Ruchira Sharma, Nathalie Pujol, Andrew D. Chisholm, Cagla Eroglu, Hiroaki Matsunami, and Dong Yan. An antimicrobial peptide and its neuronal receptor regulate dendrite degeneration in aging and infection. Neuron, 97:125-138.e5, Jan 2018. URL: https://doi.org/10.1016/j.neuron.2017.12.001, doi:10.1016/j.neuron.2017.12.001. This article has 112 citations and is from a highest quality peer-reviewed journal.
(sinner2021innateimmunitypromotes pages 1-4): Marina P. Sinner, Florentin Masurat, Jonathan J. Ewbank, Nathalie Pujol, and Henrik Bringmann. Innate immunity promotes sleep through epidermal antimicrobial peptides. Feb 2021. URL: https://doi.org/10.1016/j.cub.2020.10.076, doi:10.1016/j.cub.2020.10.076. This article has 72 citations and is from a highest quality peer-reviewed journal.
(taffoni2015mechanismsofinnate pages 5-6): Clara Taffoni and Nathalie Pujol. Mechanisms of innate immunity in c. elegans epidermis. Tissue Barriers, 3:e1078432, Oct 2015. URL: https://doi.org/10.1080/21688370.2015.1078432, doi:10.1080/21688370.2015.1078432. This article has 75 citations and is from a peer-reviewed journal.
(zugasti2016aquantitativegenomewide pages 5-6): Olivier Zugasti, Nishant Thakur, Jérôme Belougne, Barbara Squiban, C. Léopold Kurz, Julien Soulé, Shizue Omi, Laurent Tichit, Nathalie Pujol, and Jonathan J. Ewbank. A quantitative genome-wide rnai screen in c. elegans for antifungal innate immunity genes. BMC Biology, Apr 2016. URL: https://doi.org/10.1186/s12915-016-0256-3, doi:10.1186/s12915-016-0256-3. This article has 69 citations and is from a domain leading peer-reviewed journal.
(kim2018signalinginthe pages 9-12): Dennis H. Kim and J. Ewbank. Signaling in the innate immune response. WormBook : the online review of C. elegans biology, 2018:1-35, Aug 2018. URL: https://doi.org/10.1895/wormbook.1.83.2, doi:10.1895/wormbook.1.83.2. This article has 152 citations.
(pujol2008antifungalinnateimmunity pages 3-5): Nathalie Pujol, Olivier Zugasti, Daniel Wong, Carole Couillault, C. Léopold Kurz, Hinrich Schulenburg, and Jonathan J. Ewbank. Anti-fungal innate immunity in c. elegans is enhanced by evolutionary diversification of antimicrobial peptides. PLoS Pathogens, 4:e1000105, Jul 2008. URL: https://doi.org/10.1371/journal.ppat.1000105, doi:10.1371/journal.ppat.1000105. This article has 300 citations and is from a highest quality peer-reviewed journal.
(pujol2008distinctinnateimmune pages 4-5): Nathalie Pujol, Sophie Cypowyj, Katja Ziegler, Anne Millet, Aline Astrain, Alexandr Goncharov, Yishi Jin, Andrew D. Chisholm, and Jonathan J. Ewbank. Distinct innate immune responses to infection and wounding in the c. elegans epidermis. Current Biology, 18:481-489, Apr 2008. URL: https://doi.org/10.1016/j.cub.2008.02.079, doi:10.1016/j.cub.2008.02.079. This article has 388 citations and is from a highest quality peer-reviewed journal.
(zhang2015structuraldamagein pages 6-7): Yun Zhang, Wenna Li, Linfeng Li, Yuanbao Li, Rong Fu, Yi Zhu, Jie Li, Yanfeng Zhou, Sidong Xiong, and Huimin Zhang. Structural damage in the c. elegans epidermis causes release of sta-2 and induction of an innate immune response. Immunity, 42 2:309-320, Feb 2015. URL: https://doi.org/10.1016/j.immuni.2015.01.014, doi:10.1016/j.immuni.2015.01.014. This article has 86 citations and is from a highest quality peer-reviewed journal.
(zugasti2009neuroimmuneregulationof pages 5-11): Olivier Zugasti and Jonathan J Ewbank. Neuroimmune regulation of antimicrobial peptide expression by a noncanonical tgf-β signaling pathway in caenorhabditis elegans epidermis. Nature Immunology, 10:249-256, Mar 2009. URL: https://doi.org/10.1038/ni.1700, doi:10.1038/ni.1700. This article has 260 citations and is from a highest quality peer-reviewed journal.
(sinner2021innateimmunitypromotes pages 8-9): Marina P. Sinner, Florentin Masurat, Jonathan J. Ewbank, Nathalie Pujol, and Henrik Bringmann. Innate immunity promotes sleep through epidermal antimicrobial peptides. Feb 2021. URL: https://doi.org/10.1016/j.cub.2020.10.076, doi:10.1016/j.cub.2020.10.076. This article has 72 citations and is from a highest quality peer-reviewed journal.
(e2018anantimicrobialpeptide pages 10-11): Lezi E, Ting Zhou, Sehwon Koh, Marian Chuang, Ruchira Sharma, Nathalie Pujol, Andrew D. Chisholm, Cagla Eroglu, Hiroaki Matsunami, and Dong Yan. An antimicrobial peptide and its neuronal receptor regulate dendrite degeneration in aging and infection. Neuron, 97:125-138.e5, Jan 2018. URL: https://doi.org/10.1016/j.neuron.2017.12.001, doi:10.1016/j.neuron.2017.12.001. This article has 112 citations and is from a highest quality peer-reviewed journal.
(sinner2021innateimmunitypromotes pages 10-11): Marina P. Sinner, Florentin Masurat, Jonathan J. Ewbank, Nathalie Pujol, and Henrik Bringmann. Innate immunity promotes sleep through epidermal antimicrobial peptides. Feb 2021. URL: https://doi.org/10.1016/j.cub.2020.10.076, doi:10.1016/j.cub.2020.10.076. This article has 72 citations and is from a highest quality peer-reviewed journal.
(sinner2021innateimmunitypromotes pages 11-12): Marina P. Sinner, Florentin Masurat, Jonathan J. Ewbank, Nathalie Pujol, and Henrik Bringmann. Innate immunity promotes sleep through epidermal antimicrobial peptides. Feb 2021. URL: https://doi.org/10.1016/j.cub.2020.10.076, doi:10.1016/j.cub.2020.10.076. This article has 72 citations and is from a highest quality peer-reviewed journal.
(sinner2021innateimmunitypromotes pages 5-8): Marina P. Sinner, Florentin Masurat, Jonathan J. Ewbank, Nathalie Pujol, and Henrik Bringmann. Innate immunity promotes sleep through epidermal antimicrobial peptides. Feb 2021. URL: https://doi.org/10.1016/j.cub.2020.10.076, doi:10.1016/j.cub.2020.10.076. This article has 72 citations and is from a highest quality peer-reviewed journal.
(sinner2021innateimmunitypromotes pages 9-10): Marina P. Sinner, Florentin Masurat, Jonathan J. Ewbank, Nathalie Pujol, and Henrik Bringmann. Innate immunity promotes sleep through epidermal antimicrobial peptides. Feb 2021. URL: https://doi.org/10.1016/j.cub.2020.10.076, doi:10.1016/j.cub.2020.10.076. This article has 72 citations and is from a highest quality peer-reviewed journal.
(pujol2008antifungalinnateimmunity pages 7-9): Nathalie Pujol, Olivier Zugasti, Daniel Wong, Carole Couillault, C. Léopold Kurz, Hinrich Schulenburg, and Jonathan J. Ewbank. Anti-fungal innate immunity in c. elegans is enhanced by evolutionary diversification of antimicrobial peptides. PLoS Pathogens, 4:e1000105, Jul 2008. URL: https://doi.org/10.1371/journal.ppat.1000105, doi:10.1371/journal.ppat.1000105. This article has 300 citations and is from a highest quality peer-reviewed journal.
(pujol2008antifungalinnateimmunity pages 10-10): Nathalie Pujol, Olivier Zugasti, Daniel Wong, Carole Couillault, C. Léopold Kurz, Hinrich Schulenburg, and Jonathan J. Ewbank. Anti-fungal innate immunity in c. elegans is enhanced by evolutionary diversification of antimicrobial peptides. PLoS Pathogens, 4:e1000105, Jul 2008. URL: https://doi.org/10.1371/journal.ppat.1000105, doi:10.1371/journal.ppat.1000105. This article has 300 citations and is from a highest quality peer-reviewed journal.
(pujol2008antifungalinnateimmunity pages 1-2): Nathalie Pujol, Olivier Zugasti, Daniel Wong, Carole Couillault, C. Léopold Kurz, Hinrich Schulenburg, and Jonathan J. Ewbank. Anti-fungal innate immunity in c. elegans is enhanced by evolutionary diversification of antimicrobial peptides. PLoS Pathogens, 4:e1000105, Jul 2008. URL: https://doi.org/10.1371/journal.ppat.1000105, doi:10.1371/journal.ppat.1000105. This article has 300 citations and is from a highest quality peer-reviewed journal.