Picture from Bulow HE et al. (2002) Proc Natl Acad Sci U S A "Heparan sulfate proteoglycan-dependent induction of axon branching and axon ...."

Figure 1. The Kallmann syndrome gene kal-1 in C. elegans. (A) Schematic domain structure of the Kallmann syndrome proteins in humans (Hs), worms (Ce), and flies (Dm). Pairwise similarities of domains between proteins were calculated by aligning the domains as predicted by SMART. WAP, whey acidic protein domain; Fn(III), fibronectin III motif; SS, signal sequence. (B) Schematic drawing of the gene structure of C. elegans kal-1 (located on cosmid K03D10) and the transcriptional reporter fusion with green fluorescent protein (gfp) and the unc-54 3' untranslated region. (C) Expression pattern of the kal-1::gfp reporter construct in transgenic animals (otIs33IV).

Picture from den Boer BGW et al. (1998) Development "A tissue-specific knock-out strategy reveals that lin-26 is required for the ...."

Figure 2. Localization of LIN-26 protein during hermaphrodite somatic gonad development. Immunostaining of wild-type hermaphrodites with LIN-26 antiserum (A,C,E,G,I,K) and corresponding DAPI staining in the same focal planes (B,D,F,H,J,L). (A,B) Early L1 animal, dorsal view, showing LIN-26 in the somatic gonad precursors Z1 and Z4. (C,D) Mid-L1 animal with LIN-26 in Z1.a, Z1.p, Z4.a and Z4.p. (E,F) Early L2 animal, with no detectable LIN-26 in the anterior dtc. (G,H) Animal in L2/L3 molt with LIN-26 in a sheath/spermatheca precursor (SS-cell), the future AC and a DU precursor (other cells of the somatic gonad are not visible in this focal plane). Note that LIN-26 expression is weaker than in Pn.p cells (large arrow points to P6.p). (I,J) L3 animal with weak LIN-26 expression in the AC. (K,L) L4 animal with weak LIN-26 expression in uterine cells. Due to weakness and rapid fading of the uterine signal we could count up to 32 nuclei per arm but never in both arms; thus we cannot exclude that a small subset of uterine nuclei do not express LIN-26. In this as in subsequent figures, anterior is to the left and dorsal is up, unless otherwise noted. Bar 6 mm (A-D), 8 mm (E-L).

Picture from Pak SC et al. (2004) J Biol Chem "SRP-2 is a cross-class inhibitor that participates in postembryonic ...."

Figure 7. srp-2 promoter::GFP expression pattern. Lines of transgenic C. elegans carrying the srp-2 promoter::gfp reporter gene were created as described under Experimental Procedures. SRP-2::GFP expression was visible in all developmental stages of the worm. A-D, nuclear and cytoplasmic expression of srp-2 in the embryo. Note srp-2 expression in the eggshell (D, arrowheads). E-I, SRP-2 expression in the L1/L2 larvae. GFP is visible in a number of hypodermal (possibly hyp 1, 2, and 3) cells near the buccal cavity (E and F), the sensory support (sheath or socket) cells of several sensilla (F), alae (G, arrowheads), posterior intestinal cells (H), and seam cells and the body hypoderm (I). In the adult hermaphrodite, strong punctate expression is seen in the hypodermal cells surrounding the anterior and posterior bulb of the pharynx (J), the hyp 7 cells near the vulva (K and L), and the fibrous organelles (M and N). O-R, SRP-2 expression in phasmid neurons. Normaski of the hermaphrodite tail (O), GFP expression in phasmid neurons (PHA and PHB) (P), amphid neuron-specific dye, DiI, staining of phasmid neurons (Q), and overlay of GFP and DiI staining (R). The overall SRP-2::GFP expression pattern was similar in both the hermaphrodites (S) and males (T). int, intestine; ab, anterior bulb; pb, posterior bulb; sm, sphincter muscle; ss, sensory support cells; hyp, hypoderm; cut, cuticle; fo, fibrous organelles; sp, spicule.

Picture from Aurelio O et al. (2002) Science "Immunoglobulin-domain proteins required for maintenance of ventral nerve cord ...."

Fig. 1. Structure and expression of zig genes. (A) Schematic structure of the predicted ZIG proteins. Protein domain, signal sequence (SS), transmembrane (TM), and GPI-anchor- predictions were performed as described in Web fig. 1 and based on PCR-amplified cDNAs. ZIG proteins are solely defined by the presence of exclusively two Ig domains (hence "zig" for "zwei Ig"); otherwise the ZIG proteins are highly divergent among themselves both in primary sequence (Web fig. 2) and exon/intron organization [panel (B)], suggesting anancient origin of this gene family. Database searches reveal that other metazoan genomes also contain a variety of secreted and transmembrane 2-Ig domain-only proteins whose role in neural development has not been explored (Web fig. 1B). (B) Structure of zig-promoter::gfp fusion constructs and summary of expression patterns (21). (C) Transgenic animals expressing zig::gfp fusion constructs. Arrows in insets point to PVT (21). (D) Temporal dynamics of zig-4::gfp expression from the integrated array otIs20. Note the absence of zig-4::gfp expression in PVT at embryonic and early L1 stages (upper left panel). Similar temporal expression profiles in PVT are observed with chromosomally integrated zig-1, zig-2, zig-3, and zig-8::gfp reporter genes. zig-5::gfp expression can first be observed at late (>threefold) stages of embryonic development. (E) Timeline of zig gene expression in relation to C. elegans development, timing of pioneer axon outgrowth (1) and unc-6/netrin expression (3). Expression of zig genes in PVT persists in adults, yet becomes less penetrant.

Picture from Nelson MD et al. (2014) Curr Biol "FMRFamide-like FLP-13 neuropeptides promote quiescence following heat stress ...."

Figure 2. flp-13 Is Expressed in the ALA Neuron and Is Required for ALA-Induced Quiescence (A) The gene flp-13 encodes for a preproproteinthat is processed into seven distinct neuropeptides, FLP-13-FLP-13g, each of which is amidated at the C terminus. The tm2427 deletion removes all of exon 2, which results in a frame shift mutation. ''ss'' denotes signal sequence. (B) flp-13 is expressed in the ALA neuron. mCherry is expressed under the control of the flp-13 promoter, and GFP is expressed in the ALA neuron under the control of the ida-1 promoter. (C) Overexpression of LIN-3/EGF in the wild-type genetic background results in a feeding quiescence phenotype 2 hr after induction of the lin-3 transgene. In the flp-13(tm2427) background, fewer animals are quiescent during lin-3 overexpression (n = 18-20 worms per trial, four trials; ***p < 0.0005, Student's t test). flp-13 expressed in ALA using the ida-1 promoter restores the ability of LIN-3 to induce quiescence (n = 21 animals per trial, two trials; ***p < 0.0005, Student's t test). (D) flp-13(tm2427) mutation impairs the suppression of locomotion (left) and feeding (right) caused by activating ChR2 in the ALA neuron with blue light in the presence of ATR (n = 10 animals per condition; *p < 0.05 **p < 0.005, Wilcoxon rank-sum test comparing initial red to blue and initial red to finalred conditions).Error bars indicate the SEM. See also Figure S2 and Table S1.

Picture from Howell K et al. (2017) Curr Biol "Morphological Diversity of C.elegans Sensory Cilia Instructed by the ...."

Figure 1. oig-8 Expression in Sensory Neuronsand Localization to Ciliated Endings(A) oig-8 locus, oig-8 promoter fusion to assessexpression, oig-8 fosmid-based translational reportersto assess protein localization (the N-terminal fusion hasGFP inserted immediately after the signal peptidesequence; the C-terminal fusion has GFP insertedimmediately before the stop codon), CRISPR deletionallele ot818, and nonsense mutation (Q116Amber)allele gk867223. The OIG-8 protein contains a signalpeptide sequence (SS) and transmembrane (TM)domain.(B and C) GFP::OIG-8 (from the oig-8fosmid::Ngfptranslational reporter, otEx6368) localizes to amphidcilia (B) and to axonal and dendritic membranes of PVD(C). Fusing GFP to the C-terminal end of the oig-8 locus(oig-8fosmid::Cgfp, otEx6815) results in severe sortingdefects; the OIG-8::GFP protein is stuck in the cellbody, suggesting that C-terminal residues may becritical for OIG-8 trafficking (B).(D) GFP::OIG-8 expressed in individual amphidwing neurons localizes to cilia (GFP signals are colorinverted and then transformed to black/white signals).GFP::OIG-8 from odr-10prom::gfp::oig-8 (otEx6936) localizes to the cilia of AWA in L4 animals (middle).GFP::OIG-8 from str-1prom::gfp::oig-8 (otEx6807) localizes to the cilia of AWB in L4 animals (middle).GFP::OIG-8 from ceh-36prom3::gfp::oig-8 (otEx6922)localizes to the cilia of AWC L4 animals (bottom).GFP::OIG-8 also localizes to the cilia of amphid wingneurons in L1-stage animals (Figure S2F). The ciliaschematic is adapted from [2, 23].