Picture from Bhalla N et al. (2008) PLoS Genet "ZHP-3 acts at crossovers to couple meiotic recombination with synaptonemal ...."

ZHP-3 localizes to sites of meiotic crossover recombination. (A-F) The site from which the asymmetric disassembly of the SC occurs is marked by a ZHP-3 focus. Wild-type nuclei in diplotene/diakinesis stained with DAPI and antibodies against HTP-3, ZHP-3 and SYP-1. An individual bivalent from one of these nuclei is shown in DF. Scale bar in D represents 2 microns.

Picture from Zwaal RR et al. (1996) Cell "G proteins are required for spatial orientation of early cell cleavages in C. ...."

Figure 1. Expression of gpb-1. (A-G and L) Immunolocalization of anti-GPB-1 antiserum in wild-type animals. Shown are the following: 2-cell embryo, with staining concentrated at the region between the cells (A); 4-cell embryo (B); 12-cell embryo (C); 20-cell embryo (D); cleavage stage, about 200 cells (E); and a comma-stage embryo (F). In (A)-(F), staining is at the cell membrane and appears equally intense in all cells. In (B), (C), and (D), arrowheads mark staining that colocalizes with the asters.(G) L2 larva. Staining is brightest in neuronal cells. Green arrow, ventral nerve cord; green arrowhead, dorsal nerve cord; white arrow, gonad. The circumpharyngeal nerve ring, which also shows strong staining, is out of this focal plane.(L) A portion of the meiotic germline syncytium in a distal gonadal arm of a wild-type hermaphrodite. GPB-1 (green) is found at the membrane of developing gametes. Red staining shows P granules, a germline-specific marker used as a control.(H, I, and M) Rescued gpb-1(pk44 df); pkEx179 animals.(H) 20-cell embryo, showing weaker staining than wild-type (compare with [A]-[E]).(I) Comma-stage embryo with wild-type level of staining (compare with [F]).(M) Germline from adult hermaphrodite, most of whose progeny lived; staining is weaker than wild-type (compare with [L]).(J, K, N, and O) gpb-1(pk44 df); pkEx179 probable mosaic animals.(J) and (K) show a 4-cell and a 200-cell embryo, respectively, laid by gpb-1(pk44 df); pkEx179 probable germline mosaic mother, all of whose progeny died. There is no detectable GPB-1 staining in these embryos. The images were made very bright to show that there is no membrane-associated staining. The embryos were costained with an anti-P granule antibody as a control for permeability.(N and O) Probable mosaic germlines from gpb-1(pk44 df); pkEx179 mothers (all progeny from these mothers died as embryos). Staining is undetectable in (N) and very weak in (O). In (L)-(O), GPB-1 is green and P granules are red.All pictures are single-plane confocal images. Merging and false color in (L)-(O) was added using Adobe Photoshop software.

Picture from Doser, Rachel L et al. (2022) MicroPubl Biol

Figure 1. Diminished ROS levels decrease GLR-1 transport out of the cell body via a calcium-independent mechanism. A) Representative images showing expression of contents of transgenic arrays used. Scale bar = 5 μm. B) GLR-1::mCherry transport. Top: Single time points from 50 s of continuous imaging (100 ms/frame). Two GLR-1-containing vesicles (blue and green numbers) are pointed out for three timepoints. Bottom: Kymograph derived from 30 s of a 50 s image stream depicting position (x-axis) of GLR-1 transport vesicles over time (y-axis). Scale bar = 5 μm. C and E) Representative kymographs depicting GLR-1 transport vesicles (black lines) as they are transported through the length of the neurite (x-axis) over time (y- axis). Scale bar = 5 μm. D) Quantification of transport events in control (lin-15(n765ts) X; glr-1(ky176) III; csfEx63, n=15) and worms overexpressing catalase (CTL-2(OX)) in the AVA (lin-15(n765ts) X; glr-1(ky176) III; csfEx65, n=11, **:p=0024, two-tailed Student's t-test). F) Quantification of transport events from untreated (n=18) and mitoTEMPO treated (n=20) worms (glr-1(ky176) III; akIs201, ***:p=0.0008, two-tailed Student's t-test). G) Representative traces of changes in GCaMP6f fluorescence in the AVA cell body over 60 s in vivo normalized to baseline fluorescence (DF/Fmin) from untreated (n=35) and mitoTEMPO treated (n=35) worms (lin-15(n765ts) X; csfEx62). H) Average DF/Fmin normalized to untreated controls. I) Total activity (sum of fluorescence values above baseline divided by baseline) normalized to untreated controls. J) Average baseline of these groups normalized to untreated controls.

Picture from Bhalla N et al. (2008) PLoS Genet "ZHP-3 acts at crossovers to couple meiotic recombination with synaptonemal ...."

Figure 2. ZHP-3 localizes to sites of meiotic crossover recombination. (A-F) The site from which the asymmetric disassembly of the SC occurs is marked by a ZHP-3 focus. Wild-type nuclei in diplotene/diakinesis stained with DAPI and antibodies against HTP-3, ZHP-3 and SYP-1. An individual bivalent from one of these nuclei is shown in DF. Scale bar in D represents 2 microns. (G and H) ZHP-3 foci formation depends on DSB formation and crossover recombination. Late pachytene nuclei from spo-11(ok79) (G) and msh-5(me23) (H) mutants were stained with antibodies against ZHP-3. (I, J, and K) More than one ZHP-3 focus per chromosome is frequently observed in mutant oocytes with perturbed crossover control. Late pachytene nuclei from him-8(mn253) mutants were stained with ZHP-3, SYP-1 and HTP-3 antibodies. Arrows indicate unsynapsed chromosomes. Circled nuclei have greater than five ZHP-3 foci. The inset in J is a single pair of synapsed homologs with two ZHP-3 foci.

Picture from microPublication Biology

Figure 1. Behavior and Neurodegeneration assays conducted with sod-1(G85R) strain: (A) Survival of worms treated with 100 and 150 mM Paraquat (PQ) in liquid media. The sod-1(G85R)C strain showed a significant decrease in survival with PQ treatment compared to sod-1(WT)C. Three independent experiments with three replicates (n=90 worms per group) were analyzed. A log rank test is used with DF=1, p<0.0001. Error bars indicate standard deviation for each time.(B) Quantification of number of thrashes per minute of worms treated with 0 and 2.5 mM Paraquat (PQ) in liquid media. The sod-1(G85R)C strain has defects in locomotion that increased with PQ treatment compared to sod-1(WT)C. Three to six independent experiments with 10 worms per group were analyzed using a One-way ANOVA with F=152.2 and p<0.0001. Significance on the graph: *p= 0.0319; ****p<0.0001. Error bars indicate standard deviation.(C) Nose touch avoidance response of worms treated with 0 and 2.5 mM Paraquat (PQ) in liquid media. The sod-1(G85R)C strain has a defect in nose touch avoidance response and the defect increased with PQ treatment compared to sod-1(WT)C. Three to six independent experiments with 30 worms per group were analyzed using a Two-way ANOVA with p<0.0001 for genotype, p<0.0001 for treatment and p=0.0007 for interaction between genotype and treatment. Error bars indicate standard deviation.(D) Aldicarb resistance assay. No difference was observed between sod-1(WT)C and sod-1(G85R)C. The number of independent experiments were 7 for sod-1(WT)C strain, 3 for sod-1(G85R)C strain and 5 for dgk-1 and snt-1 strains with 15 worms per group. Seven to three independent experiments were analyzed using a log rank test with DF=1, p<0.0639 for sod-1(WT)C and sod-1(G85R)C, p<0.0001 for sod-1(G85R)C and dgk-1; sod-1(G85R)C and snt-1. Error bars indicate standard deviation.(E-H) Dil staining assay in worms exposed at 0 and 2.5 mM of PQ in (E, G) solid for 18 hours and in (F, H) liquid media for 4 hours. The sod-1(G85R)C strain has neurodegeneration of ASH, PHA and PHA neurons with PQ treatment regardless of solid or liquid medium. Three independent trials with 15 worms per group were analyzed using Two-way ANOVA with p<0.0001 for genotype, p<0.0001 for Paraquat treatment and p<0.0001 for interaction between genotype and PQ treatment for both solid and liquid experiments. Error bars indicate standard deviation.

Picture from Peters MA et al. (2007) Curr Biol "A calcium wave mediated by gap junctions coordinates a rhythmic behavior in C. ...."

Figure S1. Genomic Structure and Developmental Expression Pattern of inx-16. (A) The inx-16 locus. The top portion shows the location of inx-16 on chromosome I. The deficiency (Df) used for mapping and the rescuing cosmid are shown below the chromosome. The extent of the PCR rescuing fragment, containing both inx-16 and inx-17, is depicted above the genomic structure of the loci. inx-17 is downstream of inx-16 in an operon. The insertion site of green fluorescent protein (GFP) in the INX-16:GFP rescuing fusion construct is denoted. Mutations in the inx-16 alleles are also shown. ox144 is a C-to-T transition that results in an early stop after amino acid 104 of 372 predicted residues. tm1589 deletes 470 base pairs of inx-16 genomic DNA including most of exons I and II and the intervening intron (National Bioresource Project for the Experimental Animal Nematode C. elegans).(B-D) Expression of GFP driven by the inx-16 promoter (plasmid pMAP4). Fluorescence is observed in the intestine from early developmental stages. All fluorescent figures have been inverted so that fluorescence appears as black on white. In (B), GFP is observed in the developing in- testine of a comma stage embryo. In (C) is a DIC image of embryo shown in (B). In (D), GFP is observed in the intestine of an L1 stage larva.

Picture from Murayama T et al. (2013) Curr Biol "Environmental alkalinity sensing mediated by the transmembrane guanylyl ...."

Figure 2. Chemotaxis Analysis of gcy Mutants and Expression and Ca2+ Imaging of gcy-14 (A) Alkaline pH chemotaxis of mutants defective in gcy genes expressed in ASE (n = 12 assays each). (B) Specific expression of the gcy-14p::gfp reporter construct in ASEL, but not in ASER. Neurons stained with DiI are shown in magenta. ASE cell positions are indicated by arrows. Scale bars represent 10 mm. (C) Subcellular localization of GCY-14::GFP. The arrow indicates the cell body of ASEL. Open and filled arrowheads indicate the distal end of a dendrite and a sensory cilium of ASEL, respectively. The scale bar represents 10 mm. (D) Ca2+ transients in ASEL of gcy-14(pe1102) upon a pH up-step at t = 30 s. Ca2+ transients in ASEL of the wild-type in Figure 1D are also shown as a reference. (E) Ca2+ transients in ASER of wild-type, gcy- 14(pe1102), gcy-14 animals expressing the wildtype gcy-14 gene specifically in ASEL, and unc-13(e450) in response to a pH up-step from 6.8 to 9.1. pH up-steps were at t = 10 s. (F) Mean fluorescence intensity increases in ASER of wild-type and mutant animals shown in (E). Data were calculated from mean values of relative DF/F0 (%) at their peaks. **p < 0.01, Dunnett test compared to the wild-type in (B) and Mann-Whitney U test in (F). NS, not significant. Numbers of recordings are shown in parentheses. Error bars and gray bands in Ca2+ transient traces indicate the SEM. See also Figure S2.