Picture from Kullyev A et al. (2010) Genetics "A genetic survey of fluoxetine action on synaptic transmission in ...."

Figure 1.Fluoxetine treatment and mutations in mod-5/ SERTabolish anti-5-HT immunoreactivity in the RIH and AIM neurons. (a-d) Photomicrographs of animals stained with anti-5-HT antibodies. To test the effects of MOD-5/SERT inhibitors, WT animals were incubated overnight on NGM plates containing 0.5 mg/ml of fluoxetine (as shown) or 0.4 mg/ml of imipramine (not shown) before fixation for staining. (e and f) Photomicrographs of WT animals expressing tph-1Tgfp. All the animals shown have anterior to the right.

Picture from Kim HS et al. (2014) Genetics "The novel secreted factor MIG-18 acts with MIG-17/ADAMTS to control cell ...."

Figure 3 Expression and localization of MIG-17-Venus and Venus-MIG-18. (A and C) DIC (left), confocal (center), and merged (right) images. The enlarged images of the boxed areas in the center panels are shown on the right side. The arrowheads point to the fluorescence from the gonadal basement membrane. (A) Wild-type and mig-18(k140) young adults that express MIG-17-Venus. (B) Western blot analysis of wild-type and mig-18(k140) animals that expressed MIG-17-GFP. Worm extracts (200 mg protein/sample) were analyzed using rabbit anti-GFP (2 mg/ml, Molecular Probes). The red and blue arrowheads indicate pro- and mature forms MIG- 17-GFP, respectively. Intensities of the bands were quantified using ImageJ software. (C) Venus-MIG-18 expression in wild-type and mig-17(k174) animals. (D) Colocalization of Venus-MIG-18 and MIG-17-mCherry in the gonadal basement membrane. Confocal images for Venus (left) and mCherry (center) and DIC and confocal merged image (right). The strong dot-like signals on the upper right are of coelomocytes that take up secreted proteins. Posterior gonads are shown. Anterior to the left, dorsal to the top. Bar, 20 um.

Picture from Leung AC et al. (2020) MicroPubl Biol "Lipopolysaccharide stimulates egg laying in Caenorhabditis elegans"

Wild-type N2 strain of C. elegans was stimulated by Salmonella enterica lipopolysaccharide (LPS) to lay eggs in an aqueous environment: Animals were incubated in M9 buffer for 15 minutes, after which the numbers of eggs laid were recorded for adjustment purpose. The liquid medium was then supplemented with either LPS or serotonin, or with no supplement as the negative control. The final concentration of LPS was 0.1 mg/ml and that of serotonin was 1 mg/ml. After one hour, the eggs in each microtiter well were counted again. For each individual, the adjusted number of eggs laid, which considered only the eggs laid during the treatment period, is presented here. More than 100 animals under each condition were tested. Error bars represent standard errors; asterisks denotes p < 0.01 when the treatment condition (LPS or serotonin) resulted in an egg-laying level that was significantly different from that of the negative control condition (M9), when the non-parametric Mann-Whitney U Test (Mann and Whitney 1947) was performed. The horizontal bar and the asterisks above it indicate that there was a significant difference (p < 0.01, Mann-Whitney U Test; Mann and Whitney 1947) between the numbers of eggs laid under the LPS and serotonin conditions.

Picture from Loges, Luiza N. et al. (2021) MicroPubl Biol

Figure 1. The D60N and R252L mutations in GSPD-1 reduce enzyme activity, and the R252L mutation appears to alter the position of the active site residues: (A) The protein sequence alignments of C. elegans GSPD-1 (top line) and human G6PD (bottom line) surrounding the two mutation sites (underlined) are shown. The middle line of text shows identical amino acids, and a + symbol indicates a conservative substitution. The numbers show the amino acid positions at the ends of each sequence. (B) Michaelis-Menten graph of enzyme velocities (in μmol/min/mg or U/mg) for wild-type GSPD-1 (blue circles), the D60N mutant (green triangles), and the R252L mutant (purple squares) at varying glucose-6-phosphate (G6P) concentrations. All of the data points are shown, and the lines indicate the best-fit line. (C) This table shows the results from the Michaelis-Menten fits shown in B with standard errors. (D) View of the active site in GSPD-1 models. The wild-type structure is shown in beige, and the R252L structure is shown in light blue. Asp264 and His269 bind to the glucose moiety of G6P, His207 and Tyr208 bind to the phosphate moiety of G6P, and Arg252/Leu252 are at the site of the mutation. The positions of these amino acids in each structural model are shown.

Picture from Amiri A et al. (2001) Development "An isoform of eIF4E is a component of germ granules and is required for ...."

Figure 4. IFE-1, IFE-3 and IFE-5 are enriched in the germline. m7GTP affinity-purified proteins derived from 1.5 mg of total protein from wild-type (N2) or germline-deficient (glp-4) worms were resolved by SDS-PAGE on 6% (A) and 12% (B) gels. (A) The gel on the left was stained with silver nitrate, the gel on the right was immunoblotted using anti-PGL-1 antiserum. (B) The gels were immunoblotted using antibodies to isoform-specific C-terminal peptides for each of the IFE proteins. Both wild-type and glp-4 worms were grown at 25 C, the restrictive temperature for germline development in the glp-4 strain.

Picture from Denzel MS et al. (2014) Cell "Hexosamine pathway metabolites enhance protein quality control and prolong ...."

Figure 1. Developmental Tunicamycin Resistance Screen Identifies gfat-1 gof Mutations (A) Representative images of WT controls and tunicamycin (TM)-resistant C. elegans mutants after developmental screen for resistance to 10 mg/ml TM. (B) Representative images of dhEx941(Pgfat-1:: gfat-1::cfp) transgenic animal showing the GFAT-1 expression pattern in the head area of L4 animals. DIC, differential interference contrast. (C) Multiple sequence alignment of gfat-1 protein sequences surrounding the amino acid sub- stitutions of alleles dh468, dh784, and dh785. (D) The hexosamine pathway. (E) Developmental TM resistance assay using transgenic animals expressing cfp or gfat-1::cfp fusion under gfat-1 regulatory elements (n = 3). Results are presented as means ± SEM. ***p < 0.001. (F) Representative LC/MS scans of adult C. elegans extracts. (G) Quantitative LC/MS analysis of pooled L1/L2 larvae and adult animals for UDP-HexNAc levels in dh468, dh784, and dh785 alleles of gfat-1 (n = 8). Results are presented as means ± SEM. *p < 0.05 and ***p < 0.001 versus WT. (H) Representative images of developmental TM resistance assay on control or 10 mg/ml TM plates with UV-killed OP50 bacteria, supplemented with 10 mM of indicated compounds. (I) Quantification of the developmental TM resistance assay in (F). L4 or adult animals were counted 5 days after egg transfer to TM plates and displayed as a fraction of the number of eggs used (n = 6). **p < 0.01 and ***p < 0.001 versus D-Arg. Results are presented as means ± SEM.

Picture from Wang WF et al. (1997) J Mol Biol "Expression patterns and transcript processing of ftt-1 and ftt-2, two C. elegans ...."

Figure 3. Developmental profile of ftt-1 and ftt-2 ex- pression patterns. Total RNA samples from embryos (lane 1), L1 larvae (lane 2), L2/L3 larvae (lane 3), L4 lar- vae (lane 4) and adults (lane 5) were isolated, and 10 mg of each RNA sample was separated on an agarose gel and sized according to RNA molecular mass markers (BRL). The RNA panel hybridized sequentially with the ftt-1 cDNA probe (A), the ftt-2 cDNA probe (B), and 28S rRNA probe (C). The representative autoradio- graphs in A to C were scanned densitometrically across lanes to quantitatively analyze stage specific changes in individual transcripts. These results were converted into graphic form after normalizing the data for sample load- ing variations using the 28 S rRNA marker. The lowest level of each transcript was set to an arbitrary value of 1 in order to optimize comparisons of a single transcript between the staged worms. Direct comparisons cannot be made between different transcripts, since the relative abundance scales are not comparable.

Picture from Fernandez-Abascal J et al. (2022) MicroPubl Biol

Figure 1 Cl- channel CLH-1 is needed in AMsh glia for HCO3- efflux:(A) Schematic representation of the chloride channel CLH-1 in glia and its function. CLH-1 mediates both efflux (big arrowhead) and to a lesser extent influx (small arrowhead) of Cl- and HCO3- thereby regulating the concentration of Cl- and pH both inside and outside of the cell (Grant et al., 2015, Fernandez-Abascal et al., 2021). (B) Representative images of wild type (N2, left column) and clh-1(ok658) mutants (clh-1, right column) expressing the pH sensor Superecliptic pHluorin (pGM87) under the control of the AMsh glia specific promoter pT02B11.3, grown in normal conditions (NGM, top row) or in NGM plates supplemented with 150 mM KHCO3 (bottom row). Scale bar is 50 µm. (C) Violin plots showing the quantification of relative pH inside the AMsh glia as pixel intensity of pGM87 in wild type (red) and clh-1(ok658) mutants (blue) grown on NGM or NGM supplemented with KHCO3 plates. Data were normalized to N2 in NGM conditions. Each data point represents one worm (n= 58, 31, 26 and 74, respectively). Statistics were done by ANOVA followed by Tukey post-test (****p<0.0001).

Picture from Ferguson AA et al. (2013) PLoS Genet "TATN-1 mutations reveal a novel role for tyrosine as a metabolic signal that ...."

Figure 8. Control of TATN-1 protein expression by daf-2/IGFR signaling, diet and temperature. (A) Rescue of tatn-1 mediated dauer arrest by a tatn-1p:tatn-1 cDNA:GFP transgene (bafIs131). (B) daf-2 signaling positively regulates TATN-1:GFP expression. Box and whiskers plot showing comparison of GFP fluorescence between day 1 adult wild-type and daf-2(e1368) mutants expressing the TATN-1:GFP transgene and grown on OP50- 1 bacteria. N$15 worms, ** p,0.001 by t-test. (C) Bacterial food source and temperature regulate TATN-1:GFP expression. Wild-type worms expressing the TATN-1:GFP transgene were grown on the indicated bacteria until adulthood and then either kept at 20uC or shifted to 25uC overnight. N=15 worms, ** p,0.001 for 20uC versus 25uC for each bacterial strain by t-test, and p,0.001 for 25uC treatment of OP50-1 versus HB101 or HT115. (D) Supplementation of HB101 with 1 mg/mL tyrosine or tryptophan increases TATN-1:GFP expression. Wild type worms expressing the TATN- 1:GFP transgene were grown until adulthood on the indicated diet. N$15 worms, ** p,0.001 for comparison between HB101, and HB101+Tyr or HB101+Trp by t-test. (E) Representative photos showing the effects of the treatments graphed in panels B-D.

Picture from Sadeghian, Fereshteh et al. (2023) MicroPubl Biol

Figure 1. TLN-1(W387A) results in modest motility and oocyte transit defects:A) The tln-1(kq387) strain BU387 thrashed less on average compared to N2 (Student's t-test; p<0.0002). B) No significant difference in egg laying in M9 solution was observed between BU387 tln-1(kq387) and N2 (Student's t-test p = 0.7620). C) No significant difference in stimulated egg laying in 3 mg/mL serotonin creatine sulfate monohydrate solution was observed between BU387 tln-1(kq387) and N2 (Student's t p-value of 0.9828). D-E) Confocal microscopy of the AH3437 TLN-1::GFP(WT) and BU388 TLN-1::GFP(W387A) animals indicating talin expression in body wall muscles (D), spermatheca, and sheath (E), scale bar= 20 mm. F-G) Phalloidin staining indicates actin alignment in spermatheca, sheath, germline, and body wall muscle scale bar= 20 mm. H) Spermathecal occupancy 'trapping screen' scoring of TLN-1::GFP(WT) and TLN-1::GFP(W387A) indicates the presence or absence of an embryo in the spermatheca. I-K) Assessment of timing of oocyte transit through the spermatheca (oocyte entry, dwell, and exit time) of of TLN-1::GFP(WT) and TLN-1::GFP(W387A) animals (blue: fertilized oocyte, red: oocyte fragment 'small piece').