Picture from Carter JL et al. (2018) MicroPubl Biol "Chemotaxis based enrichment for transgenic animals containing the rol-6 ...."

Figure 1. (A) Graphic depicting how C. elegans worms arrange transgenic elements introduced into them. (B) Pictures showing the general look of wild-type and rol-6 mutant worms. (C) Depiction of how worms segregate via chemotaxis. (D) Data showing the number of worms, rol-6 mutant (rol) vs. wild-type (WT), counted in each region, in or out of food, for three replicates, and the ratio of rol:WT worms in the 'Out of Food' condition.

Picture from Kurz CL et al. (2007) Biochem Biophys Res Commun "Caenorhabditis elegans pgp-5 is involved in resistance to bacterial infection ...."

Supplementary Figure 2. Induction of pgp-5 expression by infection and exposure to heavy metal. Fluorescence photomicrographs of ppgp-5::gfp animals after 24 h continuous exposure to OP50 (A), PA14 (B), and OP50 with 100 μM CdCl2 (C) from the L4 larval stage. In every image, heads of the animals are on the left. Arrows point to the terminal bulb of the pharynx. Note that GFP expression in the terminal bulb is only detected in majority of animals treated with CdCl2. The scale bar represents 100 μm. (D) Quantification of GFP expression of ppgp-5::gfp animals after 24 h continuous exposure to OP50 (blue; mean fluorescence = 21 ± 7), PA14 (red; mean fluorescence = 76 ± 29) or OP50 with CdCl2 100 μM (green; mean fluorescence = 43 ± 9) from the L4 larval stage using the COPAS biosort. Green fluorescence was significantly increased upon exposure to PA14 (Student's t-test, p < 0.0001) and exposure to cadmium (Student's t-test, p < 0.0001). Each spot represents one animal. The fluorescence and Time Of Flight (TOF) are measured in arbitrary, but constant units. TOF is a measure of the length of the animal; details can be found in [1]. ([1] C. Couillault, N. Pujol, J. Reboul, L. Sabatier, J.F. Guichou, Y. Kohara, and J.J. Ewbank, TLR-independent control of innate immunity in Caenorhabditis elegans by the TIR domain adaptor protein TIR-1, an ortholog of human SARM. Nat. Immunol. 5 (2004) 488-494.)

Picture from Gallo M et al. (2011) PLoS One "MISC-1/OGC links mitochondrial metabolism, apoptosis and insulin ...."

Figure 1. MISC-1::GFP reporter expression and its subcellular localization during C. elegans development. (A-B) GFP image and GFP/ DIC overlay of MISC-1::GFP expression in an early embryo. Expression is in intestinal precursor cells and has a typically mitochondrial sub-cellular localization. (C-D) GFP image and GFP/DIC overlay of reporter expression in a newly hatched L1 animal. Expression can be observed in the intestine (arrowhead points to one typical cell) and in four head neurons (arrows). As in (A,B), the GFP reporter also has a string-like appearance typical of mitochondria. (E-F) GFP image and GFP/DIC overlay of reporter expression in an adult. Expression is strongest in the pharyngeal corpus. (G) Muscles of a MISC-1::GFP adult. MISC-1::GFP co-localizes with muscle mitochondria stained with the dye Mitotracker CMXRos (MT), as seen in the overlay. (H) Seam cell syncytium of a MISC-1::GFP adult. Mitochondria were stained with Mitotracker CMXRos and nuclei were counterstained with DAPI. The overlay shows the alternating pattern of mitochondria and nuclei in the seam cell syncytium, and illustrates how MISC-1::GFP co-localizes with the mitochondria.

Picture from Juanico, Iris Y et al. (2021) MicroPubl Biol

Figure 1. : Position of paternal DNA within meiotic embryos. Hermaphrodites expressing GFP::SPCS-1, which labels the endoplasmic reticulum, were mated with control or rmd-2, 3, 6 triple mutant males expressing MEV-1::mCherry, which labels mitochondria. (A, B) Representative z projections of methanol-fixed meiotic embryos stained with DAPI and anti-GFP antibodies. Blue indicates DAPI-stained DNA. Red indicates mCherry-labeled paternal mitochondria from the sperm. Green indicates maternal endoplasmic reticulum labeled with anti-GFP, which labels GFP::SPCS-1. Arrows indicate paternal DNA. Control and rmd-2,3,6 indicate paternal genotypes. The control embryo shown is in anaphase I. The triple mutant embryo shown is in metaphase I. Bar = 5 um. (C) Diagram indicates how sperm DNA position relative to the future posterior tip was measured. PS indicates the distance from the future posterior tip of the ellipsoid embryo to the sperm DNA. EL indicates embryo length from the future posterior tip to the future anterior tip of the ellipsoid embryo. PS was divided by EL and the mean and SEM for the resulting ratios are shown. n indicates the number of embryos analyzed. Results of Students unpaired t test indicated no significant difference (NS) between control and rmd-2,3,6 (p=0.42).

Picture from Lemieux J et al. (2001) Genetics "Regulation of physiological rates in Caenorhabditis elegans by a ...."

Figure 4. Subcellular expression of GRO-1::GFP. (A-D) GFP fluorescence in a muscle cell in three different planes of focus to show how the fluorescence pervades the entire cytoplasm and nucleus. The weak striations that can be observed are the results of partial exclusion of the fluorescence from the contractile elements of the muscle. The dark granules that can be seen in D are not mitochondria but some other unidentified cytoplasmic inclusions. (E) Mitochondrial localization of the long form of GRO-1 [product of gro-1(Met1- 5Ile)::gfp; see main text]. The mitochondrial distribution of CLK-1 is shown in H for comparison. (F) A muscle cell adjacent to the vulva expressing the short form of GRO-1 [product of gro-1(Met1Ile)::gfp; see main text]. Only one plane of focus is shown. The observed distribution is indistinguishable from the distribution of GRO-1::GFP as shown in A-D. (G) Distribution of GRO-1::GFP in a neuron. Note the fluorescence is also found in the neuronal projection and that it is slightly less intense in the nucleus. (H) The mitochondrial distribution of CLK-1 (Felkai et al. 1999). (I) Distribution of the long form of GRO-1 in the mitochondria of a neuron. Note the granular cytoplasmic distribution and the exclusion from the nucleus.

Picture from Maeder CI et al. (2018) Cell "The THO Complex Coordinates Transcripts for Synapse Development and Dopamine ...."

Figure 7. CREB Physically Interacts with THOC to Recruit It onto Activity-Dependent Transcripts(A) Localization of GFP-tagged THOC components in PDE cell body.(B) Co-expression analysis of fluorescently tagged THOC-1::tdTomato and CREB::GFP in PDE neurons.(C) Quantification of simPULL assay showing that THOC-1 and CREB transiently interact in C. elegans. GFP serves as negative control. ****p < 0.0001 Student'st test.(D) Quantification of simPULL assay showing that THOC1 and CREB transiently interact in mouse striatal brain lysate. No lysate and non-specific IgG antibodiesserved as negative control. ***p < 0.0001 one-way ANOVA.(E) Immunoprecipitation of THOC-1-bound RNAs from WT and crh-1 mutant neurons. Red, synaptic genes; purple, postsynaptic genes; blue, cell adhesionmolecules; green, cytoskeletal genes; black, other pan-neuronal and control genes.(F) Current model of how THOC functions to regulate presynaptic gene expression in DA neurons. In WT, CREB recruits THOC onto presynaptic transcripts tofacilitate their efficient nuclear export for concerted translation. In THOC mutant background, these transcripts are retained in the nucleus, hence leading todecreased presynaptic proteins and defective synapse assembly. This defect can be alleviated by removal of CREB, thereby allowing for a constitutive backupexport pathway to kick in and to re-establish efficient export of presynaptic transcripts. Averages and SEM are plotted in all graphs.See also Figures S5 and S7.

Picture from Lamitina, Todd (2022) MicroPubl Biol

Figure 1. Characterization of a C. elegans G4C2 repeat model. A) Description of G4C2 expression clones and their expression products. Characteristics of these expression clones are listed above the G4C2 repeat domain. B) In situ hybridization to detect G4C2 -containing mRNA in muscle cell nuclei. Arrowheads point to examples of RNA foci, which were only observed in muscle cell nuclei (dashed circle). Scale bar = 1 micron. C) Quantification of the percentage of animals with observable RNA foci. The number above each bar represents the number of animals examined. **** - p<0.0001, Fisher's exact test with Bonferroni correction. D) Canonical translation or RAN translation was detected using GFP expression. Note in the '+ATG' lines how GFP expression transitions from soluble to puncta as the number of repeats increase. This is consistent with the production of a (Gly-Ala)x-GFP fusion protein with increasing number of repeats, which is known to form aggregates in C. elegans (Rudich et al. 2017). Without a start ATG, GFP expression is not observed until repeats ≥33, which fits the definition of RAN translation (Zu et al. 2011). All images were taken using identical exposure times. Scale bar = 100 microns. E) Quantification of RAN translated GFP. Data were normalized to the mean of the 5 repeat measurements. Graph shows the mean ± S.D. with individual data points shown. **-p<0.01, ***-p<0.001, ****-p<0.0001, One-way ANOVA with Welch test.

Picture from Rasmussen JP et al. (2008) Dev Cell "Notch signaling and morphogenesis of single-cell tubes in the C. elegans ...."

Figure 4. Ventral Migration and Lumen Formation in pm8 and vpi1. (A-D) ref-1::GFP-PM expression in pm8 and the group 3 marginal cell mc3V in successively older embryos. Images are optical sections through the midline of the cyst; a complete image series corresponding to (D) is shown in Movie S4.(E-E'') vpi1 expressing eff-1::EFF-1::GFP and stained with phalloidin to visualize F-actin at the midline (arrow); note relative absence of actin in pm8 (asterisk indicates position of pm8 nucleus).(E''') Diagram of vpi1 with the approximate position of the pm8 cell body included for reference (see Figure S3D).(F) Electron micrograph and diagram of a cross-section through pm8 in an embryo near hatching. The three marginal cell fingers (numbered 1-3) are evident in the Y-shaped lumenal channel (white) of pm8.(G) Apical junctions in a wild-type, third stage (L3) larva; cells in the pharynx and valve do not divide during larval development, but increase in size and allow better visualization of apical junctions. Apical surfaces of cell like pm7 resemble broad triangles, while the group 3 marginal cells (numbered 1-3) have long, thin apical surfaces (see also Movie S1). Note how fingers from the marginal cells extend through the apical surface of pm8. The region indicated by the double-headed arrow is diagrammed to show a superposition of the pm8 and vpi1 cell bodies on their apical surfaces; apical junctions are drawn in black. (H and I) Same region as in (F) in wild-type (H) and lin-12 glp-1 mutant (I) embryos near hatching. Bars = 1 um (F) and 5 um (G-H).

Picture from Anderson C et al. (2012) PLoS Genet "SLI-1 Cbl inhibits the engulfment of apoptotic cells in C. elegans through a ...."

Fig-1. Core molecular pathways required for the engulf-ment of apoptotic cells. Proteins of the CED-10 Rac pathway are labeled in yellow. Proteins of the CED-1 pathway are labeled in green. C. elegans protein names are indicated above and their mammalian homologs below. The Wave Regulatory Complex (WRC) contains ABI-1, GEX-2, GEX-3, WVE-1 and NUO-3. The dashed arrow from CED-6 to CED-10 indicates that CED-1, CED-6 and CED-7 might also signal through CED-10 [6]. The CED-1 pathway is required for engulfment only, whereas the CED-10 Rac pathway is required for both engulfment and DTC migration. doi:10.1371/journal.pgen.1003115.g001Author SummaryCell death is a normal part of organismal development. When cells die, other cells engulf them. In the roundworm C. elegans, engulfment is facilitated by one pathway that rearranges the actin cytoskeleton and another that recruits membrane. Together they cause the formation of cellular extensions that surround the dead cell. Notably, little is known about how engulfment is inhibited. The cytoskel-etal regulatory pathway, which also promotes cell migra-tion, includes CED-10 and ABI-1, homologs of the actin regulators Rac and the Abi proteins, respectively. In mammals, the c-Cbl proto-oncogene interacts with Rac and Abi2 and has been shown to regulate the actin cytoskeleton, so we tested whether the C. elegans homolog of Cbl, SLI-1, regulates engulfment and cell migration. We found that SLI-1 inhibits both processes. Our analysis further showed that SLI-1 does not function by inhibiting other known engulfment proteins. Cbl proteins have ubiquitin ligase domains through which they target proteins for destruction or sequestration. Most of the known functions of Cbl proteins require that domain, but we found that SLI-1 did not require it to block engulfment and cell migration. We propose that SLI-1 inhibits engulfment and cell migration through a previ-ously unidentified pathway.

Picture from Roy, Peter J. (2022) MicroPubl Biol

Figure 1. Additional Temporal Regulation of Gene Expression in C elegans Larvae is Revealed through the Intersection of Multiple mRNA Sequencing Datasets :A. A schematic illustrating the translation of C. elegans developmental time at 25oC (top timeline) to 'degrees' as articulated by Hendriks et al., (2014) (bottom timeline). On the top timeline, red vertical lines indicate the approximate time points at which Hendriks et al. sequenced mRNAs from whole animals. Longer vertical lines denote the transition from one stage to the next. On the bottom timeline, the 360 degrees is the timeline of a repeating pattern of larval gene expression that has a periodicity of ~eight hours. For example, genes that peak in expression at one time point (blue diagonal lines) were observed to peak again ~eight hours later (pink diagonal lines). E, embryogenesis (~14 hours); A, adulthood. See Hendriks et al., (2014) for more details. B. UMAP plots of six major post-mitotic tissue types. Red arrows highlight obvious archipelagos. C. UMAP plots from the pharynx, excluding the gland cells cluster (topmost cluster in the top panel in 'B') and two smaller clusters (on the bottom right of the top panel in 'B'). Each of the 14 exemplar genes shown are enriched in pharynx gene expression (see (Kamal et al., 2022)) and peak in expression at different times (indicated by the degree in the upper right-hand corner of each panel) that illustrate how expression progresses along each archipelago over time. The black arrows in the upper left panel indicate the flow of time. D. UMAP plots of genes expressed within the pharynx gland cells archipelago. Gene names in green are characterized HLH-6 targets and described in more detail in panel 'D'. The description is the same as for 'C'. The scale of expression intensity is shown below 'C' and 'D'. All panels in B-D are unmanipulated screen shots from the VisCello server (see text for details). E. Four transcriptional targets of the HLH-6 and PHA-4 transcription (trnsc) factors and their associated properties. The source of the data in each column is as follows: a- (Hendriks et al., 2014); b- (Cao et al., 2017); c- (Smit et al., 2008); d- (Smit et al., 2008) and WormBase (WS284); e-(Smit et al., 2008); f- (Smit et al., 2008) and WormBase; g-i- WormBase. The bottom two rows show the correlation (r2) between the indicated data columns as calculated in excel.