Picture from Angeles-Albores D et al. (2018) MicroPubl Biol "Two new functions in the WormBase Enrichment Suite"

Figure 1. Enrichment results for Tissue, Gene and Phenotype ontologies for genes overexpressed in a ciliary transcriptome (Wang et al. 2015).

Picture from Tsuda H et al. (2008) Cell "The amyotrophic lateral sclerosis 8 protein VAPB is cleaved, secreted, and acts ...."

(B-C) An efn-2::GFP transcriptional reporter (Wang et al., 1999) shows GFP expression in hyp7 (arrowhead) during the time of DTC migration (B), but not before DTC migration (C). The bright spots in panel C are nonspecific gut autofluorescence.

Picture from Park YS et al. (2000) Biochem Biophys Res Commun "Alternative splicing of gar-1, a Caenorhabditis elegans G-protein-linked ...."

Figure 5. RT-PCR of the three gar-1 mRNAs at various develop- mental stages. RT-PCR was performed, with a primer pair flanking the i3 loop (MF-i3/MR-i3), using stage-specific RNA as a template (see Materials and Methods). The PCR products were analyzed on an 1% agarose gel. The expected sizes of the PCR products for gar-1a, gar-1b, and gar-1c are 1281, 1188, and 1008 bp, respectively (from top to bottom). E, embryo; L1, first larval stage; L2, second larval stage; L3, third larval stage; L4, fourth larval stage; and A, young adult.

Picture from Kimura K et al. (2007) J Biol Chem "Knockdown of mitochondrial heat shock protein 70 promotes progeria-like ...."

Figure 1. Localization of HSP-6 to mitochondria. A, transgenic worms expressing an HSP-6-GFP fusion protein (HSP-6::GFP; top panels) or a mitochondria targeting signal-GFP fusion protein (MTS::GFP; bottom panels) were produced as described under Experimental Procedures. Confocal images of the body wall muscles are shown. Phase-contrast images are shown on the right. Both MTS::GFP and HSP-6::GFP (leftmost panels) co-localized with MitoTracker mitochondrial dye in muscle cells (2nd panels from the left, also see yellow color in merged images in the right panels). Scale bar = 10 μm. a.a., amino acids. B, wild-type worms (N2) were homogenized and cell-fractionated by differential centrifugation. 1 μg of mitochondrial fraction (MF) and 10 μg of post-mitochondrial supernatant (PMS) and the total fraction (TF) were analyzed by Western blotting as described under Experimental Procedures. The blot was probed for mitochondrial markers (HSP-6, HSP-60, ATP-2, and CLK-1) and cytoplasmic controls (HSP-1 and actin) using antibodies as indicated. An asterisk indicates a nonspecific reaction band.

Picture from Hyun M et al. (2016) Genetics "BLIMP-1/BLMP-1 and Metastasis Associated Protein (MTA1) Regulate Stress ...."

Figure 1 The levels of BLMP-1 during development and the growth rate and lethality of blmp-1 mutants. (A and B) The levels of blmp-1 mRNA measured by qPCR (A) and BLMP-1 protein measured by Western blot analysis (B) are highest at L2 stage compared to other stages in wild-type C. elegans. In A, the values are average 6 SEM of three independent experiments. Em, embryos;YA, young adults. In B, actin is shown as a loading control. (C) The numbers of wild-type animals and blmp-1 mutants in different development stages (L2, L3, L4, and dead) were counted at 48 hr from egg hatching to yield the fraction of each stage and the death rate. blmp-1 mutants show more L2/L3 stages and dead worms compared to wildtype animals. (D) Growth rates of wild-type animals and blmp-1 mutants. Starting at 43 hr after hatching, the numbers of adult worms were counted every hour until 100% became adults (Lee et al. 2012; Wang et al. 2015). blmp-1 mutants showed grossly normal grow rate.

Picture from Kim KW et al. (2018) Neuron "A Neuronal piRNA Pathway Inhibits Axon Regeneration in C.elegans."

Figure 3. prde-1 mRNA Is Present in PLM, and prde-1 Inhibits Axon Regeneration Cell-Autonomously(A) smFISH shows prde-1 mRNAs in the cytoplasm of PLM neuron labeled with Pmec-7-gfp (muIs32). Right bottom shows no probe control.(B) Schematic of gfp KI into prde-1 genomic locus (ju1534). See also Figure S2A.(C) Confocal image of endogenous GFP::PRDE-1 fluorescence in the germline nuclei in the prde-1 (ju1534) gfp KI animals.(D) Schematic of depletion of GFP-tagged PRDE-1 protein using GFP-DEGRON (modeled after Wang et al., 2017).(E) PLM axon regrowth 24 hr post-axotomy. Data are represented as mean +- SEM. Student's t test. Number of animals is shown within columns. Bottom:representative images of PLM neurons 24 hr post-axotomy. Red-orange arrowhead, site of axotomy.(F) PLM axon regrowth 24 hr post-axotomy in transgenic animals expressing prde-1 driven by tissue-specific promoters for mechanosensory neurons (Pmec-4),motor neurons (Punc-25), or muscle (Pmyo-3) in a prde-1(mj207) background. Data are represented as mean +- SEM. One-way ANOVA followed by Tukey'smultiple comparison tests. Number of animals is shown within columns.

Picture from Brunschwig K et al. (1999) Development "Anterior organization of the Caenorhabditis elegans embryo by the labial-like ...."

Figure 2. ceh-13 expression. (A-D) Four different focal planes of a comma-stage embryo stained with the anti-CEH-13 antibody; (E-H) corresponding DAPI stainings. Strong CEH-13 staining is detected in the lateral hypodermal cells H2 and V1 and in cells of the prospective ventral nerve cord (asterisks, VNC). CEH-13 expression in anterior dorsal hypodermal cells (arrowheads, hyp) and in anterior body wall muscle cells is indicated. Expression is also found in some unidentified cells located in the anterior part of the embryo. (I) CEH-13 distribution in a 15-16 hour L1 larva; (J) corresponding DAPI staining. V1 to V6 are lateral hypodermal cells, Vx/Vx.x are descendants of these cells; a, anterior; p, posterior (left view). V1.pxx cells are not fluorescing in the L1 larva. In contrast, all V1 to V4 descendants express ceh-13 in L2 larvae (data not shown). (K-M) Embryonic expression pattern of the C. elegans Hox genes. Immunostainings of CEH-13 (K) and LIN-39::LACZ (L) in 1.5-fold embryos. Arrows indicate the borders of the LIN-39::LACZ expression domain. (M) Schematic drawing showing the expression domains of the different C. elegans Hox genes (adapted from Wang et al., 1993). Anterior, left. Bar, 10 µm.

Picture from Tsuda H et al. (2008) Cell "The amyotrophic lateral sclerosis 8 protein VAPB is cleaved, secreted, and acts ...."

Figure S7. Phenotypic studies of wild type and mutant hermaphrodites. (A-C) DTC migration and EFN-2 expression. (A) The DTC migrates along the ventral body wall muscle (blue) between the hyp7 hypodermal syncytium (green) during phase 1. The DTC then turns and crosses hyp7 during phase 2. In phase 3, the DTC turns again and migrates along the dorsal body wall muscle. Its final resting position is shown in red. Wild type and mutant hermaphrodites were scored for defects in each phase of DTC migration. (B-C) An efn-2::GFP transcriptional reporter (Wang et al., 1999) shows GFP expression in hyp7 (arrowhead) during the time of DTC migration (B), but not before DTC migration (C). The bright spots in panel C are nonspecific gut autofluorescence. These results are consistent with EFN-2 functioning in hyp7 to repel the DTC, keeping it migrating along the body wall muscle. (D) Embryonic [E] and larval [L] lethality of wild type and mutant hermaphrodites. (E) 4D time-lapse DIC micrographs of wild-type and mutant embryos undergoing ventral enclosure. During enclosure, the ventral hypodermal cells (brown cells, diagram) migrate and meet at the ventral midline. The blue cells and green cells are the seam and dorsal hypodermal cells, respectively. vpr-1(tm1411) embryos have incompletely penetrant and variably expressed enclosure defects that are similar to vab-1(dx31) null embryos. vpr-1(tm1411); vab-1(dx31) double mutants exhibit similar defects as the single mutants, although the double mutants exhibit increased embryonic lethality (D).

Picture from Walton SJ et al. (2017) MicroPubl Biol "Mapping results for a set of cGAL effectors and drivers."

Recently, the GAL4-UAS system (cGAL) has been adapted for use in C. elegans for control of gene expression across 15C - 25C (Wang et al., 2017). In order to create a desired gene expression pattern, one crosses a transgenic strain containing a driver construct with another strain containing an effector gene. Here we mapped several cGAL driver and effector integrations. We first crossed each of the cGAL driver and effector strains with N2 males, picked the heterozygous male progeny, crossed them with hermaphrodites of the mapping strain (DA438), picked L4 hermaphrodites with the corresponding transgenic marker of the driver or effector strain and scored the progeny in the next generation. The DA438 strain contains six recessive mutations, each of which locates on one of the six chromosomes and produces visible phenotypes (Bli on chromosome I, Rol on II, Vab on III, Unc on IV, Dpy on V, and Lon on X (Avery, 1993). F2 progeny with each of the six phenotypes were selected and examined for the presence or absence of the dominant marker associated with the transgene. In the cases where the dominant transgene marker is unlinked to the recessive phenotypic marker, about three quarters of the F2 progeny will have the dominant marker. If the two markers are linked, very few or no animals are expected to have the dominant transgenic marker. The following tables summarize the mapping results for each cGAL strain, stating the ratios of the F2 mutant progeny with and without the dominant transgenic marker.

Picture from microPublication Biology

Figure 1. CRISPR Design and Cuticle Integrity Characterization of rab-33 mutants: A) Diagram showing the rab-33 and taf-11.3 loci and the ok1561 deletion, dashed lines represent additional sequence upstream of the rab-33 locus. The diagram also shows the genetic construct (STOP-IN cassette, adapted from Wang et al. 2018) used in this study and the CRISPR insertion site in the rab-33 gene; HDR arms are highlighted (green) on both ends of the construct, Synthetic Nhe-1 restriction enzyme site (purple), early stop codon is noted by an asterisk, external and internal genotyping primers are shown. Lower panel shows sanger sequencing data using a rev primer, confirming the correct insertion of the STOP-IN cassette in rab-33(axr2) homozygotes. B) Genotyping results confirming correct insertion of STOP-IN cassette in our mutants. The external amplicon is also digested with NheI to confirm insertion. C) Results of 150 μM Tetramisole paralysis assays on day-1 adult N2 worms (wild type), rab-6.2(ok2254) worms, rab-33 taf11-.3 (ok1561) and the newly engineered rab-33(axr2). P-value < 0.0001, Log-rank (Mantel-Cox) test. D) Results of 125 μM Levamisole paralysis assays after 30 minutes on day 1 adult N2 worms, dpy-10(cn64) worms, and rab-33(axr2). Error bars denote standard deviation. P-value < 0.001. E) images of heads and tails of N2, dpy-10(cn64), and rab-33(axr2) D1 adult worms stained with Hoescht 33258. Arrowheads show stained nuclei in the dpy-10(cn64) worms, which both the N2 and rab-33(axr2) do not exhibit. F) percentage of animals displaying nuclear stains in heads or tails. Scale bar = 20mm. Error bars denote standard deviation. p < 0.001.