Picture from Michelet X et al. (2009) Biol Cell "The ESCRT-III protein CeVPS-32 is enriched in domains distinct from CeVPS-27 and ...."

Figure 3. CeVPS-32 protein localizes to residual bodies in the male germline.Confocal images of CeVPS-32 antibody staining in hermaphrodite (A, B) and male (C, D) reproductive organs. A strong accumulation of CeVPS-32 (arrows) is detected as a vesicular pattern in the proximal gonad (go) near the spermatheca (sp) or the vas deferens (vd). Note the expression in the epithelial cells of the vulva (vu), the spermatheca and the gonad. (D) High magnification shows that CeVPS-32 is not detected in spermatids (blue), but in residual bodies (arrowheads), which are cytoplasts produced during spermatid maturation. (D') is the Nomarski view of (D). Apical junctions and the nucleus of spermatids are visualized with the MH27 antibody and Hoechst staining respectively. Scale bars: 10 μm (A-C) and 1 μm (D, D').

Picture from Hashmi S et al. (2004) J Biol Chem "The Caenorhabditis elegans cathepsin Z-like cysteine protease, Ce-CPZ-1, has a ...."

Figure 2. Temporal pattern of Ce-cpz-1 gene expression as determined by real-time PCR. The levels of the cpz-1 transcript in each stage of development were compared. The graph shows the ratio (+/- S.D.) between cpz-1 levels and those of the constitutively expressed control gene ama-1 (y axis). We used the ama-1 gene as an internal control transcript to allow the relative quantification of cpz-1 expression in each stage. The mRNA was isolated from mixed-stage embryos and synchronized larval and adult populations collected at 2-h intervals and used for the preparation of stage-specific cDNA as indicated on x axis. Stage-specific molting within the life cycle is indicated by vertical and horizontal arrows. Note that cpz-1 transcripts increased in the intermolt period of each larval stage and at 40 h when the fertilized embryos go through the process of embryogenesis. Each experimental point was repeated at least twice.

Picture from Gladden JM et al. (2007) Genetics "A ONECUT homeodomain protein communicates X chromosome dose to specify ...."

Figure 4.-CEH-39 accumu- lates in nuclei of young embryos, consistent with its role as an XSE, and also in germline nuclei. (A- D) Partial projections of false-col- ored confocal images of wild-type and ceh-39 mutant embryos stained with DAPI (red) and anti- bodies (CA1184) against CEH-39 (green). (A and B) CEH-39 local- izes in a diffuse pattern within in- terphase nuclei of young (50-cell) and older (150- to 200-cell) XX embryos; CEH-39 also associates with mitotic chromosomes (arrow and inset in A). (C) CEH-39 is greatly reduced in embryos with .200 cells. (D) No CEH-39 anti- body staining was detectable in ceh-39 deletion mutant embryos, which lack the antibody epitope, demonstrating specificity of the CEH-39 antibody. Bars, 10 μm. (E and F) Partial projections of false-colored confocal images of wild-type and ceh-39 mutant go- nads stained with DAPI (red) and CEH-39 antibodies (green) (CA1183). Two focal planes (sep- arated by a dashed white line in E) were used to show pachytene and diplotene diakinesis. In late pachytene and early diplotene, CEH-39 staining appears diffuse nuclear and excluded from the nucleolus. In late diplotene and diakinesis, staining colocalizes with condensed chromosomes. Enlargement of the nucleus in diakinesis is shown in insets in E. Staining is absent in gonads of ceh-39 deletion mutants.

Picture from Raman D et al. (2024) MicroPubl Biol "PALS-14 promotes resistance to Nematocida parisii infection in ...."

Figure 1. Loss of pals-14 causes increased susceptibility to N. parisii infection.A) The lifecycle of N. parisii starts with an extracellular infectious spore that fires an invasion apparatus called a polar tube that delivers a parasite cell, or sporoplasm, directly into the C. elegans intestinal cytoplasm. This sporoplasm replicates into a multinucleated cell called a meront, which eventually differentiates back into spores that egress from the cell, exit the organism, and go on to infect new hosts.B) pals genes induced by N. parisii infection listed in order found in the genome, together with information about whether they are induced in pals-22(jy3) and pals-25(jy111) strains, based on RNAseq analysis (Gang et al., 2022). Induced pals genes are listed as present in pals-2-6(vir6); pals-25(jy111) mutants if they are not deleted by the pals-2-6(vir6) deletion. (RNAseq analysis has not yet been performed on pals-2-6(vir6); pals-25(jy111) mutants.)C) N. parisii sporoplasms per animal infected at the L1 stage, quantified 3 hours post-inoculation (hpi).D) N. parisii sporoplasms per animal infected at the L1 stage after RNAi treatment of the previous generation (see Methods), quantified at 3 hpi.E) N. parisii meront (pathogen) load per animal infected at the L4 stage after RNAi treatment, quantified at 30 hpi.F) N. parisii meront (pathogen) load per animal infected at the L4 stage, quantified at 30 hpi.C-F) Three experimental replicates were infected and quantified, with 100 animals (C&D) or 50 animals (E&F) per strain per replicate. **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05, Kruskal-Wallis test with Dunn's multiple comparisons test using Prism v10. Bars represent mean values, and error bars standard deviation. Select statistically significant comparisons are being shown for clarity.

Picture from Eisenmann DM et al. (2000) Genetics "Protruding vulva mutants identify novel loci and Wnt signaling factors that ...."

Figure 2.-Four stages of C. elegans vulval development. (A) Generation of P1.p-P12.p during the L1 stage. P3.p-P8.p make up the Vulval Equivalence Group. The remaining six cells fuse with the hypodermis of the animal during the L1 stage. (B) In the late L2 stage, the fates of the six vulval precursor cells (P3.p-P8.p) are determined in response to several extracellular signals: an inductive signal from the anchor cell, a lateral signal acting between Pn.p cells, and a general inhibitory signal acting between the Pn.p cells and the surrounding hypodermal syncytium. The outcome of these signaling events is that P6.p adopts the 1 vulval cell fate, its neighbors, P5.p and P7.p, adopt the 2 vulval cell fate, and P3.p, P4.p, and P8.p adopt the 3, nonvulval cell fate. Note that P3.p also adopts the F fate 50% of the time in wild-type animals. (C) The vulval precursor cells execute their cell fates in the L3 stage. Shown are P3.p-P8.p with their patterns of cell division and the fate of their progeny cells (vulval or hypodermal). For P5.p-P7.p, the letters indicate the plane of the axis of the last cell division (see Table 2). (D) The 22 vulval cells go through morphogenetic movements during the L4 larval stage to form the vulval opening. A diagram of an intermediate stage in that process, referred to as the 'Christmas tree' stage, is shown here. The 8 cells descended from P6.p occupy the center of the developing vulva, and the 7 cells each descended from P5.p and P7.p occupy the sides of the developing vulva. To the right of each diagram are indicated the genes examined in this work that are likely to function at that stage in vulval development.