Picture from Jonathan J. Ewbank (2006) WormBook "Signaling in the immune response."

Figure 6. The TIR-1/NSY-1/SEK-1 cassette is part of a broader signaling network. Figure based on published information (Huffman et al., 2004; Kim et al., 2004; Koga et al., 2000; Mizuno et al., 2004; Sakaguchi et al., 2004; Villanueva et al., 2001). The MAP3K presumed to act upstream of SEK-1 and JKK-1 have not been identified. It is noteworthy that there is some uncertainty as to whether JNK-1 really plays a role in the resistance to the stress associated with heavy metal exposure (Mizuno et al., 2004) as originally reported (Villanueva et al., 2001).

Picture from Shaye DD et al. (2005) Development "LIN-12/Notch trafficking and regulation of DSL ligand activity during vulval ...."

Figure 4. Trans-acting factors required for LIN-12 downregulation. (A) Beta-Galactosidase filter lift assay showing that ALX-1 interacts with LIN-12(region 1) in the yeast two-hybrid system. Four independent transformants carrying the activation domain (AD) and DNA-binding domain (DBD) fusions indicated are shown. (B) Domain structure of Ce ALX-1, Saccharomyces cerevisiae (Sc) Bro1p and H. sapiens (Hs) Alix, showing the N-terminal BRO1 domain, which mediates localization to late endosomes (Kim et al., 2005), a highly conserved Src kinase phosphorylation consensus site, one or two coiled-coils and a C-terminal proline-rich domain (PRD). (C) A GFP::ALX-1 translational reporter is highly and widely expressed (data not shown), and is seen in all the VPCs. This is a lateral view, with AJM-1 (red) detected by immunofluorescence, while native fluorescence of fixed GFP::ALX-1 is visualized without the need for anti-GFP staining. Note that GFP::ALX-1 appears to accumulate in vesicular structures (arrowheads) that are probably LE/MVEs. (D) Domain structure of Ce WWP-1, D. melanogaster (Dm) Su(dx) and Mus musculus (Mm) Itch, showing the C2 phospholipid-binding motif, WW motifs, and the ubiquitin-conjugating HECT domain (reviewed by Ingham et al., 2004). (E) Phylogenetic relationship among Nedd4-family members from C. elegans, Drosophila and mouse. Neighbor-joining analysis of the full-length proteins was done with MacVector (Accelrys), using an uncorrected p' setting for distance calculation and 1000 bootstrap repetitions to calculate the percent branch support, shown above each branch. CeD2085.4 (HECT domain only) and CeF45H7.6 (WW repeats and HECT domain) were used to anchor the tree. Scale bar: 10 μm.

Picture from Tsukamoto T et al. (2017) Genetics "LIN-41 and OMA Ribonucleoprotein Complexes Mediate a Translational ...."

Figure S2. Effects of RNA interference with lin-41 and oma-1/2 on expression of several transcripts that selectively associate with LIN-41. Fluorescence and DIC microscopy were used to examine the expression of GFP::3xFLAG::CYB-3 (A-F; strain DG4271) SPN-4::GFP::3xFLAG (G-L; strain DG4158), and GFP::3xFLAG::MEG-1 (M-R; strain DG4213) after lin-41(RNAi), oma-1(RNAi; oma-2(RNAi); or control(RNAi) treatment. Living animals were examined on the second day of adulthood. In several species, translational regulation of B-type cyclins has been observed to contribute to the regulation of meiotic maturation (reviews by Kim et al. 2013). cyb-3 mRNA, which encodes cyclin B3, is a 6.7-fold enriched in the LIN-1 immunopurified samples (File S3). Thus, we examined expression of cyb-3 expression pattern using GFP::3xFLAG::CYB-3 is expressed in all eugenic nuclei in the adult hermaphrodite gonad (panel B) and that lin-41(RNAi) did not alter the GFP::3xFLAG::CYB-3 expression pattern (panel D; n=25). We also examined GFP::3xFLAG::CYB-3 expression on day 1 of adulthood in lin-41(n2914) (strain DG4386, n=25) and obtained similar results. Thus, misregulation of cyb-3 expression is unlikely to contribute to the premature M-phase entry defect in lin-41 null mutant oocytes. We did observe a slight reduction in GFP::3xFLAG::CYB-3 expression in the most proximal oocytes (-1 to -4) after oma-1(RNAi); oma-2(RNAi) on day 2 of adulthood (indicated by arrowheads in panel F; n=28) and in oma-1(zu405te33); oma-2(te51) null mutants on day 1 of adulthood (strain DG4390; n=60). Whether this slight reduction in CYB-3 levels contributes to (or is a consequence of) the M-phase entry defect in oma-1; oma-2 mutants will require further study. Surprisingly, we observed an expansion of GFP::3xFLAG::MEG-1 expression following oma-1(RNAi); oma-2(RNAi) treatment (panel R; n=33). This phenotype differs from that observed in the oma-1(zu405te33); oma-2(te51) double null mutant in the background in which GFP::3xFLAG::MEG-1 exhibits weak but not expanded expression (see Figure 11 and its discussion in the main text). The expression level of GFP::3xFLAG::MEG-1 appeared lower following oma-1(RNAi); oma-2(RNAi) as compared to that observed in the fog-2(oz40) and acy-4(ok1806) genetic backgrounds (see Figure 12, E-H). A possible explanation is that the RNAi treatment might reduce but not eliminate OMA-1/2 function. There may be sufficient residual function to enable the OMA-1/2 promotion of some MEG-1 expression. This combined with the low meiotic maturation rate might lead to the accumulation and expansion of GFP::3xFLAG::MEG-1 expression, analogous to that observed in unmated fog-2(oz40) females and acy-4(ok1806) hermaphrodites. Bars, 50 um.