Picture from Chao LF et al. (2017) PLoS Genet "An SMC-like protein binds and regulates Caenorhabditis elegans ...."

Fig 3. SMCL-1 expression and protein features. (A) Adult hermaphrodites from wild-type (WT) and a straincarrying the map::smcl-1 transgene driven by endogenous smcl-1 5' and 3' elements. A section of thegermline is shown, imaged by DIC to show structures and fluorescent microscopy to detect mVenusexpression from the MAP tag. Arrowheads denote the first four oocytes. (B) A typical SMC protein folds backon itself at a hinge domain, bringing coil regions together and creating a "head domain" (yellow) from ATPasedomains in the N- and C-termini. SMCL-1 lacks predicted coil and hinge domains, but has N- and C-terminalATPase domains that may be capable of forming a head domain (purple). (C) SMC head domain and theATPase cycle, showing binding of ATP (red circle), ATP-dependent engagement of heads from two SMCproteins, and disengagement upon ATP hydrolysis. (D) SMCL-1 amino acid sequence aligned to C. eleganscondensin SMC proteins. Shown are regions surrounding three conserved motifs found in SMCs and relatedATPases: the Walker A motif, ABC transporter signature motif, and Walker B motifs, and their consensussequences. SMCL-1 shares a conserved Walker A motif, but differs from consensus signature motif andWalker B motif at residues shown in red. Asterisk denotes catalytic amino acid required for ATP hydrolysis.x = any amino acid and h = hydrophobic amino acid.

Picture from Lyssenko NN et al. (2008) BMC Dev Biol "An unexpectedly high degree of specialization and a widespread involvement in ...."

Figure 3. tat-5 is a housekeeping gene. The 5' end of the tat-5 locus and structure of the two tat-5 expression cassettes (A). Expression of tat-5b::nls::gfp in the lcIs481.4 line in embryos (B and C) and a head region of an adult (D), and in the lcEx481.2 isolate atthe head-intestine junction (E) and in a developing somatic gonad (F). Necrotic death of tat-5(RNAi) embryos (G). Abbreviations:DTC-distal tip cell; in-intestinal nucleus; sg-somatic gonad.

Picture from Zhu Z et al. (2016) Dev Cell "Functional Coordination of WAVE and WASP in C.elegans Neuroblast ...."

Figure 3. Identification of MIG-13 and SEM-5 Interaction(A) A color-coded heatmap scoring the position of AQR. n > 50 for all genotypes. Statistical significance compared with the control (-) with a matching color codeis based on Student's t test, ***p < 0.001.(B) Interaction of MIG-13 with SEM-5, CED-2, or NCK-1 in a GST-tagged protein pull-down assay.(C) Representative still images and quantification of SEM-5 (GFP knockin) in AQR. Traces in the lower panel are line-scan intensity plots (a.u.) of the SEM-5::GFPand Myri-mCherry signals along the leading edge. The trajectory and direction of the scanning line are shown in the upper and bottom panels. Asterisks show thepositions of the leading edge.(D) Quantification of AQR that contains SEM-5::GFP signal at the leading edge.(E-G) Fluorescence time-lapse images of F-actin, plasma membrane, and histone during AQR migration in abl-1(ok171) (E), sem-5-sg (F), or abl-1(ok171);sem-5-sg double (G) mutant animals. Asterisks denote nuclei.(H-J) Quantification of migration speed (box plots, H) F-actin GFP fluorescence intensity ratio (the leading edge to cytosol, I; data are presented as mean +- SEM),and the number of filopodia-like structures (J) of AQR.n = 10-20. Statistical significances compared with WT (*) or between underlined pairs (#) are based on Student's t test: **p < 0.01, ***p < 0.001, #p < 0.05, and ###p < 0.001. Scale bars, 5 um.

Picture from Rousakis A et al. (2014) PLoS One "Diverse functions of mRNA metabolism factors in stress defense and aging of ...."

Figure S7 Spatial overlapping of PB and SG components in somatic cells of worms. Representative confocal images of 1-day adults, under normal conditions (-HS) or after heat-shock at 35C for 3 h (+HS), co-expressing: (A) rfp::tiar-1 and ife-2::gfp (BRF312 in Table S1), (B) rfp::tiar-1 and dcap-1::gfp (BRF328 in Table S1), (C) gfp::tiar-2 and dcap-1::rfp (BRF369 in Table S1), (D) rfp::tiar-1 and gfp::tiar-2 (BRF361 in Table S1). B and C are confocal optical sections. All fusions are driven by their own promoters. Arrows point to induced granules. Scale bar: 25 um.

Picture from Yang Y et al. (2017) Dev Cell "Spectraplakin Induces Positive Feedback between Fusogens and the Actin ...."

Figure S2, related to Figure 2. Generation of conditional knockout animals using thesomatic CRISPR-Cas9 strategy. (A) The embryo survival rates in WT and conditionalknockout animals before and after heat-shock treatment; n = 180-300. (B) Invertedfluorescence time-lapse images of F-actin (GFP::moesinABD) in a seam cell from V.abirth (0 min, the completion of V cell cytokinesis) to fusion pore formation (redasterisks, the loss of F-actin fluorescence in V.a) in WT, wve-1-sg, arx-2-sg, syg-1 andsyg-2 animals. (C-D) Fluorescence still imagesshow the loss of GFP fluorescence in GFPknock-in animals that were introduced with the corresponding conditional mutationswith (right) or without (left) heat-shock treatment. (E) Quantification of GFP knock-outefficiency in (C-D). The target gene was scored as knocked out in cells in which its GFPfluorescence wasindistinguishable from the background fluorescence. n = 104-117. (F)Fluorescence of GFP::WVE-1 knock-in in seam cells. (G) Fluorescence time-lapseimages of ARX-2::GFP knock-in and mCherry::PH during the seam-hyp7 cell fusion. 0min, the completion of V cell cytokinesis. White asterisks, V.a. (H) Duration from F-actin enrichment to fusion pore formation. n = 11-27. (I) Time interval from thecleavage furrow formation to the end of cytokinesis in WT and mutant animals. n =10.Error bars indicate the mean +- SD. n.s., not significant based on Student's t-test. Scalebars in (B), (C), (D), (F) and (G), 5 um.

Picture from Duan Z et al. (2015) Genetics "Guanine nucleotide exchange factor OSG-1 confers functional aging via ...."

Figure 3 OSG-1 is expressed in muscle and nervous system. (A) Fluorescence microscopy image taken from a Posg1::GFPnematode (FDX2533), showing Posg-1 expression in head and body wall muscle. (B) Image of the head of a Posg-1::GFP nematode demonstrating Posg-1::GFP expression in head muscle and FLP neurons. (C) DiD staining of amphid neurons of a Posg-1::GFP nematode, demonstrating OSG-1 expression in the ASE neuron. (D) Number of thrashes in 4-day-old N2 or SG-1 KO worms. n $ 20 animals/genotype. (E) Representative images of ASER neurons marked with GFP in 4-day-old N2 or OSG-1 KO genotypes. Images were taken with a BX61 Olympus microscope equipped with Nomarsky optics and a digital camera.

Picture from Duan Z et al. (2015) Genetics "Guanine nucleotide exchange factor OSG-1 confers functional aging via ...."

Figure 3 OSG-1 is expressed in muscle and nervous system. (A) Fluorescence microscopy image taken from a Posg1::GFPnematode (FDX2533), showing Posg-1 expression in head and body wall muscle. (B) Image of the head of a Posg-1::GFP nematode demonstrating Posg-1::GFP expression in head muscle and FLP neurons. (C) DiD staining of amphid neurons of a Posg-1::GFP nematode, demonstrating OSG-1 expression in the ASE neuron. (D) Number of thrashes in 4-day-old N2 or SG-1 KO worms. n $ 20 animals/genotype. (E) Representative images of ASER neurons marked with GFP in 4-day-old N2 or OSG-1 KO genotypes. Images were taken with a BX61 Olympus microscope equipped with Nomarsky optics and a digital camera.

Picture from Achanzar WE et al. (1997) J Cell Sci "A nematode gene required for sperm vesicle fusion."

Fig. 4. In situ hybridization showing fer-1 expression in the testis. (A) Hybridization with the fer-1 antisense probe. fer-1 message is only detected in the testis and not in the gut or carcass that includes other tissues. Expression starts near the turn of the gonad and is not seen in spermatogonial cells (sg). (B) Control with a fer-1 sense probe showing no hybridization to the testis. Bar, 50 um (A and B). (C-D) Higher magnification of the testis loop region with paired Nomarski differential interference contrast optics (C,E) and DAPI fluorescence images (D,F). (C,D) fer-1 expression begins as the cells mature from mitotic spermatogonial cells to primary spermatocytes (1o). (E,F) The fer-1 message is not detected past the first meiotic division and is not seen in either the secondary spermatocytes (2o) or spermatids (sd). Bar, 10 um (C-F).

Picture from Cao S et al. (2005) J Neurosci "Torsin-mediated protection from cellular stress in the dopaminergic neurons of ...."

Torsin-mediated protection of C. elegans DA neurons against 6-OHDA. A, Different stages of DA neurodegeneration. From left to right, representative temporally staged images depicting CEP DA neuron morphology of wild type, neuronal process blebbing, process loss and cell body rounding, and cell body loss are shown. Scale bar, 20 μm. B, Schematic representation of torsin domains and mutations. Top, Human torsinA; bottom, C. elegans TOR-2; black region, signal peptide; green region, putative hydrophobic transmembrane domain; A, Walker A domain; B, Walker B domain; 1, sensor 1 domain; 2, sensor 2 domain. The asterisks mark the approximate positions of mutations that were analyzed. Mutations within sensor 2 correspond to the EOTD- associated mutation [torsinA(ΔE302/303)] and the structurally analogous change in worm TOR-2 [TOR-2(Δ367)]. The mutation within the Walker A domain corresponds to an alteration within a conserved ATP-binding site [TOR-2(K171T)]. C, TOR-2 protection against 6-OHDA. After 6-OHDA treatment, worms were examined for the presence of all four wild-type CEP neurons at specific time points: green, TOR-2; blue, TOR-2(K171T); red, TOR-2(Δ367); black, Pdat-1::GFP without TOR-2 overexpression. D, TorsinA protection against 6-OHDA. Green, TorsinA; blue, torsinA/torsinA (ΔE302/303) combination; red, torsinA(ΔE302/303); black, Pdat-1::GFP without torsinA overexpression. Statistical significance between Pdat-1::GFP and each of the six torsin-overexpressing lines was assessed at each time point between all transgenic lines by the ANOVA Bonferroni's test (*p < 0.05; NS, not significant). Error bars in C and D indicate SEM between independent experiments. E, Immunolocalization of torsinA in DA neurons in human torsin-overexpressing worms. Top, Two CEP neurons marked by GFP fluorescence; middle, torsinA antibody immunostaining in CEP cell bodies (arrows); bottom, merge of top and middle images. Scale bar, 20 μm. F, Immunolocalization of torsinA in torsinA(ΔE302/303)-overexpressing worms in CEP cell bodies (arrows). Scale bar, 20 μm. The GFP and merge images are not shown because they were reminiscent of those in Figure 1 E. G, Western analysis to verify TOR-2 overexpression in TOR-2- overexpressing worms. Actin was probed for each sample as a loading control. H, Native TOR-2 expression pattern in transgenic worms in which GFP is driven by a genomic region upstream and inclusive of the C. elegans tor-2 gene. Left, Entire worm depicting expression in the AVE neurons (large arrowhead), vulva muscle cells (small arrowhead), and PVW neurons (arrow); gut autofluorescence is also observed throughout the intestinal tract. Right, Close-up of the anterior head region, showing expression in the M1 pharyngeal neuron (large arrowhead), the AW class of neurons (2 small arrowheads), and the AVE interneurons (2 arrows). Expression in DA neurons is not observed. Scale bar, 20 μm

Picture from Zhu Z et al. (2016) Dev Cell "Functional Coordination of WAVE and WASP in C.elegans Neuroblast ...."

Figure 1. MIG-13 and Arp2/3 Regulate theC. elegans Q Neuroblast Migration(A) Schematic overview of Q cell migration. TheQR descendant (QR.x), AQR, migrates anteriorly,and the QL descendant (QL.x), PQR, migratesposteriorly. Apoptotic Q.aa cells are indicated bya black cross.(B) MIG-13 protein domains. The amino acidchanges or deletion in mig-13 mutant alleles areindicated.(C) A color-coded heatmap scoring the distribution of AQR position in L4 animals of various genotypes as indicated. The full length between URXand PLM cells is divided into ten blocks, and thepercentage of AQR that stopped within eachblock is given. The color (green) darkness of theblocks symbolizes the range of percentagevalues. n > 50 for all genotypes. Statistical significance compared with the control (-) with amatching color code is based on Student's t test,*p < 0.05. N.S., not significant.(D and E) Fluorescence time=lapse images ofF-actin and plasma membrane and histone duringAQR migration in WT (D) or mig-13(cas15) mutant(E) animals. Merged images, left; inverted fluorescence images of AQR morphology, right; whitearrows, migration direction; white arrowhead,mispolarized leading edge; asterisks, nuclei;double-headed arrows, migration distance.(F) Quantification of the F-actin fluorescence intensity ratio of the leading edge to the rear partof AQR in WT (n = 19) or mig-13 mutant (n = 15)animals. The corresponding mCherry-membraneintensity ratio was used as an internal control.Data are presented as mean +- SEM.(G) Box plots show the distributions of the AQRmigration speed in WT (n = 17), mig-13 mutant(n = 15), and arx-2-sg mutant (n = 14) animals. Theanterior migration is referred to as ''positive.''(H) Quantification of the mean counts of filopodialike structures. Bar segments represent the percentage of filopodia-like structures within thelength range as indicated. The same imaging datasets as in (G) were used for analysis.(I) Inverted fluorescence images of AQRmorphology in arx-2-sg mutants. Arrows, leadingedges; asterisks, nuclei.(J-L) Fluorescence images (J) and quantification(K and L) of ARX-2 (GFP knockin). (J) Upper,merged image; middle, plasma membrane andhistone; lower, ARX-2. Arrows, leading edges;asterisks, ARX-2::GFP from an adjacent apoptoticcell. Box plots show the quantification of ARX2::GFP enrichment (K) or distribution (L) at theleading edge of AQR (n=10-15 animals). Thequantification method is described in Figure S1and Experimental Procedures.Statistical significances in (F)-(H), (K), and (L) arebased on Student's t test, *p < 0.05, ***p < 0.001.Scale bars, 5 um. See also Figure S1; Movies S1,S2, and S3.