Figure 1. A) Map of the exons, and intron of spch-3 (T27A3.4) with the location of the xc2 deletion in red. B) Map of the new spch-3 allele after mutation, with frameshifted nucleotides to the first stop codon in purple.
Figure 1. A. Map of exons, introns and the 3'UTR of cls-2 (R107.6). B. The eighth exon and 3'UTR of cls-2 (R107.6) with the position of the xc3, xc4, and xc5 mutations indicated in red. C. Alignment of DNA and amino acid sequences in mutant and wildtype worms with mutations in red.
Side-by-side comparison of markers disregarding the temporal aspect,demonstrating that six different cell types can be distinguished based on the expression pattern.
Figure 10. Working model for Mn and Fe uptake by SMF transporters in C. elegans.A: Regulation of Mn, Fe contents and SMF transporters upon low Mn exposure (0.001 mM to 3 mM), which is believed to be beneficial for the worm physiology [92]. B: Regulation of Mn, Fe contents and SMF transporters upon high Mn exposure (50 mM to 150 mM), which was shown to be toxic (Fig. 3, 4). We propose that SMF-3* is the main transporter responsible for Mn uptake (A), and that it is degraded upon exposure to high Mn concentrations (B). Since high Fe content limit Mn uptake, SMF-3 may be inhibited by intracellular Fe (A). SMF-1 would be involved in Mn uptake to a lesser extent, and together with SMF-2*, would be responsible for Fe uptake. Upon Low Mn exposure SMF-2 would be mostly required for Fe uptake (A), whereas upon high Mn exposure, SMF-2 would be inhibited and SMF-1 would partially compensate for Fe uptake (B). In the case of SMF-2 and SMF-1, metal uptake could essentially take place in acidified endosomal compartments, as SMF-2 is mainly cytoplasmic and SMF-1 is detected in sub-apical compartments. Gap-junction communications between pharyngeal epithelia, vpi cells and intestinal cells permit Mn2+ and Fe2+ to diffuse distant from their site of uptake, allowing metal-dependent regulation of smf mRNA stability or transcription. A prediction of our model is that the Fe gradient established by SMF-2 activity would be reversed upon high Mn exposure (B), and could constitute the signal for smf expression regulation. Since basal smf mRNA levels depend on the integrity of each smf genomic sequence (Fig. 9), transcriptions of smf genes are assumed to be interdependent, maybe because they require a common transcription factor. * SMF-2 might transport Mn and SMF-3 might transport Fe, but these possibilities are not explored in this model. The size of the text reflects the concentration of the species.
REC-8 can not be detected in embryos (C). It is homogeneously distributed in early nuclei of the gonad (F) and is condensed into threads in pachytene nuclei (J).
Fig 3. unc-6/netrin signaling via the unc-5/UNC5 receptor requires lon-2/glypican. (A) The axon of PVM normally migrates ventrally in the wild type, but it can be forced to migrate dorsally by misexpressing the repulsive receptor unc-5/UNC5. We quantified PVM since AVM could not be reliably identified (bothAVM and neighboring ALMR axons project dorsally in Pmec-7::unc-5 transgenic animals.)