Figure S1.
The genetic interaction of atg-9(bp1532) with autophagy mutants. (A–C) In the hypodermis of wild-type animals at the L4 larval stage, SQST-1::GFP is weakly expressed and diffusely localized (A′). A large number of SQST-1::GFP aggregates accumulate in epg-5 mutants (B), which are largely absent in epg-5; atg-9(bp1532) double mutants (C). The C. elegans strains used in this experiment carry a single-copy SQST-1::GFP transgene (bpIs443). Panel A shows the DIC image of the animal in A′. (D–F) In the hypodermis of wild-type L4 larvae, GFP::LGG-1 shows weak accumulation (D′). Numerous GFP::LGG-1 puncta accumulate in epg-5 mutants (E), and this accumulation is largely suppressed in epg-5; atg-9(bp1532) double mutants (F). The C. elegans strains used in this experiment carry a single-copy GFP::LGG-1 transgene (qxIs13). Panel D shows the DIC image of the animal in D′. (G and H) Quantification of the number of SQST-1::GFP aggregates (G) and GFP::LGG-1 puncta (H) per confocal plan in the indicated strains shown (n = 3 animals for each genotype). Data are shown as mean ± SEM; ***, P < 0.001. For comparison, the middle body region of animals at the same developmental stage was analyzed. (I) Immunoblot showing the levels of SQST-1::GFP in extracts from wild-type animals, epg-5 mutants, and epg-5; atg-9(bp1532) double mutants. (J) Quantification of the number of SQST-1::GFP aggregates in the indicated genotypes shown in K–M and Q–V (n = 3 animals for each strain). Data are shown as mean ± SEM; *, P < 0.05. (K–M) Visualization of SQST-1::GFP aggregates in the head region of animals with the indicated genotypes. In the head of wild-type L4 larvae, SQST-1::GFP is weakly expressed and diffusely localized (K′). SQST-1::GFP aggregates accumulate in cpl-1 mutants (L), and the accumulation is suppressed in atg-9(bp1532) cpl-1 double mutants (M). The C. elegans strains used in this experiment carry bpIs151(Psqst-1::sqst-1::GFP+unc-76). Panel K shows the DIC image of the animal in K′. (N and O) No GFP::SEPA-1 aggregates are detected in wild-type embryos at the comma stage. A large number of SQST-1::GFP aggregates accumulate in atg-9(bp1527) null mutants (O). The dashed contour outlines the embryo in N′. Panel N shows the DIC image of the animal in N′. (P) Quantification of the number of GFP::SEPA-1 aggregates in embryos of the indicated strains (n = 3 embryos for each genotype). Data are shown as mean ± SEM; ***, P < 0.001. (Q–V) The number of SQST-1::GFP aggregates in the head region of animals with various genetic backgrounds. SQST-1::GFP aggregates accumulate in epg-7 mutants (Q), atg-18 hypomorphic mutants (S), and bec-1 hypomorphic mutants (U). The number of aggregates is further enhanced in atg-9(bp1532); epg-7 double mutants (R). atg-9(bp1532)atg-18 double mutants (T) and bec-1; atg-9(bp1532) double mutants (V). The C. elegans strains used in this experiment carry bpIs151(Psqst-1::sqst-1::GFP+unc-76). (W–Z) A large number of GFP::SEPA-1 aggregates accumulate in epg-6 null mutant embryos (X), epg-8 null mutant embryos (Y) and epg-9 null mutant embryos (Z) at the comma stage, and this accumulation is not suppressed by atg-9(bp1532). Panel W shows quantification of the number of GFP::SEPA-1 aggregates in embryos of the indicated strains in X–Z (n = 3 embryos for each genotype). Data are shown as mean ± SEM; n.s., no significant difference. Scale bars: 10 μm for A–F; 20 μm for K–M and Q–V; 5 μm for N and O and X–Z. Source data are available for this figure: SourceData FS1.

The genetic interaction of atg-9(bp1532) with autophagy mutants. (A–C) In the hypodermis of wild-type animals at the L4 larval stage, SQST-1::GFP is weakly expressed and diffusely localized (A′). A large number of SQST-1::GFP aggregates accumulate in epg-5 mutants (B), which are largely absent in epg-5; atg-9(bp1532) double mutants (C). The C. elegans strains used in this experiment carry a single-copy SQST-1::GFP transgene (bpIs443). Panel A shows the DIC image of the animal in A′. (D–F) In the hypodermis of wild-type L4 larvae, GFP::LGG-1 shows weak accumulation (D′). Numerous GFP::LGG-1 puncta accumulate in epg-5 mutants (E), and this accumulation is largely suppressed in epg-5; atg-9(bp1532) double mutants (F). The C. elegans strains used in this experiment carry a single-copy GFP::LGG-1 transgene (qxIs13). Panel D shows the DIC image of the animal in D′. (G and H) Quantification of the number of SQST-1::GFP aggregates (G) and GFP::LGG-1 puncta (H) per confocal plan in the indicated strains shown (n = 3 animals for each genotype). Data are shown as mean ± SEM; ***, P < 0.001. For comparison, the middle body region of animals at the same developmental stage was analyzed. (I) Immunoblot showing the levels of SQST-1::GFP in extracts from wild-type animals, epg-5 mutants, and epg-5; atg-9(bp1532) double mutants. (J) Quantification of the number of SQST-1::GFP aggregates in the indicated genotypes shown in K–M and Q–V (n = 3 animals for each strain). Data are shown as mean ± SEM; *, P < 0.05. (K–M) Visualization of SQST-1::GFP aggregates in the head region of animals with the indicated genotypes. In the head of wild-type L4 larvae, SQST-1::GFP is weakly expressed and diffusely localized (K′). SQST-1::GFP aggregates accumulate in cpl-1 mutants (L), and the accumulation is suppressed in atg-9(bp1532) cpl-1 double mutants (M). The C. elegans strains used in this experiment carry bpIs151(Psqst-1::sqst-1::GFP+unc-76). Panel K shows the DIC image of the animal in K′. (N and O) No GFP::SEPA-1 aggregates are detected in wild-type embryos at the comma stage. A large number of SQST-1::GFP aggregates accumulate in atg-9(bp1527) null mutants (O). The dashed contour outlines the embryo in N′. Panel N shows the DIC image of the animal in N′. (P) Quantification of the number of GFP::SEPA-1 aggregates in embryos of the indicated strains (n = 3 embryos for each genotype). Data are shown as mean ± SEM; ***, P < 0.001. (Q–V) The number of SQST-1::GFP aggregates in the head region of animals with various genetic backgrounds. SQST-1::GFP aggregates accumulate in epg-7 mutants (Q), atg-18 hypomorphic mutants (S), and bec-1 hypomorphic mutants (U). The number of aggregates is further enhanced in atg-9(bp1532); epg-7 double mutants (R). atg-9(bp1532)atg-18 double mutants (T) and bec-1; atg-9(bp1532) double mutants (V). The C. elegans strains used in this experiment carry bpIs151(Psqst-1::sqst-1::GFP+unc-76). (W–Z) A large number of GFP::SEPA-1 aggregates accumulate in epg-6 null mutant embryos (X), epg-8 null mutant embryos (Y) and epg-9 null mutant embryos (Z) at the comma stage, and this accumulation is not suppressed by atg-9(bp1532). Panel W shows quantification of the number of GFP::SEPA-1 aggregates in embryos of the indicated strains in X–Z (n = 3 embryos for each genotype). Data are shown as mean ± SEM; n.s., no significant difference. Scale bars: 10 μm for A–F; 20 μm for K–M and Q–V; 5 μm for N and O and X–Z. Source data are available for this figure: SourceData FS1.

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