Figure 6. Loss of germ cell pluripotency in gld-1-deficient animals does not occur in response to all stresses.

(A) Representative micrographs (x400) of gonads of ced-3(+) day 2 animals which were stained with SYTO12 to detect apoptotic cell corpses. White bar graphs present number of apoptotic nuclei per gonad arm (n = 60 gonads per genotype). (B) Representative micrographs (x400) of gonads of gld-1(RNAi); ced-3(RNAi) day-4 animals which were stained with DAPI to detect germline and somatic nuclei within the animals' gonads. Black bar graph presents the percentage of gonad area occupied by large nuclei (n = 60 gonads per genotype). ER stress was induced by tfg-1 RNAi. Osmotic stress was induced by osm-8 inactivation. Mitochondrial stress was induced by RNAi targeting ddl-3. Genotoxic stress was induced by rad-51 RNAi. Asterisks mark Student's T-test of p < 0.001 relative to control RNAi-treated animals. Note that the stresses that did not induce germ cell transdifferentiation in gld-1(−); ced-3(−)animals also failed to suppress the germline tumor in gld-1(−); ced-3(+) animals (see Figure 6—figure supplement 1).

DOI: http://dx.doi.org/10.7554/eLife.08005.015

Figure 6—figure supplement 1. Not all stresses suppress the germline tumor in gld-1-deficient animals.

Representative micrographs (x400) of DAPI-stained gonads of gld-1(RNAi) day-4 animals (n = at least 50 gonads per genotype). Note that the ability to execute apoptosis has not been manipulated in these animals, in contrast to the animals in Figure 6B. ER stress was induced by tfg-1 RNAi. Osmotic stress was induced by osm-8 inactivation. Mitochondrial stress was induced by RNAi targeting ddl-3. Genotoxic stress was induced by rad-51 RNAi. Only tfg-1 RNAi suppressed tumor progression.

DOI: http://dx.doi.org/10.7554/eLife.08005.016