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. Author manuscript; available in PMC: 2009 Oct 12.
Published in final edited form as: Science. 2008 Nov 7;322(5903):957–960. doi: 10.1126/science.1162011

Fig. 2. Regulation of fat metabolism by GSC proliferation.

Fig. 2

(A to D) fem-3(e2006) loss-of-function mutants (lf) producing only oocytes or fem-3(q20) gain-of-function mutants (gf) generating only sperm showed the same fat storage as in the wild type (P > 0.1) (n = 15 for each). (E) Shift to 25°C during early or late larval development did not affect fat storage in the wild type (P > 0.1) but caused a 50% decrease in glp-1(e2141) mutants (P < 0.0001) (n = 15 for each genotype and treatment). (F) GSC arrest, caused by temperature shifting of 1-day-old glp-1 adults, caused a decrease in fat storage (0 hours, P > 0.5; 30 hours, P < 0.005; 48 hours, P < 0.0001)(n = 17 for each genotype and treatment). (G) lag-2(q420) showed reduced fat (P < 0.0001) (N2, n = 12; lag-2, n = 15). (H to K) GSC overproliferation in the glp-1(ar202) gain-of-function mutant causes increased fat (P < 0.0001). In contrast, the loss-of-function mutant of gld-1(q485), in which early-phase meiotic germ cells overproliferate, did not change fat storage (P > 0.1) (N2, n = 12; glp-1, n = 15; gld-1, n = 13).