Research Paper Volume 12, Issue 16 pp 16255—16269

Figure 4. dpMPK-1 is activated by glucose and cholesterol, and daf-12 is needed to induce Q-cell divisions. The activated form of MPK-1 (dpMPK-1) is detected in glucose- (A) and cholesterol- (C) treated L1-arrested worms. daf-12(-) can suppress Q-cell divisions and block dpMPK-1 formation in glucose- (B) and cholesterol- (D) treated L1-arrested worms. (E) Worms with and without dpMPK-1 fluorescence were counted, and the percentage of worms expressing dpMPK-1 was calculated. Data are the average of at least ten independent experiments (sample size >50 in each experiment). Error bars: Standard Deviation (SD). ***: P<0.001. White bar: 50 μm. (F) The glucose and cholesterol treatment is only performed in F0-F1 culture period. F1 and F2 worms were collected and assessed for Q-cell divisions. (G) The F1 progeny of glucose- and cholesterol-treated worms also present aberrant Q-cell divisions, but the F2 generation shows no abnormal Q-cell division. Data are the average of at least three independent experiments (sample size >50 in each experiment). Error bars: Standard Deviation (SD). (H) The survival of the F1 and F2 progeny of F0 worms treated with glucose and cholesterol. (I) Working model: cholesterol and glucose can work through DAF-12 and DAF-16 independent of the IIS pathway to activate MPK-1 to induce neuronal Q-cell divisions in L1-arrested worms, and these effects can also affect the F1 generation.