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. Author manuscript; available in PMC: 2012 Nov 18.
Published in final edited form as: Mol Cell. 2011 Nov 18;44(4):532–544. doi: 10.1016/j.molcel.2011.08.045

Figure 7. Depletion of siah-1 or drp-1 from Hatch Decreases the Life Span of C. elegans.

Figure 7

(A) RNAi-mediated depletion of C. elegans drp-1 and siah-1 resulted in reduction of mean life span N2-control (black line, mean 20.1 ± 0.3 days), N2-drp-1 (red line, 15.5 ± 0.3 days), and N2-siah-1 (green line, 17.5 ± 0.4 days, log rank p < 0.0001 in each case). RNAi depletion was initiated from hatch.

(B) A proposed model. AKAP121 regulates mitochondria dynamics through (1) facilitating Drp1 phosphorylation via PKA binding domain (RII) (2) providing a docking site for Drp1 at C-terminal domains and (3) via inhibition of Drp1-Fis1 interaction by mitochondria fission regulatory domain (MRD) within central region. Upon hypoxia or ischemia, Siah2 reduces availability of AKAP121 via Siah degron (SD), which decreases AKAP121-mediated Drp1 phosphorylation and increases Drp1-Fis1 interaction, resulting in mitochondria fission and cell death of cardiomyocytes under myocardial ischemia. Question marks indicate an unidentified component(s) that is expected to be involved in AKAP121-mediated regulation of Fis1-Drp1 complex.