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. Author manuscript; available in PMC: 2014 Mar 4.
Published in final edited form as: Neuron. 2013 Sep 4;79(5):903–916. doi: 10.1016/j.neuron.2013.06.035

Figure 7. EBAX-1 and DAF-21/Hsp90 Facilitate the Folding and Degradation of Misfolded SAX-3.

Figure 7

(A) The effects of ebax-1 and daf-21 on AVM guidance in the sax-3(ky200) mutant background. Control (ctrl), the sax-3(ky200) mutant alone. EBAX-1 WT (+) and EBAX-1 ΔSWIM (+), overexpression of Pebax-1::EBAX-1 WT and Pebax-1::EBAX-1 ΔSWIM in the sax-3 mutants. Data represent means ± SEM. **p<0.01 and ***p<0.001 relative to indicated controls; one-way ANOVA.

(B) EBAX-1 overexpression has no effect in sax-3(ky123) null mutants.

(C) Model of the EBAX-1-mediated triage mechanism for SAX-3 quality control during axon guidance. The amount of non-native SAX-3 caused by translational errors, environmental stress or genetic mutations is restricted by collaborative efforts between EBAX-1 and DAF-21/Hsp90. On one hand, EBAX-1 recruits DAF-21/Hsp-90 to promote the folding and refolding of non-native SAX-3. On the other hand, EBAX-1 degrades irreparable proteins through its connection to the CRL complex.