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which is called the mixed equilibrium problem (MEP) [1].
The phenotype resembles that in mutants for SUMO-recruited Mec complex factors MEP-1 and LET-418 (Stielow et al., 2008; Wu et al., 2012).
(B D) RNAi inactivation of lsy-2 (B), mep-1 (C), and let-418 (D) caused ectopic expression of GCY-5::GFP in ASEL neurons.
After RNAi inactivation of mep-1 and let-418, 25% (n = 32) and 12% (n = 40) animals showed ectopic expression of GCY-5::GFP in ASEL, respectively (Fig. 6C and 6D).
Interestingly, mep-1 is also a synMuv B gene, notwithstanding that MEP-1 is not a stable member of the C. elegans NuRD complexes in solution.
We found that CHD-3 did not co-precipitate with MEP-1 (Figure 1F).
Given the similar phenotype of let-418 RNAi) let-418 RNAiand animep-1 RNAihe mep-1 RNAinteranimalsof LET-418 and MEP-1, we expecthe a comphysicalgene expressinteraction.
By analogy to the Drosophila dMec, we named the C. elegans LET-418 and MEP-1 containing complex "MEC complex".
However, we could not co-precipitate MEP-1 with LIN-53 (Figure 1F) nor with LIN-40 GFP LIN-40 GFP.
This suggested that mep-1 and let-418 must act prior to this stage to ensure normal development.
LET-418 and MEP-1 may generally act during embryonic development before the onset of morphogenesis, when cells still divide.
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