Skip to main content
. Author manuscript; available in PMC: 2018 Jan 22.
Published in final edited form as: Neuron. 2017 Jan 4;93(1):80–98. doi: 10.1016/j.neuron.2016.11.036

Figure 4. Additional class-specific repressors control motor neuron identity.

Figure 4

A: In ot718 animals, unc-129 is derepressed in AS MNs (phenocopied by the unc-55 mutant allele, e1170) and this phenotype is unc-3-dependent. ot718 fails to complement e1170 and is thus confirmed to be an unc-55 mutant allele. del-1 expression is unaffected in unc-55 mutants, but is derepressed in AS MNs in mab-9; unc-55 double mutants – indicating a redundant role of these two genes. The individual defects of bnc-1, mab-9, and unc-55 mutants are additive since the expression of unc-129 in bnc-1; unc-55 and del-1 in mab-9; unc-55 double mutants is no longer class-specific. WT and mab-9 mutant images repeated from Fig.2A and Fig.3F, respectively; all images show anterior half of worm; all scale bars = 50 µm.

B: unc-55 gene locus.

C: DA/DB/VA/VB-specific and unc-3-dependent effector genes acr-2, dbl-1, and slo-2 are derepressed in AS MNs in unc-55 mutants. See Fig.S3A for quantification.

D: In unc-4 mutants, acr-16 is derepressed in DA MNs in an unc-3-dependent manner. Additive effect of double mutant bnc-1; unc-4 causes acr-16 to no longer be as class-specific.

E: In vab-7 mutants, unc-53 is derepressed in DB MNs in an unc-3-dependent manner. Additive effect of double mutant bnc-1; vab-7 causes unc-53 to no longer be as class-specific.

F: Quantification for A, D, and E; error bars show SD. Unpaired t-tests were performed for all mutants compared to WT unless otherwise indicated; ***p < 0.001; n ≥ 13.

G: Genetic model depicting the interactions of repressors on class-specific effector genes in VNC MNs. In AS MNs, acr-16 and acr-5 are likely repressed by as yet unidentified AS-specific repressors, perhaps redundantly with UNC-55.