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. Author manuscript; available in PMC: 2016 Aug 19.
Published in final edited form as: Neuron. 2015 Aug 19;87(4):733–750. doi: 10.1016/j.neuron.2015.07.031

Fig. 7. Distinct Regulation of Pan-neuronal and Neuron-Type Specific Identity Features.

Fig. 7

A: Summary of distinct regulatory effects of terminal selectors on neuron-type specific and pan-neuronal genes. Mutagenesis of Terminal Selector motifs in neuron type-specific gene fosmid reporters abolishes expression in the respective neuron types, shown in panels B, C and D. Primary data for A is shown in Fig 6A – H; Fig. S7L, M, N except for cases with footnotes* MNs = motor neurons, TRN = light touch receptor neurons. n.d. = not determined. 1: (Wenick and Hobert, 2004), 2: (Hwang and Lee, 2003), 3: (Kratsios et al., 2011), 4: (Eastman et al., 1999), 5: (Howell et al., 2015), 6: (Zhang et al., 2014), 7: (Gordon and Hobert, 2015), 8: (Serrano-Saiz et al., 2013), 9: (Wightman et al., 2005), 10: (Chang et al., 2003) 11: Pereira et al., in preparation.

B: cho-1/ChT (choline transporter) fosmid reporter expression in the cholinergic VNC MN and the head interneuron AIY is controlled by the terminal selector unc-3 (Kratsios et al., 2011) and ttx-3 (Altun-Gultekin et al., 2001). Mutagenesis of the AIY motif (replacement by FRT) and of the COE motif (GG to CC substitution) in the nuclear cho-1fosmid::SL2::NLS::yfp::H2B reporter abolishes expression in AIY and VNC MNs respectively. Mutagenesis in the fosmid reporters was done by recombineering an FRT sequence in the place of a binding site (Tursun et al., 2009). A control cho-1fosmid reporter containing only the FRT scar, without the mutations in the COE and AIY motif, drives expression in AIY and VNC MNs same as the not mutated cho-1fosmid reporter.

C: gcy-5 expression in the ASER neuron depends on the ASE terminal selector che-1 (Uchida et al., 2003). Mutagenesis of the ASE motif (replacement by FRT*) of the gcy-5fosmid reporter, abolishes expression in ASER.

D: eat-4 expression in the Touch Receptor Neurons (TRN) depends on the terminal selector unc-86 (Serrano-Saiz et al., 2013). Mutagenesis of the POU homeodomain motif (replacement by FRT) of the eat-4fosmid reporter abolishes expression in the TRNs.