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. 2008 Dec 4;136(2):231–240. doi: 10.1242/dev.028043

Fig. 4.

Fig. 4.

Nolz1 and Grg5 interact and function as transcriptional repressors. (A) In situ hybridization of Grg5 mRNA expression in transverse sections of chick embryonic spinal cords. (B) Co-immunoprecipitation (IP) analyses of Grg5 protein interactions with Nolz1. (C) Schematic of the Nolz1 coding region. FKPY, putative Grg consensus binding site; Btd, Buttonhead domain; ZF, atypical zinc-finger domain. Lines beneath indicate the regions deleted within the Nolz1 coding sequence; the numbers indicate the corresponding amino acids that are deleted. Whether Nolz1 retains (+) or loses (-) its ability to interact with Grg5 in co-IP is indicated alongside. (D) Luciferase-based transcriptional assays using extracts from transfected COS-7 cells. Data are from three replicate experiments, mean ± s.e.m. Student's t-test compared with Nolz1: Nolz1+Grg5, P=0.0055; Nolz1ΔC22, P=0.0016. (E) Luciferase-based transcriptional assays using extracts from electroporated chick spinal cords. n=6-8 embryos, mean ± s.e.m. Student's t-test compared with Nolz1: Nolz1+Grg5, P<0.000001; Nolz1ΔC22, P=0.0029. Compared with GAL4-only: Nolz1+Grg5, P=0.0003.