Figure 6

NM23 inhibits p27Xic1-mediated gliogenesis through their interaction. (A) Co-expression of a NM23 member with p27Xic1 inhibits p27Xic1-mediated gliogenesis. (B) Interaction of NM23-X4 with deleted versions of p27Xic1. Full length, amino-terminal NT(1–96), and 1–91 portions of p27Xic1 interact with NM23-X4, but the 31–96 portion does not. (C) The interaction between p27Xic1 and NM23 is responsible for the inhibitory function of NM23 on Müller glial cell phenotype. NM23-X4 blocked glial induction by interacting with the amino-terminal and 1–91 portions of p27Xic1 but not with the 31–96 portion. (D) NM23-X4 cannot inhibit gliogenesis mediated by p16Xic2. Müller glial cell percentage in the retina after co-introduction of NM23-X4 and Xic1 or Xic2. (E) Effect of co-introduction of shX4-B and -B constructs in the retina. Activation of gliogenesis by shX4-B requires p27Xic1. (F) Interaction of p27Xic1 with mutants of NM23-X4. Wild type (wt), H148C (H), S150G (S) and ΔKPN were tested for their interaction with p27Xic1. (G) Wild type and the ΔKPN blocked Müller cell induction by p27Xic1, but H148C and S150G did not. Double and triple asterisks correspond to P ≤ 0.01, and 0.001, respectively; error bars indicate standard error of the mean.