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. Author manuscript; available in PMC: 2007 May 8.
Published in final edited form as: Hum Mol Genet. 2006 Mar 2;15(7):1087–1098. doi: 10.1093/hmg/ddl023

Figure 4.

Figure 4

Missense mutations and deletions of human NF1 modulate Drosophila MAPK activity. (A) Position of four hNF1 missense mutations, and size of five hNF1 deletion constructs, that have been expressed and analyzed in Drosophila Nf1 null mutants (CSRD, Cys–Ser-rich domain; GRD, GAP-related domain; LRD, Leu-rich domain). Crosses required to generate F1 progeny expressing UAS-hNF1 mutants or deletion constructs under control of the nervous system specific elav-Gal4 driver (B) on the X chromosome or the globally expressing e22c-Gal4 driver (C) on the second chromosome. (D) Representative western blot of head extracts from flies expressing normal and mutant hNF1s and deletions, probed with anti-phospho-MAPK then stripped and re-probed with anti-MAPK antibodies. (E) Levels of phospho-MAPK versus total MAPK levels in flies expressing hNF1 mutants and deletions, normalized to K33 wild-type (+) control values (see Materials and Methods). (D and E) Expression is under control of the e22c-Gal4 driver. (E) Values are mean ± SEM (*P < 0.05; **P < 0.01; n = 4–6).