Protein O-GlcNAcylation Is Required for Fibroblast Growth Factor Signaling in Drosophila

Daniel Mariappa, Kathrin Sauert, Karina Mariño, Daniel Turnock, Ryan Webster, Daan M. F. van Aalten, Michael A. J. Ferguson, H.-Arno J. Müller*

*To whom correspondence should be addressed. E-mail: h.j.muller{at}dundee.ac.uk

This PDF file includes:

• Fig. S1. Hexosamine biosynthesis pathway.
• Fig. S2. EGFR-dependent MAPK activation in the ectoderm in nst^MZ embryos.
• Fig. S3. Molecular cloning and transgenic rescue of nst.
• Fig. S4. O-GlcNAc immunostaining is reduced in nst^16923MZ embryos.
• Fig. S5. Changes in protein O-GlcNAcylation upon modulation of OGT and OGA activity in S2 cells.
• Fig. S6. Lack of mesoderm phenotype in sxc, nst double mutants.
• Table S1. Genetic interaction between nst and htl.
• Table S2. Rescue of hatching defects in nst^MZ embryos.
• Table S3. Measurement of UDP-HexNAc in mmy and nst embryos.
• Table S4. Tissue-specific rescue of the nst phenotype.
• Table S5. Epistasis experiment of nst mutants with λHtl.
• Table S6. Suppression of nst phenotype by GlcNAcstatin C.
• Table S7. Overexpression of O-GlcNAc–cycling enzymes in nst mutants.
• Table S8. Oligonucleotide primers used in this study.
  

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© 2011 American Association for the Advancement of Science