Supplementary Materials

Supplementary Materials for:

Gain-of-function mutations in the gene encoding the tyrosine phosphatase SHP2 induce hydrocephalus in a catalytically dependent manner

Hong Zheng, Wen-Mei Yu, Ronald R. Waclaw, Maria I. Kontaridis, Benjamin G. Neel, Cheng-Kui Qu*

*Corresponding author. Email: cheng-kui.qu{at}emory.edu

This PDF file includes:

  • Fig. S1. The Ptpn11E76K mutation induces brain developmental defects with aberrant behaviors.
  • Fig. S2. Neurons are reduced, and astrocytes are increased in the cerebral cortex and hippocampus of adult Ptpn11E76K/+/Nestin-Cre+ mice.
  • Fig. S3. Total number and survival of NSPCs in the developing brain of Ptpn11E76K/+/Nestin-Cre+ mice are not significantly changed.
  • Fig. S4. Neuron and ependymal cell differentiation is decreased, whereas astrocyte differentiation is increased in Ptpn11E76K/+/Nestin-Cre+ NSPCs.
  • Fig. S5. ERK activity in the developing brain of Ptpn11E76K/+/Nestin-Cre+ mice is enhanced, but cell proliferation does not change.
  • Fig. S6. Similar abundance of bFGF and CNTF receptors in Ptpn11E76K/+/Nestin-Cre+ and Ptpn11+/+/Nestin-Cre+ NSPCs.
  • Fig. S7. Defects of ependymal cilia are proportionate to the catalytic activity of various mutant forms of SHP2.
  • Fig. S8. Generation and characterization of Ptpn11E76K,C459S/+ mice.

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