Ablation of the Kinase NDR1 Predisposes Mice to the Development of T Cell Lymphoma

Hauke Cornils,* Mario R. Stegert, Alexander Hergovich, Debby Hynx, Debora Schmitz, Stephan Dirnhofer, Brian A. Hemmings*

*To whom correspondence should be addressed. E-mail: hauke.cornils{at}fmi.ch (H.C.); brian.hemmings{at}fmi.ch (B.A.H.)

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• Fig. S1. Generation of NDR1-deficient mice.
• Fig. S2. Mature T cells from NDR1^+/– and NDR1^–/– mice show slightly increased
  resistance to apoptosis.
• Fig. S3. Activation of NDR is unchanged in NDR1-deficient thymocytes in response
  to induction of apoptosis by dexamethasone or antibody against Fas together with
  cycloheximide.
• Fig. S4. NDR1 and NDR2 show distinct patterns in mice.
• Fig. S5. The expression of NDR2 and the abundance of NDR2 protein remain
  unchanged upon loss of NDR1.
• Fig. S6. Reduction of the abundance of NDR2 in NDR1-deficient MEFs results in
  increased resistance to apoptosis.
• Fig. S7. Increased development of MPDs in NDR1^+/– and NDR1^–/– mice after ENU
  treatment.
• Fig. S8. An increase in the abundance of Pou2af1 correlates with a low abundance of
  NDR in tumors.
• Fig. S9. Loss of NDR1 results in minor defects in the proliferation of mature T cells
  after stimulation of the TCR.
• Fig. S10. Cells from NDR-high and NDR-low tumors show no consistent differences
  in Ki67 staining.
• Fig. S11. siRNA against MEF2c does not rescue apoptosis defects in cells depleted
  of NDR1 and NDR2.
• Fig. S12. Characterization of a murine antibody against NDR1.
• Fig. S13. Validation of siRNA against MEF2c and overexpression of E47 in
  transfected cells.
• Fig. S14. Testing of different shNDR2 constructs.
• Table S1. Aged mice analyzed for tumor development.
• Table S2. Overview of tumors identified in ENU-treated mice.
• Table S3. Classification of human T cell lymphoma samples.
• Table S4. Classification of tumors according to the abundances of NDR1 and NDR2.
• Table S5. Genes whose expression was significantly altered in NDR-low tumors.

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