Supplementary Materials

Supplementary Material for:

Histone deacetylase inhibition rescues structural and functional brain deficits in a mouse model of Kabuki syndrome

Hans T. Bjornsson,* Joel S. Benjamin, Li Zhang, Jacqueline Weissman, Elizabeth E. Gerber, Yi-Chun Chen, Rebecca G. Vaurio, Michelle C. Potter, Kasper D. Hansen, Harry C. Dietz

*Corresponding author. E-mail: hbjorns1{at}

Published 1 October 2014, Sci. Transl. Med. 6, 256ra135 (2014)
DOI: 10.1126/scitranslmed.3009278

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Integration site of gene trap in the Kmt2dβGeo allele.
  • Fig. S2. Kmt2d+/βGeo mice show overlapping phenotypic features with patients with Kabuki syndrome.
  • Fig. S3. Kmt2d+/βGeo mice have context-related memory defects.
  • Fig. S4. Kmt2d+/βGeo mice show no deficit in flag trial.
  • Fig. S5. Assessment of motor function in Kmt2d+/βGeo and Kmt2d+/+ mice.
  • Fig. S6. Escape latencies during Morris water maze training.
  • Fig. S7. H3K4me3 is decreased in the pyramidal layer in Kmt2d+/βGeo mice compared to Kmt2d+/+ littermates.
  • Fig. S8. Body and brain size in Kmt2d+/βGeo mice.
  • Fig. S9. EdU incorporation.
  • Fig. S10. Decreased dendrites in DCX+ cells in the granule cell layer of Kmt2d+/βGeo mice.
  • Fig. S11. Staining for activated caspase 3 does not reveal increased apoptosis in the granule cell layer of Kmt2d+/βGeo mice compared to Kmt2d+/+ littermates.
  • Fig. S12. HDAC3 attenuates signal of the H4ac indicator.
  • Fig. S13. Both indicators demonstrate a deficiency in Kmt2d+/βGeo mice.
  • Fig. S14. Improved H3K4 trimethylation activity in Kmt2d+/βGeo cells transiently transfected with H3K4 trimethylation indicator and treated with MS275.
  • Fig. S15. In vivo responses to AR-42.
  • Fig. S16. AR-42–induced expression of a known KMT2D target gene.
  • Fig. S17. MA plots indicate a shift in the balance of H3K4me3 upon treatment with AR-42.
  • Fig. S18. A visualization of shifts in balance between the two states (genotype or AR-42) as a function of intensity demonstrates an abnormality in Kmt2d+/βGeo that is responsive to AR-42.
  • Fig. S19. Serum control experiments for antibodies used for immunofluorescence.
  • Table S1. A summary of genotypes, drugs, and quality measures of ChIP-seq experiments.
  • References (52, 53)

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