Histone deacetylase knockouts modify transcription, CAG instability and nuclear pathology in Huntington disease mice.

At 5 months of age the expansion index was significantly reduced in Hdac2 ΚO striata ( Hdac2 WT: mean 15.22, 95% CI [14.16, 16.28]; Hdac2 ΚO: mean 12.69, 95% CI [10.91, 14.47]; 2-tailed unpaired t-test p=0.0094), while at 10 months of age, we again observed a small reduction in expansion in Hdac2 ΚO striata; this was most apparent from the GeneMapper traces of closely CAG repeat-matched mice (panel A), though this did not reach statistical significance ( Hdac2 WT: mean 21.55, 95% CI [19.62–23.48]; Hdac2 ΚO: mean 20.02, 95% CI [17.1–22.94]; two-tailed unpaired t-test p=0.26) across this cohort of mice with a wide range of CAG lengths ( Source data 1 ).

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There was a highly significant overlap in the DEGs and enriched pathways due to the Hdac2 KO or the Htt Q111 allele, largely reflecting overlaps in DEGs and enriched pathways altered in the same direction, i.e. up- or down-regulated in both conditions (statistical tests of enrichment were performed using one-sided Fisher exact tests – see Materials and methods, and results are shown in Figure 3—figure supplement 1C ).

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