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Fig. 2 | BMC Genomics

Fig. 2

From: SWI/SNF complexes act through CBP-1 histone acetyltransferase to regulate acute functional tolerance to alcohol

Fig. 2

SWI/SNF-regulated genes in neurons. a Constructs for single-copy rescue of swsn-9(ok1354) mutants in neurons. The empty MosSCI vector (top) serves as a negative control and contains the unc-119+ selectable marker. The neuronal rescue plasmid (bottom) expresses SWSN-9::GFP under control of the ric-19 promoter; it also contains the unc-119+ selectable marker. b Animals were tested on 0 mM and 400 mM exogenous ethanol. Relative speeds were calculated as treated over untreated speeds. The development of AFT is indicated by a statistically significant recovery of speed between 10 and 30 min of exposure. All genotypes on the same graph were tested simultaneously on the same plates. Wild-type (WT) animals develop AFT, while swsn-9(ok1354) mutants fail to develop AFT (n = 6). A single copy insertion of Pric-19::SWSN-9::GFP (rescue) was able to rescue the AFT defect of swsn-9(ok1354) mutants, while a single copy insertion of the empty MosSCI vector (control) did not rescue the AFT defect. Error bars indicate S.E.M. Paired one-tailed Student’s t tests were used for statistical comparisons of speeds at 10 and 30 min. One-way ANOVA, with Tukey’s multiple comparison test, was used to compare initial sensitivity across the strains; no significant difference was observed. For indicated comparisons: ns, not significant; **p ≤ 0.01 c Principal component analysis with gene expression plotted relative to the first two principal components (PC1 and PC2). swsn-9(ok1354) mutant replicates containing the rescue or control constructs are most similar to replicates of the same genotype. d Volcano plot shows genes that are up-regulated (red) and down-regulated (blue) in swsn-9(ok1354) mutant neurons. Dashed lines indicate the FDR and fold change cutoffs (FDR ≤ 0.05 and fold change ≥1)

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