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Resolution: standard / high Figure 1.
Clustering of drug sensitive gene deletion mutants. The haploid non-essential yeast gene deletion array was subjected to sub-inhibitory
concentrations of five inhibitory compounds. Colony size reduction was used to detect
sensitivity. (A) Drug sensitive yeast gene deletion mutants were clustered according
to the cellular processes in which their deleted genes participated. The overall distributions
of gene functions were comparable for different treatments with protein biosynthesis
as a major group for all treatments. (B) Chemical profiles were clustered according
to drug sensitivities to two or more drugs. Hierarchical clustering of mutants is
illustrated using complete linkage. Absolute correlation coefficient (centered) is
used for comparability and displayed in Java TreeView. Several regions of interest
(a-e) are enlarged. The cellular processes of the deleted genes are color-coded. On
the basis of sensitivity profiles, paromomycin is grouped with neomycin. Cycloheximide
is grouped with 3-AT, which then merges with streptomycin. Sensitivity indexes of
the gene deletion mutants are shown as high to low (light to dark red). (C) Sensitivity
overlaps for gene deletion mutants to different drug treatments. The number of gene
deletion mutants with a particular sensitivity, for example paromomycin (P) alone
(89), paromomycin and 3-AT (17) and paromomycin, 3-AT and neomycin (3), are indicated.
(D) The overlapping drug sensitive yeast gene deletion mutants are clustered according
to the cellular processes in which their deleted genes participate. No significant
enrichment for protein biosynthesis genes among overlapping sensitive strains was
observed. The number of sensitive strains is presented on the z-axis. C: cycloheximide;
P: paromomycin; A: 3-AT; N: neomycin; and S: streptomycin. The sensitivity overlaps
between P and N, C and 3-AT, C and S, and 3-AT and S were significant with P-values ≤ 5 × 10-14. Other overlaps are significant with P-values of ≤ 0.029.
Alamgir et al. BMC Chemical Biology 2010 10:6 doi:10.1186/1472-6769-10-6 |