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. 2000 Sep;20(17):6449–6465. doi: 10.1128/mcb.20.17.6449-6465.2000

FIG. 10.

FIG. 10

Modulation of transcription by the HP1 binding regions from KAP-1, SP100, LBR, and CAF-1 p150. (A) Direct assessment of the effect on basal transcription of the HP1 binding regions from KAP-1, SP100, LBR, and CAF-1 p150. Plasmids expressing G4DBD fusions were cotransfected as outlined in the legend to Fig. 8, and fold repression was plotted. The amino acids encoded are indicated below the constructs. For comparison, full-length human HP1α was also tested. Also shown are the results for a point mutation engineered in the human HP1α CD (V21M), corresponding to the D. melanogaster mutant allele Su(var)2-0502 (14). H, HP1BD. (B) Squelching of human HP1α-mediated transcription repression. A series of cotransfections were conducted with a constant amount of pM-HP1α2-191 (2 μg) and increasing amounts of plasmids expressing six-His fusions with the HP1 binding regions from KAP-1, SP100, LBR, and CAF-1 p150 (amounts, in micrograms, are indicated on the y axis). Asterisks indicate the position of mutations in HP1α (V21M) and in KAP-1 (mut1 and mut2).