The rat histone H1d gene has intragenic activating sequences that are absent from the testis-specific variant H1t
In some cases core histone genes in the mouse depend on intragenic sequence elements for high level expression [Gene 176 (1996) 1]. Here we report that the highly expressed gene for rat linker histone H1d also contains an intragenic activating region (IAR). Using transient transfection assays in mou...
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Veröffentlicht in: | Biochimica et biophysica acta. Gene structure and expression 2003-01, Vol.1625 (2), p.165-172 |
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Zusammenfassung: | In some cases core histone genes in the mouse depend on intragenic sequence elements for high level expression [Gene 176 (1996) 1]. Here we report that the highly expressed gene for rat linker histone
H1d also contains an intragenic activating region (IAR). Using transient transfection assays in mouse fibroblast NIH3T3 cells, we showed that rat
H1d contains a downstream region (+21 to +116) that imparts a two- to threefold up-regulation of fused reporters. This region also activated expression when moved to the promoter region, though the effect was dependent on its distance from other promoter elements. The IAR contains sequence homologies to the core α and Ω elements identified as functional protein binding sites within the mouse
H3.2 coding region activating sequence (CRAS). A pair of Ω elements (+32 and +66) accounts for the activating effect of the
H1d intragenic region as shown by targeted mutations as well as stepwise deletions. The
H1d and
H3.2 Ω sequences bound similar and perhaps identical proteins by gel shift analysis. The
H1d α-like sequence at +56 overlaps the translational start codon and was therefore not mutated. Like the mouse
H3.2 α element, it bound transcription factor YY1 in gel shift assays.
H1t, the gene for the testis-specific linker histone, did not demonstrate an IAR. While
H1t has a similar α sequence and did bind YY1, it lacks the Ω homologies of
H1d. Sequence comparison shows that the YY1/α site as well as the adjacent Ω site are likely present in genes for other standard H1 variants, but that the +32 Ω site in the 5′ untranslated region (UTR) of
H1d is unique. We conclude that the +32 and +66 Ω sequences of the rat
H1d gene contribute significantly to its high-level expression. |
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ISSN: | 0167-4781 1879-2634 |
DOI: | 10.1016/S0167-4781(02)00604-8 |