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Regulation of transcription of the testis-specific histone H1t gene by multiple promoter elements

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Abstract

This is a review of mechanisms that contribute to testis-specific transcription of the histone H1t gene.The mammalian testis-specific histone H1t gene is transcribed only in primary spermatocytes during spermatogenesis. Linker histones bind to DNA and contribute to chromatin condensation by formation of the 30 nm chromatin fiber. Furthermore, linker histones contribute to regulation of transcription of specific genes. Histone H1t, which binds more weakly to DNA than the other six known linker histones, is expressed in cells that are involved in the essential processes of crossing over and mismatch repair of DNA and in cells that undergo a dramatic alteration in gene expression. However, contributions of this linker histone to these processes are unknown. Subtle differences are found in the H1t promoter compared to the other H1 promoters. Nevertheless, several lines of evidence support the hypothesis that a sequence element designated TE that is located within the H1t promoter is essential for enhanced testis-specific transcription of this gene. Transgenic mice bearing a rat H1t transgene which contains a replacement of the TE element with stuffer DNA fail to express rat H1t mRNA. In addition, an upstream sequence appears to function as a silencer element that leads to transcriptional repression of the H1t gene in nongerminal cells. Thus, multiple promoter elements appear to contribute to regulation of transcription of the histone H1t gene.

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Authors and Affiliations

  1. Research Service, VA Medical Center and Department of Biochemistry and Molecular Biology, LSU Medical Center, Shreveport, LA, 71101–4295, USA

    Sidney R. Grimes Jr., Jane van Wert & Steven A. Wolfe

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  1. Sidney R. Grimes Jr.
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  2. Jane van Wert
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  3. Steven A. Wolfe
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Grimes, S.R., van Wert, J. & Wolfe, S.A. Regulation of transcription of the testis-specific histone H1t gene by multiple promoter elements. Mol Biol Rep 24, 175–184 (1997). https://doi.org/10.1023/A:1006807716339

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