z-logo
Premium
Binding of nuclear proteins to a conserved histone H1t promoter element suggests an important role in testis‐specific transcription
Author(s) -
vanWert Jane M.,
Wolfe Steven A.,
Grimes Sidney R.
Publication year - 1996
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(19960301)60:3<348::aid-jcb7>3.0.co;2-w
Subject(s) - microbiology and biotechnology , biology , promoter , response element , gene , transcription (linguistics) , nuclear protein , histone , e box , gene expression , transcription factor , genetics , linguistics , philosophy
The testis‐specific histone H1t gene is transcribed only in primary spermatocytes during spermatogenesis. Recently, expression of the rat gene was shown to be limited to primary spermatocytes in transgenic mice, revealing that promoter elements sufficient for regulating tissue‐specific transcription were present in the cloned rat gene. In this study the mouse histone H1t gene has been cloned, and sequenced and its promoter region has been compared to the rat H1t promoter with regard to conserved elements and protein binding activity. The amino acid sequence of each of the three H1t coding region domains is conserved when compared to the homologous domain in H1t derived from other species. H1t mRNA is found only in testis, where it accumulates to a high steady‐state level, and examination of enriched testis cell populations shows that expression is limited to primary spermatocytes. Protein binding assays using nuclear extracts from various mouse tissues reveal testis‐specific binding to TE1 and TE2, imperfect inverted repeat elements within the larger TE element. Although the H1t promoter contains an Sp1 consensus motif within the H1t/TE element, binding of testis Sp1 to the motif could not be detected using specific anti‐Sp1 antibodies. © 1996 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here