Skip to main content

Some NLM-NCBI services and products are experiencing heavy traffic, which may affect performance and availability. We apologize for the inconvenience and appreciate your patience. For assistance, please contact our Help Desk at info@ncbi.nlm.nih.gov.

Nucleic Acids Research logoLink to Nucleic Acids Research
. 1999 Sep 15;27(18):3685–3689. doi: 10.1093/nar/27.18.3685

Messenger RNAs encoding mouse histone macroH2A1 isoforms are expressed at similar levels in male and female cells and result from alternative splicing.

T P Rasmussen 1, T Huang 1, M A Mastrangelo 1, J Loring 1, B Panning 1, R Jaenisch 1
PMCID: PMC148623  PMID: 10471737

Abstract

Two protein isoforms of histone macroH2A1 (mH2A1) are found in mammalian cells. One isoform, mH2A1.2 is highly concentrated on the heterochromatinized inactive X chromosome (Xi) of female cells. mH2A1.2 protein is also present in male cells, but fails to form dense concentrations. Another protein isoform, mH2A1.1, differs from mH2A1.2 by a single short segment of amino acids. In this study, we cloned and characterized the genomic locus of the mouse mH2A1 gene and mapped it to chromosome 13. Two alternatively spliced transcripts derived from the mH2A1 locus are responsible for the generation of the two mH2A1 protein isoforms with mH2A1.2 mRNA being the most abundant spliced form in all tissues examined. The absolute amount of mH2A1 mRNA is similar in male and female cells for most tissues with the exception of testes where it is par-ticularly abundant. Both spliced forms are present in all adult tissues analyzed as well as in female embryonic stem cells. In contrast, male embryonic stem cells expressed mH2A1.1 at low levels if at all. The relatively abundant expression of mH2A1 in both sexes suggests that mH2A1 has functions in addition to a possible involvement in X chromosome inactivation.

Full Text

The Full Text of this article is available as a PDF (360.6 KB).


Articles from Nucleic Acids Research are provided here courtesy of Oxford University Press

RESOURCES