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Expression Analysis of Mammalian Linker-histone Subtypes
Published on: March 19, 2012
Individual somatic H1 subtypes are dispensable for mouse development even in mice lacking the H1(0) replacement
Y Fan1, A Sirotkin, R G Russell
1Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Molecular and Cellular Biology
|November 2, 2001
Summary
Mice lacking individual H1 linker histone subtypes develop normally, as other subtypes compensate. Even losing two subtypes is tolerated if H1-to-nucleosome stoichiometry is maintained, suggesting dispensability of single subtypes for mouse development.
Area of Science:
- Molecular Biology
- Genetics
- Epigenetics
Background:
- H1 linker histones are crucial for chromatin folding into the 30-nm fiber.
- Mice possess eight H1 subtypes with diverse sequences and developmental expression patterns.
- Previous studies indicated H1(0) knockout mice develop normally due to compensation by other H1 subtypes.
Purpose of the Study:
- To investigate the in vivo roles of individual mammalian H1 subtypes (H1c, H1d, H1e) in mouse development.
- To determine if specific H1 subtypes compensate for the loss of H1(0).
- To assess the impact of losing one or two H1 subtypes on mouse development and chromatin structure.
Main Methods:
- Generation of knockout mice lacking individual H1c, H1d, or H1e subtypes using homologous recombination.
- Breeding single-knockout lines with H1(0) knockout mice to create double-knockout (H1c/H1(0), H1d/H1(0), H1e/H1(0)) mice.
- Phenotypic analysis (anatomic, histologic, fertility) and chromatin examination (H1-to-nucleosome ratio) of knockout mice.
Main Results:
- Mice lacking any single H1 subtype (H1c, H1d, or H1e) exhibited normal growth, reproduction, and no obvious phenotypes.
- Double-knockout mice (H1c/H1(0), H1d/H1(0), H1e/H1(0)) were fertile and showed no anatomic or histological abnormalities.
- Chromatin analysis revealed no significant change in the total H1-to-nucleosome ratio in any of the double-knockout strains.
Conclusions:
- Individual H1 linker histone subtypes are dispensable for normal mouse development.
- The loss of up to two H1 subtypes is tolerated, provided normal H1-to-nucleosome stoichiometry is maintained.
- Disrupting compensation within the H1 multigene family likely requires generating multiple compound H1 knockouts.
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