Somatic linker histones cause loss of mesodermal competence in Xenopus

Oliver C. Steinbach, Alan P. Wolffe and Ralph A.W. Rupp ()
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Oliver C. Steinbach: Friedrich Miescher Laboratorium der Max Planck-Gesellschaft
Alan P. Wolffe: Laboratory of Molecular Embryology, National Institute of Child Health and Human Development, NIH
Ralph A.W. Rupp: Friedrich Miescher Laboratorium der Max Planck-Gesellschaft

Nature, 1997, vol. 389, issue 6649, 395-399

Abstract: Abstract In Xenopus, cells from the animal hemisphere are competent to form mesodermal tissues from the morula through to the blastula stage1. Loss of mesodermal competence at early gastrula is programmed cell-autonomously, and occurs even in single cells at the appropriate stage2. To determine the mechanism by which this occurs, we have been investigating a concomitant, global change in expression of H1 linker histone subtypes. H1 histones are usually considered to be general repressors of transcription3, but in Xenopus they are increasingly thought to have selective functions in transcriptional regulation4,5,6. Xenopus eggs and embryos at stages before the midblastula transition7 are deficient in histone H1 protein, but contain an oocyte-specific variant called histone B4 or H1M. After the midblastula transition, histone B4 is progressively substituted by three somatic histone H1 variants, and replacement is complete by early neurula8,9. Here we report that accumulation of somatic H1 protein is rate limiting for the loss of mesodermal competence. This involves selective transcriptional silencing of regulatory genes required for mesodermal differentiation pathways, like muscle, by somatic, but not maternal, H1 protein.

Date: 1997
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DOI: 10.1038/38755

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