Somatic linker histones cause loss of mesodermal competence in Xenopus.
In Xenopus, cells from the animal hemisphere are competent to form mesodermal tissues from the morula through to the blastula stage. Loss of mesodermal competence at early gastrula is programmed cell-autonomously, and occurs even in single cells at the appropriate stage. 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 transcription, but in Xenopus they are increasingly thought to have selective functions in transcriptional regulation. Xenopus eggs and embryos at stages before the midblastula transition 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 neurula. 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.
Steinbach
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OC
Friedrich Miescher Laboratorium der Max-Planck-Gesellschaft, Tübingen, Germany.
Wolffe
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AP
Rupp
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RA
D028341:Activins; D000818:Animals; D001755:Blastocyst / Q000187:drug effects / Q000502:physiology; D004625:Embryo, Nonmammalian / Q000502:physiology; D047108:Embryonic Development; D004627:Embryonic Induction; D018507:Gene Expression Regulation, Developmental; D006657:Histones / Q000502:physiology*; D007265:Inhibins / Q000494:pharmacology; D008648:Mesoderm / Q000502:physiology*; D009132:Muscles / Q000196:embryology; D017570:MyoD Protein / Q000235:genetics / Q000502:physiology; D015398:Signal Transduction; D014981:Xenopus
D006657:Histones; D017570:MyoD Protein; D028341:Activins; D007265:Inhibins