SOMATIC LINKER HISTONES CAUSE LOSS OF MESODERMAL COMPETENCE IN XENOPUS

In Xenopus, cells from the animal hemisphere are competent to form mes odermal tissues from the morula through to the blastula stage(1). Loss of mesodermal competence at early gastrula is programmed cell-autonom ously, arid occurs even in single cells at the appropriate stage(2). T o determine the mechanism by which this occurs, we have been investiga ting a concomitant, global change in expression of H1 linker histone s ubtypes. H1 histones are usually considered to be general repressors o f transcription(3), but in Xenopus they are increasingly thought to ha ve selective functions in transcriptional regulation(4-6). Xenopus egg s and embryos at stages before the midblastula transition(7) are defic ient in histone H1 protein, but contain an oocyte-specific variant cal led histone B4 or H1M. After the midblastula transition, histone B4 is progressively substituted by three somatic histone H1 variants, and r eplacement is complete by early neurula(8,9). Here we report that accu mulation of somatic H1 protein is rate limiting for the loss of mesode rmal competence. This involves selective transcriptional silencing of regulatory genes required for mesodermal differentiation pathways, lik e muscle, by somatic, but not maternal, H1 protein.