Epigenetic alterations brought about by lithium treatment disrupt mouse embryo development.
The commonly accepted mechanism by which LiCl dorsalizes amphibian embryos is a respecification of ventral blastomeres, presumably through realignment of dorsal positional information in the embryo. An alternative mechanism, however, is an epigenetic change in the competence of cells to respond to cues they may be normally exposed to without effect. In order to test this hypothesis, we treated mouse preimplantation embryos, which do not possess any axial positional information, with LiCl, and observed axial abnormalities which must have been elaborated several days after treatment. We interpret this as support for the hypothesis that cellular competence rather than positional information is altered by LiCl, and suggest that this competence may be altered through the action of lithium sensitive enzymes that interact with chromatin.
Rogers
I
I
Department of Zoology, University of Toronto, Ontario, Canada.
Varmuza
S
S
D000818:Animals; D001755:Blastocyst / Q000187:drug effects*; D002478:Cells, Cultured; D005314:Embryonic and Fetal Development / Q000187:drug effects*; D005260:Female; D008094:Lithium / Q000633:toxicity*; D051379:Mice; D011247:Pregnancy
D008094:Lithium