A POU protein regulates mesodermal competence to FGF in Xenopus.

Abstract:

:XLPOU91, a POU-homeobox gene is expressed in a narrow window during early Xenopus development. We show that ectopic expression of XLPOU91 RNA causes severe posterior truncations in embryos without inhibiting the formation of Spemann's organizer. Ectopic XLPOU91 expression also inhibits mesoderm induction by fibroblast growth factor (FGF) and activin in animal cap explants. Using antisense RNA, we depleted endogenous XLPOU91 protein in animal caps. Gastrula-stage animal caps expressing XLPOU91 antisense RNA do not lose competence to FGF, unlike controls, these animal caps express XBra after FGF treatment. Endogenous XLPOU91 levels are peaking when FGF mesoderm-inducing competence is lost in animal caps. Thus XLPOU91 protein may act as a competence switch during early development, as XLPOU91 levels increase in the embryo, the mesoderm response to FGF is lost.

journal_name

Mech Dev

authors

Henig C,Elias S,Frank D

doi

10.1016/s0925-4773(98)00006-9

subject

Has Abstract

pub_date

1998-02-01 00:00:00

pages

131-42

issue

1-2

eissn

0925-4773

issn

1872-6356

pii

S0925-4773(98)00006-9

journal_volume

71

pub_type

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