pou5f1, also known as
Oct4, is required to establish the pluripotent cell population necessary for embryogenesis in mouse [
1]. Additional roles during development, including endoderm formation, have been proposed [
2 and
3]. In zebrafish, the zygotic
pou5f1/
pou2 mutant
spiel ohne grenzen (
spg) [
4,
5 and
6] shows neural plate patterning defects and reduced endoderm at the tailbud stage [
7]. To investigate the function of maternal and early zygotic
pou5f1 expression, we rescued zygotic
spgm793 mutants by injecting
pou5f1 mRNA at the one-cell stage and raised them into fertile homozygous
spgm793 adults that mate to produce maternal-zygotic
spg (
MZspg) mutant embryos. Although neurectoderm, mesoderm, and germ cells develop in
MZspg mutants, gastrulation is delayed and proceeds abnormally. Further,
MZspg mutants do not maintain expression of
sox32/casanova, express little or no
sox17, and fail to develop endodermal tissue. Constitutively active
Nodal receptor TARAM-A or
sox32 overexpression induces ubiquitous
sox17 expression in wild-type embryos [
8,
9 and
10], but not in
MZspg mutants. Overexpression of a Pou5f1-VP16 activator fusion protein can rescue gastrulation and endodermal tissues in
MZspg mutants. We propose that
pou5f1 plays an activating role in zebrafish endodermal development, where it maintains
sox32 expression during gastrulation and acts with
sox32 to induce
sox17 expression in endodermal precursor cells.