Elsevier

Developmental Biology

Volume 250, Issue 2, 15 October 2002, Pages 263-279
Developmental Biology

Regular Article
Maternally Supplied Smad5 Is Required for Ventral Specification in Zebrafish Embryos Prior to Zygotic Bmp Signaling

https://doi.org/10.1006/dbio.2002.0805Get rights and content
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Abstract

We have previously shown that the maternal effect dorsalization of zebrafish embryos from sbndtc24 heterozygous mothers is caused by a dominant negative mutation in Smad5, a transducer of ventralizing signaling by the bone morphogenetic proteins Bmp2b and Bmp7. Since sbndtc24 mutant Smad5 protein not only blocks wild-type Smad5, but also other family members like Smad1, it remained open to what extent Smad5 itself is required for dorsoventral patterning. Here, we report the identification of novelsmad5 alleles: three new isolates coming from a dominant enhancer screen, and four former isolates initially assigned to the cpt and pgy complementation groups. Overexpression analyses demonstrate that three of the new alleles, m169, fr5, and tc227, are true nulls (amorphs), whereas the initial dtc24 allele is both antimorphic and hypomorphic. We rescued m169 mutant embryos by smad5 mRNA injection. Although adult mutants are smaller than their siblings, the eggs laid by m169−/− females are larger than normal eggs. Embryos lacking maternal Smad5 function (Mm169−/− embryos) are even more strongly dorsalized thanbmp2b or bmp7 null mutants. They do not respond to injected bmp2b mRNA, indicating that Smad5 is absolutely essential for ventral development and Bmp2/7 signaling. Most importantly, Mm169−/− embryos display reducedbmp7 mRNA levels during blastula stages, when bmp2b and bmp7 mutants are still normal. This indicates that maternally supplied Smad5 is already required to mediate ventral specification prior to zygotic Bmp2/7 signaling to establish the initial dorsoventral asymmetry.

Keywords

Smad5
Bmp2b
Bmp7
dorsoventral patterning
maternal effect
enhancer screen
zebrafish
body size
oogenesis

Cited by (0)

1

These authors contributed equally to this work.

2

These authors contributed equally to this work.

3

To whom correspondence should be addressed. Fax: +001-215-898 9871. E-mail: [email protected] (MCM). Fax: +0049-761-5108 358. E-mail: [email protected] (MH).