PUBLICATION

Short- and long-range functions of Goosecoid in zebrafish axis formation are independent of Chordin, Noggin 1 and Follistatin-like 1b

Authors

Dixon Fox, M., and Bruce, A.E.

ID

ZDB-PUB-090417-12

Date

2009

Source

Development (Cambridge, England) 136(10): 1675-1685 (Journal)

Registered Authors

Bruce, Ashley

Keywords

none

MeSH Terms

Mutation
Bone Morphogenetic Proteins/physiology
Body Patterning/physiology
Zebrafish Proteins/genetics
Zebrafish Proteins/physiology*
Follistatin-Related Proteins/physiology*
Goosecoid Protein/genetics
Goosecoid Protein/physiology*
Zebrafish/embryology*
Zebrafish/physiology
Signal Transduction/physiology
Animals, Genetically Modified
Animals
Glycoproteins/genetics
Glycoproteins/physiology*
Receptors, Notch/physiology
Carrier Proteins/physiology*
Intercellular Signaling Peptides and Proteins/genetics
Intercellular Signaling Peptides and Proteins/physiology*
Embryo, Nonmammalian/physiology

(all 20)

PubMed

19369398 Full text @ Development

Abstract

The organizer is essential for dorsal-ventral (DV) patterning in vertebrates. Goosecoid (Gsc), a transcriptional repressor found in the organizer, elicits partial secondary axes when expressed ventrally in Xenopus, similar to an organizer transplant. Although gsc is expressed in all vertebrate organizers examined, knockout studies in mouse suggested that it is not required for DV patterning. Moreover, experiments in Xenopus and zebrafish suggest a role in head formation, although a function in axial mesoderm formation is less clear. To clarify the role of Gsc in vertebrate development, we used gain- and loss-of-function approaches in zebrafish. Ventral injection of low doses of gsc produced incomplete secondary axes, which we propose results from short-range repression of BMP signaling. Higher gsc doses resulted in complete secondary axes and long-range signaling, correlating with repression of BMP and Wnt signals. In striking contrast to Xenopus, the BMP inhibitor Chordin (Chd) is not required for Gsc function. Gsc produced complete secondary axes in chd null mutant embryos and gsc-morpholino knockdown in chd mutants enhanced the mutant phenotype, suggesting that Gsc has Chd-independent functions in DV patterning. Even more striking was that Gsc elicited complete secondary axes in the absence of three secreted BMP antagonists, Chd, Follistatin-like 1b and Noggin 1, suggesting that Gsc functions in parallel with secreted BMP inhibitors. Our findings suggest that Gsc has dose dependent effects on axis induction and provide new insights into molecularly distinct short- and long-range signaling activities of the organizer.

Genes / Markers

Figures

Show all Figures

Expression

Gene	Antibody	Fish	Conditions	Stage	Anatomy	Assay	Figure
tbxta	ab1-ta	AB	standard conditions	Prim-5	notochord	IHC	Fig. 7
tbxta	ab1-ta	AB + MO1-chrd	standard conditions	Prim-5	notochord	IHC	Fig. 7
tbxta	ab1-ta	AB + MO1-chrd + MO1-gsc	standard conditions	Prim-5	notochord	IHC	Fig. 7
tbxta	ab1-ta	AB + MO1-gsc	standard conditions	Prim-5	notochord	IHC	Fig. 7
tbxta	ab1-ta	chrd^tt250/tt250	standard conditions	Prim-5	notochord	IHC	Fig. 7
tbxta	ab1-ta	chrd^tt250/tt250 + MO1-gsc	standard conditions	Prim-5	notochord	IHC	Fig. 7
wnt8a		AB + MO1-chrd + MO1-gsc	standard conditions	Shield	margin	ISH	Fig. 7
wnt8a		AB + MO1-gsc	standard conditions	Shield	margin	ISH	Fig. 7

1 - 8 of 8

Show

Phenotype

Fish	Conditions	Stage	Phenotype	Figure
AB + MO1-chrd	standard conditions	Prim-5	head decreased size, abnormal	Fig. 7
AB + MO1-chrd	standard conditions	Prim-5	notochord decreased width, abnormal	Fig. 7
AB + MO1-chrd	standard conditions	Prim-5	notochord truncated, abnormal	Fig. 7
AB + MO1-chrd	standard conditions	Prim-5	whole organism wholly ventralized, abnormal	Fig. 7
AB + MO1-chrd + MO1-gsc	standard conditions	Prim-5	head decreased size, abnormal	Fig. 7
AB + MO1-chrd + MO1-gsc	standard conditions	Prim-5	notochord decreased width, abnormal	Fig. 7
AB + MO1-chrd + MO1-gsc	standard conditions	Prim-5	notochord truncated, abnormal	Fig. 7
AB + MO1-chrd + MO1-gsc	standard conditions	Prim-5	whole organism wholly ventralized, abnormal	Fig. 7
AB + MO1-gsc	standard conditions	Prim-5	notochord morphology, normal	Fig. 7
chrd^tt250/tt250	standard conditions	Prim-5	notochord decreased width, abnormal	Fig. 7

1 - 10 of 17

Show

Mutations / Transgenics

Human Disease / Model

Sequence Targeting Reagents

Fish

Antibodies

Orthology

Engineered Foreign Genes

Mapping

Dixon Fox et al., 2009 ZDB-PUB-090417-12 PMID:19369398

Short- and long-range functions of Goosecoid in zebrafish axis formation are independent of Chordin, Noggin 1 and Follistatin-like 1b

Dixon Fox et al., 2009

ZDB-PUB-090417-12
PMID:19369398