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ZFIN ID: ZDB-FIG-120814-26
Ellertsdottir et al., 2012 - Developmental Role of Zebrafish Protease-Activated Receptor 1 (PAR1) in the Cardio-Vascular System. PLoS One   7(7):e42131 Full text @ PLoS One
Knockdown Reagents:
Observed In:
Stage: Prim-15

Fig. 4 par1 knockdown impairs vascular remodeling in the cardinal vein.

(A–B) Lateral views of double transgenic embryos (Tg(kdrl:EGFP)s843;Tg(gata1:dsRed)sd2) at 35 hpf. (A) The intersegmental vessels are connected to the CV and the one intersegmental artery (most posterior) seen in the figure has blood flowing from the dorsal aorta. (A2) In the mid-cross section, the intersegmental artery is visible (green bracket), the dorsal aorta can be seen as one tube (red bracket), and the CV is seen as two tubes (blue bracket). (B) par1 morphant lateral view. ISVs are lumenized (asterisk) (B2) In cross section, the CV tube does not show a defined number. Due to mislaid vein remodeling the tube is disorganized, cell clusters are apparent instead of a round tube. (C) The tnnt2 knockdown shows no mature inflation of the dorsal aorta and only a minor primary lumen in the ISV. The CV is bulged and full of blood cells in this region. (C′) The small dorsal aorta is a clear difference to the par1 knockdown, additionally to the lack of lumen in the ISVs and blood cells always clogging in the region of origin, PBI.

Gene Expression Details No data available
Antibody Labeling Details No data available
Phenotype Details
Fish Conditions Stage Phenotype
s843Tg; sd2Tg + MO1-f2r standard conditions Prim-15 caudal vein dilated, abnormal
Prim-15 caudal vein disorganized, abnormal
Prim-15 dorsal aorta decreased size, abnormal
Prim-15 intersegmental vessel collapsed, abnormal
s843Tg; sd2Tg + MO1-tnnt2a standard conditions Prim-15 blood increased accumulation caudal vein, abnormal
Prim-15 blood circulation arrested, abnormal
Prim-15 blood vessel lumenization disrupted, abnormal
Prim-15 dorsal aorta structure, abnormal
Prim-15 intersegmental vessel structure, cavities, abnormal
ZFIN wishes to thank the journal PLoS One for permission to reproduce figures from this article. Please note that this material may be protected by copyright. Full text @ PLoS One