FIGURE

Fig. 5

ID

ZDB-FIG-120216-66

Publication

Yoruk et al., 2012 - Ccm3 functions in a manner distinct from Ccm1 and Ccm2 in a zebrafish model of CCM vascular disease

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Fig. 5

Co-injection of suboptimal ccm3a/b (0.25 ng) and stk25b (3 ng) MO results in cranial vasculature defects at 54 hpf. Embryos injected with low doses of ccm3a/b (0.25 ng) or stk25b morpholino (3 ng) showed no obvious defects in their cranial vessels (A-D). Co-injection of both morpholinos at the same dosages resulted in gross dilation of the prosencephalic arteries (PrA), anterior cerebral veins (AceV), as well as enlargement and mispatterning of the mesencephalic veins (MsV) in 71% of the embryos (E–H, yellow arrows, n = 83).

Expression Data

Gene:	EGFP
Fish:	s843Tg + MO3-stk25b s843Tg + MO1-pdcd10a,pdcd10b s843Tg + MO1-pdcd10a,pdcd10b + MO3-stk25b
Knockdown Reagents:	MO1-pdcd10a,pdcd10b MO3-stk25b
Anatomical Term:	cranial vasculature
Stage:	Long-pec

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	s843Tg + MO1-pdcd10a,pdcd10b + MO3-stk25b
Knockdown Reagents:	MO1-pdcd10a,pdcd10b MO3-stk25b
Observed In:	anterior cerebral vein mesencephalic vein prosencephalic artery
Stage:	Long-pec

Phenotype Detail

Acknowledgments

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Reprinted from Developmental Biology, 362(2), Yoruk, B., Gillers, B.S., Chi, N.C., and Scott, I.C., Ccm3 functions in a manner distinct from Ccm1 and Ccm2 in a zebrafish model of CCM vascular disease, 121-131, Copyright (2012) with permission from Elsevier. Full text @ Dev. Biol.