ZFIN Morpholino: MO3-acvrl1

Target Location

Genome Build: GRCz11Chromosome: 23

Genomic Features

No data available

Expression

Gene expression in Wild Types + MO3-acvrl1

No data available

Phenotype

Phenotype resulting from MO3-acvrl1

Phenotype	Fish	Figures
aortic arch 1 constricted, abnormal	pt505Tg + MO3-acvrl1	Fig. 2 from Rochon et al., 2016
aortic arch 1 morphology, abnormal	pt505Tg + MO3-acvrl1	Fig. 2 from Rochon et al., 2016
aortic arch 1 blood vessel development process quality, abnormal	pt505Tg + MO3-acvrl1	Fig. 2 , Fig. 5 from Rochon et al., 2016
aortic arch 1 blood vessel endothelial cell migration decreased process quality, abnormal	y7Tg + MO3-acvrl1	Fig. 5 from Rochon et al., 2016
aortic arch 1 blood vessel endothelial cell migration process quality, abnormal	rk8Tg; ubs4Tg + MO3-acvrl1	Fig. 4 from Rochon et al., 2016

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Phenotype of all Fish created by or utilizing MO3-acvrl1

Phenotype	Fish	Conditions	Figures
pericardium edematous, abnormal	WT + MO3-acvrl1	standard conditions	Fig. 4 from Walcott, 2014
whole organism morphology, abnormal	WT + MO3-acvrl1	standard conditions	Fig. 4 from Walcott, 2014
caudal division of the internal carotid artery increased size, abnormal	pt504Tg + MO3-acvrl1	standard conditions	Fig. 3 from Rochon et al., 2015
primordial midbrain channel increased size, abnormal	pt504Tg + MO3-acvrl1	standard conditions	Fig. 3 from Rochon et al., 2015
basal communicating artery increased size, abnormal	pt504Tg + MO3-acvrl1	standard conditions	Fig. 3 from Rochon et al., 2015

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Citations

Include unpublished citations

Sidhwani, P., Leerberg, D.M., Boezio, G.L.M., Capasso, T.L., Yang, H., Chi, N.C., Roman, B.L., Stainier, D.Y.R., Yelon, D. (2020) Cardiac function modulates endocardial cell dynamics to shape the cardiac outflow tract. Development (Cambridge, England). 147(12):
Ando, K., Wang, W., Peng, D., Chiba, A., Lagendijk, A., Barske, L., Crump, J.G., Stainier, D.Y.R., Lendahl, U., Koltowska, K., Hogan, B.M., Fukuhara, S., Mochizuki, N., Betsholtz, C. (2019) Peri-arterial specification of vascular mural cells from naïve mesenchyme requires Notch signaling. Development (Cambridge, England). 146(2):
Neal, A., Nornes, S., Payne, S., Wallace, M.D., Fritzsche, M., Louphrasitthiphol, P., Wilkinson, R.N., Chouliaras, K.M., Liu, K., Plant, K., Sholapurkar, R., Ratnayaka, I., Herzog, W., Bond, G., Chico, T., Bou-Gharios, G., De Val, S. (2019) Venous identity requires BMP signalling through ALK3. Nature communications. 10:453
Rochon, E.R., Menon, P.G., Roman, B.L. (2016) Alk1 controls arterial endothelial cell migration in lumenized vessels. Development (Cambridge, England). 143(14):2593-602
Rochon, E.R., Wright, D.S., Schubert, M.M., Roman, B.L. (2015) Context-specific interactions between Notch and ALK1 cannot explain ALK1-associated arteriovenous malformations. Cardiovascular research. 107(1):143-52
Walcott, B.P. (2014) BMP signaling modulation attenuates cerebral arteriovenous malformation formation in a vertebrate model. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism. 34(10):1688-94
Laux, D.W., Young, S., Donovan, J.P., Mansfield, C.J., Upton, P.D., and Roman, B.L. (2013) Circulating Bmp10 acts through endothelial Alk1 to mediate flow-dependent arterial quiescence. Development (Cambridge, England). 140(16):3403-12
Corti, P., Young, S., Chen, C.Y., Patrick, M.J., Rochon, E.R., Pekkan, K., and Roman, B.L. (2011) Interaction between alk1 and blood flow in the development of arteriovenous malformations. Development (Cambridge, England). 138(8):1573-1582

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