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Abstract
Spleen tyrosine kinase (Syk) plays critical roles in B-cell and T-cell development,
the maintenance of vascular integrity, and proper partitioning of the blood vascular
and lymphatic vascular system. Here, we utilize the zebrafish as an in vivo system
to demonstrate novel roles for Syk and the related kinase Zeta associated protein
(Zap-70) in promoting angioblast migration. Partial knockdown of either gene results
in early angiogenic delay of the intersegmental vessels, dorsal intersegmental vessel
patterning defects, and partial loss of the thoracic duct. Higher dose knockdown of
both genes results in little to no angiogenic sprouting of the intersegmental vessels,
a phenotype which resembles knockdown of vegfa. Di-phosphorylated ERK, an effector
of the vegfa pathway, is also downregulated in the aorta of syk:zap double morphants.
Over-expression of syk under the control of a blood-specific or vascular-specific
promoter rescues sprouting defects after loss of vegfa. Together these results suggest
that syk and zap-70 function redundantly in an early progenitor to promote the migration
of intersegmental vessel angioblasts and lymphangioblasts that contribute to the thoracic
duct, either downstream of, or in parallel to vegfa.
Copyright 2010 Elsevier Inc. All rights reserved.