Tek (Tie2) is not required for cardiovascular development in zebrafish
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Tek (Tie2) is not required for cardiovascular development in zebrafish. / Jiang, Zhen; Carlantoni, Claudia; Allanki, Srinivas; Ebersberger, Ingo; Stainier, Didier Y R.
in: DEVELOPMENT, Jahrgang 147, Nr. 19, dev193029, 12.10.2020.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Tek (Tie2) is not required for cardiovascular development in zebrafish
AU - Jiang, Zhen
AU - Carlantoni, Claudia
AU - Allanki, Srinivas
AU - Ebersberger, Ingo
AU - Stainier, Didier Y R
N1 - © 2020. Published by The Company of Biologists Ltd.
PY - 2020/10/12
Y1 - 2020/10/12
N2 - Angiopoietin/TIE signalling plays a major role in blood and lymphatic vessel development. In mouse, Tek (previously known as Tie2) mutants die prenatally due to a severely underdeveloped cardiovascular system. In contrast, in zebrafish, previous studies have reported that although embryos injected with tek morpholinos (MOs) exhibit severe vascular defects, tek mutants display no obvious vascular malformations. To further investigate the function of zebrafish Tek, we generated a panel of loss-of-function tek mutants, including RNA-less alleles, an allele lacking the MO-binding site, an in-frame deletion allele and a premature termination codon-containing allele. Our data show that all these mutants survive to adulthood with no obvious cardiovascular defects. MO injections into tek mutants lacking the MO-binding site or the entire tek locus cause similar vascular defects to those observed in MO-injected +/+ siblings, indicating off-target effects of the MOs. Surprisingly, comprehensive phylogenetic profiling and synteny analyses reveal that Tek was lost in the largest teleost clade, suggesting a lineage-specific shift in the function of TEK during vertebrate evolution. Altogether, these data show that Tek is dispensable for zebrafish development, and probably dispensable in most teleost species.
AB - Angiopoietin/TIE signalling plays a major role in blood and lymphatic vessel development. In mouse, Tek (previously known as Tie2) mutants die prenatally due to a severely underdeveloped cardiovascular system. In contrast, in zebrafish, previous studies have reported that although embryos injected with tek morpholinos (MOs) exhibit severe vascular defects, tek mutants display no obvious vascular malformations. To further investigate the function of zebrafish Tek, we generated a panel of loss-of-function tek mutants, including RNA-less alleles, an allele lacking the MO-binding site, an in-frame deletion allele and a premature termination codon-containing allele. Our data show that all these mutants survive to adulthood with no obvious cardiovascular defects. MO injections into tek mutants lacking the MO-binding site or the entire tek locus cause similar vascular defects to those observed in MO-injected +/+ siblings, indicating off-target effects of the MOs. Surprisingly, comprehensive phylogenetic profiling and synteny analyses reveal that Tek was lost in the largest teleost clade, suggesting a lineage-specific shift in the function of TEK during vertebrate evolution. Altogether, these data show that Tek is dispensable for zebrafish development, and probably dispensable in most teleost species.
KW - Animals
KW - Cardiovascular System/cytology
KW - Gene Editing
KW - Organogenesis/genetics
KW - Phylogeny
KW - Receptor, TIE-2/genetics
KW - Zebrafish
KW - Zebrafish Proteins/genetics
U2 - 10.1242/dev.193029
DO - 10.1242/dev.193029
M3 - SCORING: Journal article
C2 - 32928907
VL - 147
JO - DEVELOPMENT
JF - DEVELOPMENT
SN - 0950-1991
IS - 19
M1 - dev193029
ER -