Rescue of the early vascular defects in Tek/Tie2 null mice reveals an essential survival function

Disruption of the signaling pathways mediated by the receptor tyrosine kina se Tek/Tie2 has shown that this receptor plays a pivotal role in vasculariz ation of the developing embryo. In this report, we have utilized the tetrac ycline-responsive binary transgenic system to overcome the early lethal car diovascular defects associated with the tek(Delta sP) null allele in order to investigate the role of Tek in later stages of vessel growth. We show fo r the first time in vivo that synchronized loss of tek expression correlate s with rapid endothelial cell apoptosis in hemorrhagic regions of the embry o, demonstrating an ongoing requirement for Tek-mediated signal transductio n in vascular maintenance.