Klf12 is required for vessel organization in zebrafish embryos

Perkins, Andrew C., Gunaratnam, Dinushka, Gardiner, Melissa R. and Robinson, Kathleen C. (2005). Klf12 is required for vessel organization in zebrafish embryos. In: Blood. American Society of Hematology 47th Annual Meeting, Atlanta, Georgia, (1029A-1029A). 10-13 December 2005.


Author Perkins, Andrew C.
Gunaratnam, Dinushka
Gardiner, Melissa R.
Robinson, Kathleen C.
Title of paper Klf12 is required for vessel organization in zebrafish embryos
Formatted title
Klf12 is required for vessel organization in zebrafish embryos
Conference name American Society of Hematology 47th Annual Meeting
Conference location Atlanta, Georgia
Conference dates 10-13 December 2005
Proceedings title Blood   Check publisher's open access policy
Place of Publication Washington, D.C., USA
Publisher American Society of Hematology
Publication Year 2005
Sub-type Poster
ISSN 0006-4971
1528-0020
Volume 106
Issue 11
Start page 1029A
End page 1029A
Total pages 1
Language eng
Abstract/Summary The process of forming a lumenised vessel from an angioblast cord is a crucial part of both vasculogenesis and angiogenesis. The Krüppel like factors (klfs) are a family of zinc finger transcription factors which play important roles in many aspects of differentiation. Klf2 knockout mice die in utero from haemorrhaging due to arterial wall defects. Due to the similarity of vascular and haematopoietic systems to those of mammals, the zebrafish was chosen as a model in which to study the function of klf12, the only zebrafish representative of the repressor subfamily of mammalian klfs which includes klf3, klf8 and klf12. Klf12 is first detected by WISH at 12 somites in the lateral plate mesoderm (LPM) and continues in these cells as they from the ICM at 18–22hpf, the site of vasculogenesis and haematopoiesis. From 24hpf klf12 is expressed in short stripes extending from the ICM dorsally towards the notochord. This expression pattern is similar but not identical to that of fli1 and flk1, two vascular markers. Expression subsequently decreases and is absent by 30hpf. Targeted knockdown of klf12 by translantion-inhibiting and splicing morpholinos (MOs) produces a vascular defect. At 24hpf morphants display correct expression of primitive blood, kidney and vascular markers such as gata1, ßE3globin, biklf, pax2.1 and fli1. However, circulation is absent in 65% of embryos at 48 hpf and reduced in most, as seen by both brightfield microscopy and fluorescent microbead microangiography. Embryos also display a slower heartbeat, pericardial oedema and oedema over the yolk/duct of Cuvier, all likely to be secondary effects due to the circulatory defect. Injection of klf12 MOs into fli1-eGFP transgenic embryos reveals correct differentiation of endothelial cells, but disorganised angiogenesis. In summary, klf12 morphants display correct specification of angioblasts and differentiation of endothelial cells but a defect in tubulogenesis of endothelial cords.
Subjects 1103 Clinical Sciences
1102 Cardiovascular Medicine and Haematology
Q-Index Code EX
Q-Index Status Provisional Code
Institutional Status Unknown
Additional Notes Abstract number: 3695

 
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