Journal
GENESIS
Volume 32, Issue 3, Pages 218-230Publisher
WILEY-LISS
DOI: 10.1002/gene.10060
Keywords
quaking; QKI; vasculogenesis; RNA binding protein; mouse; endothelial cell maturation; smooth muscle differentiation
Categories
Funding
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [U01HD039372] Funding Source: NIH RePORTER
- NATIONAL CANCER INSTITUTE [R01CA063229, P01CA075719] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL061408] Funding Source: NIH RePORTER
- NCI NIH HHS [P01CA75719, R01CA63229] Funding Source: Medline
- NHLBI NIH HHS [R01HL61408] Funding Source: Medline
- NICHD NIH HHS [U01HD39372] Funding Source: Medline
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For nearly 40 years functional studies of the mouse quaking gene (qkl) have focused on its role in the postnatal central nervous system during myelination. However, the homozygous lethality of a number of ENU-induced alleles reveals that quaking has a critical role in embryonic development prior to the start of myelination. In this article, we show that quaking has a previously unsuspected and essential role in blood vessel development. Interestingly, we found that quaking, a nonsecreted protein, is expressed in the yolk sac endoderm, adjacent to the mesodermal site of developing blood islands, where the differentiation of blood and endothelial cells first occurs. Antibodies against PE-CAM-1, TIE-2 and SM-alpha-actin reveal that embryos homozygous for the qk(k2) allele have defective yolk sac vascular remodeling and abnormal vessels in the embryo proper at midgestation, coinciding with the timing of embryonic death. However, these mutants exhibit normal expression of Nkx2.5 and alpha-sarcomeric actin, indicating that cardiac muscle differentiation was normal. Further, they had normal embryonic heart rates in culture, suggesting that cardiac function was not compromised at this stage of embryonic development. Together, these results suggest that quaking plays an essential role in vascular development and that the blood vessel defects are the cause of embryonic death. genesis 32:218-230, 2002. (C) 2002 Wiley-Liss, Inc.
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