PMID- 16354681
OWN - NLM
STAT- MEDLINE
DCOM- 20060329
LR  - 20211203
IS  - 0270-7306 (Print)
IS  - 1098-5549 (Electronic)
IS  - 0270-7306 (Linking)
VI  - 26
IP  - 1
DP  - 2006 Jan
TI  - Defects in yolk sac vasculogenesis, chorioallantoic fusion, and embryonic axis 
      elongation in mice with targeted disruption of Yap65.
PG  - 77-87
AB  - YAP is a multifunctional adapter protein and transcriptional coactivator with 
      several binding partners well described in vitro and in cell culture. To explore 
      in vivo requirements for YAP, we generated mice carrying a targeted disruption of 
      the Yap gene. Homozygosity for the Yap(tm1Smil) allele (Yap-/-) caused 
      developmental arrest around E8.5. Phenotypic characterization revealed a 
      requirement for YAP in yolk sac vasculogenesis. Yolk sac endothelial and 
      erythrocyte precursors were specified as shown by histology, PECAM1 
      immunostaining, and alpha globin expression. Nonetheless, development of an 
      organized yolk sac vascular plexus failed in Yap-/- embryos. In striking 
      contrast, vasculogenesis proceeded in both the allantois and the embryo proper. 
      Mutant embryos showed patterned gene expression domains along the anteroposterior 
      neuraxis, midline, and streak/tailbud. Despite this evidence of proper patterning 
      and tissue specification, Yap-/- embryos showed developmental perturbations that 
      included a notably shortened body axis, convoluted anterior neuroepithelium, 
      caudal dysgenesis, and failure of chorioallantoic fusion. These results reveal a 
      vital requirement for YAP in the developmental processes of yolk sac 
      vasculogenesis, chorioallantoic attachment, and embryonic axis elongation.
FAU - Morin-Kensicki, Elizabeth M
AU  - Morin-Kensicki EM
AD  - Department of Cell and Developmental Biology, University of North Carolina at 
      Chapel Hill, Chapel Hill, NC 27599-7090, USA. emkunc@med.unc.edu
FAU - Boone, Brian N
AU  - Boone BN
FAU - Howell, Michael
AU  - Howell M
FAU - Stonebraker, Jaclyn R
AU  - Stonebraker JR
FAU - Teed, Jeremy
AU  - Teed J
FAU - Alb, James G
AU  - Alb JG
FAU - Magnuson, Terry R
AU  - Magnuson TR
FAU - O'Neal, Wanda
AU  - O'Neal W
FAU - Milgram, Sharon L
AU  - Milgram SL
LA  - eng
GR  - R01 HL063755/HL/NHLBI NIH HHS/United States
GR  - HL63755/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Mol Cell Biol
JT  - Molecular and cellular biology
JID - 8109087
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Phosphoproteins)
RN  - 0 (Proteins)
RN  - 0 (Transcription Factors)
RN  - 0 (YAP-Signaling Proteins)
RN  - 0 (Yap1 protein, mouse)
RN  - EC 2.3.- (Acyltransferases)
RN  - EC 2.3.- (tafazzin protein, mouse)
SB  - IM
MH  - Acyltransferases
MH  - Adaptor Proteins, Signal Transducing/*genetics/metabolism
MH  - Animals
MH  - Cell Cycle Proteins
MH  - Chorioallantoic Membrane/*abnormalities/*blood supply
MH  - Embryo, Mammalian/abnormalities/blood supply/cytology
MH  - Embryonic Development/genetics
MH  - Gene Expression
MH  - Gene Targeting
MH  - Genes, Lethal
MH  - Homozygote
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Mutation
MH  - Neovascularization, Physiologic/*genetics
MH  - Phosphoproteins/*genetics/metabolism
MH  - Proteins/genetics/metabolism
MH  - Transcription Factors/genetics/metabolism
MH  - YAP-Signaling Proteins
MH  - Yolk Sac/*abnormalities/*blood supply/cytology
PMC - PMC1317614
EDAT- 2005/12/16 09:00
MHDA- 2006/03/30 09:00
PMCR- 2006/05/01
CRDT- 2005/12/16 09:00
PHST- 2005/12/16 09:00 [pubmed]
PHST- 2006/03/30 09:00 [medline]
PHST- 2005/12/16 09:00 [entrez]
PHST- 2006/05/01 00:00 [pmc-release]
AID - 26/1/77 [pii]
AID - 0843-05 [pii]
AID - 10.1128/MCB.26.1.77-87.2006 [doi]
PST - ppublish
SO  - Mol Cell Biol. 2006 Jan;26(1):77-87. doi: 10.1128/MCB.26.1.77-87.2006.