Document Detail


Cell polarity regulator PARD6B is essential for trophectoderm formation in the preimplantation mouse embryo.
MedLine Citation:
PMID:  20505164     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In preimplantation mouse development, the first cell lineages to be established are the trophectoderm (TE) and inner cell mass. TE possesses epithelial features, including apical-basal cell polarity and intercellular junctions, which are crucial to generate a fluid-filled cavity in the blastocyst. Homologs of the partitioning defective (par) genes in Caenorhabditis elegans are critical regulators of cell polarity. However, their roles in regulating TE differentiation and blastocyst formation remain unclear. Here, the role of mouse Pard6b, a homolog of par-6 gene and a component of the PAR-atypical protein kinase C (aPKC) complex, was investigated. Pard6b expression was knocked down by microinjecting RNA interference construct into zygotes. Pard6b-knockdown embryos cleaved and compacted normally but failed to form the blastocyst cavity. The cavitation failure is likely the result of defective intercellular junctions, because Pard6b knockdown caused abnormal distribution of actin filaments and TJP1 (ZO-1) tight junction (TJ) protein and interfered with cavitation in chimeras containing cells from normal embryos. Defective TJ formation may be caused by abnormal cell polarization, because the apical localization of PRKCZ (aPKCzeta) was absent in Pard6b-knockdown embryos. Pard6b knockdown also diminished the expression of CDX2, a TE-lineage transcription factor, in the outer cells. TEAD4, a transcriptional activator that is required for Cdx2 expression and cavity formation, was not essential for the transcription of Pard6b. Taken together, Pard6b is necessary for blastocyst morphogenesis, particularly the development of TE-specific features-namely, the apical-basal cell polarity, formation of TJ, paracellular permeability sealing, and up-regulated expression of Cdx2.
Authors:
Vernadeth B Alarcon
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-05-26
Journal Detail:
Title:  Biology of reproduction     Volume:  83     ISSN:  1529-7268     ISO Abbreviation:  Biol. Reprod.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-23     Completed Date:  2010-11-30     Revised Date:  2011-09-13    
Medline Journal Info:
Nlm Unique ID:  0207224     Medline TA:  Biol Reprod     Country:  United States    
Other Details:
Languages:  eng     Pagination:  347-58     Citation Subset:  IM    
Affiliation:
Institute for Biogenesis Research, Department of Anatomy, Biochemistry, and Physiology, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii 96813, USA. vernadet@hawaii.edu
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MeSH Terms
Descriptor/Qualifier:
Adaptor Proteins, Signal Transducing / genetics,  metabolism*
Animals
Blastocyst / physiology*
Cell Line, Tumor
Cell Lineage
Cell Polarity / physiology*
Cells, Cultured
DNA-Binding Proteins / genetics,  metabolism
Down-Regulation
Epithelial Cells / physiology
Fluorescent Antibody Technique
Homeodomain Proteins / genetics,  metabolism
Mice
Microinjections
Microscopy, Confocal
Morphogenesis / physiology*
Muscle Proteins / genetics,  metabolism
Protein Kinase C / genetics,  metabolism
RNA Interference
Reverse Transcriptase Polymerase Chain Reaction
Tight Junctions / physiology
Transcription Factors / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
G12RR003061/RR/NCRR NIH HHS; P20RR016453/RR/NCRR NIH HHS; P20RR024206/RR/NCRR NIH HHS; R03HD050475/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Cdx2 protein, mouse; 0/DNA-Binding Proteins; 0/Homeodomain Proteins; 0/Muscle Proteins; 0/Par6 protein, mouse; 0/Tead4 protein, mouse; 0/Transcription Factors; EC 2.7.11.13/Protein Kinase C
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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