Different molecular mechanisms underlie placental overgrowth phenotypes caused by interspecies hybridization, cloning, and Esx1 mutation

Dev Dyn. 2004 May;230(1):149-64. doi: 10.1002/dvdy.20024.

Abstract

To obtain a deeper insight into the genes and gene networks involved in the development of placentopathies, we have assessed global gene expression in three different models of placental hyperplasia caused by interspecies hybridization (IHPD), cloning by nuclear transfer, and mutation of the Esx1 gene, respectively. Comparison of gene expression profiles of approximately 13,000 expressed sequence tags (ESTs) identified specific subsets of genes with changed expression levels in IHPD, cloned, and Esx1 mutant placentas. Of interest, only one gene of known function and one EST of unknown function were found common to all three placentopathies; however, a significant number of ESTs were common to IHPD and cloned placentas. In contrast, only one gene was shared between IHPD and Esx1 mutant, and cloned and Esx1 mutant placentas, respectively. These genes common to different abnormal placental growth genotypes are likely to be important in the occurrence of placentopathy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Blotting, Northern
  • Cell Nucleus / metabolism
  • Cloning, Molecular
  • DNA / metabolism
  • DNA, Complementary / metabolism
  • Expressed Sequence Tags
  • Gene Expression Regulation, Developmental*
  • Genomic Imprinting
  • Genotype
  • Homeodomain Proteins / genetics*
  • Hyperplasia
  • Image Processing, Computer-Assisted
  • In Situ Hybridization
  • Mice
  • Mutation
  • Nucleic Acid Hybridization
  • Oligonucleotide Array Sequence Analysis
  • Phenotype
  • Placenta / metabolism*
  • Placenta / pathology*
  • Proto-Oncogene Proteins / genetics*
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transcription Factors / genetics*

Substances

  • DNA, Complementary
  • Esx1 protein, mouse
  • Homeodomain Proteins
  • Proto-Oncogene Proteins
  • RNA, Messenger
  • Transcription Factors
  • DNA