title: Different molecular mechanisms underlie placental overgrowth phenotypes caused by interspecies hybridization, cloning, and Esx1 mutation.
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.
authors.affiliation: Department of Development and Genetics, Uppsala University, Uppsala, Sweden.
authors.forename: Umashankar
authors.initials: U
authors.lastname: Singh
authors.forename: Laurel E
authors.initials: LE
authors.lastname: Fohn
authors.forename: Teruhiko
authors.initials: T
authors.lastname: Wakayama
authors.forename: Jun
authors.initials: J
authors.lastname: Ohgane
authors.forename: Christine
authors.initials: C
authors.lastname: Steinhoff
authors.forename: Bettina
authors.initials: B
authors.lastname: Lipkowitz
authors.forename: Ralph
authors.initials: R
authors.lastname: Schulz
authors.forename: Annie
authors.initials: A
authors.lastname: Orth
authors.forename: H Hilger
authors.initials: HH
authors.lastname: Ropers
authors.forename: Richard R
authors.initials: RR
authors.lastname: Behringer
authors.forename: Satoshi
authors.initials: S
authors.lastname: Tanaka
authors.forename: Kunio
authors.initials: K
authors.lastname: Shiota
authors.forename: Ryuzo
authors.initials: R
authors.lastname: Yanagimachi
authors.forename: Ulrike A
authors.initials: UA
authors.lastname: Nuber
authors.forename: Reinald
authors.initials: R
authors.lastname: Fundele
mesh_terms: D000818:Animals; D015152:Blotting, Northern; D002467:Cell Nucleus / Q000378:metabolism; D003001:Cloning, Molecular; D004247:DNA / Q000378:metabolism; D018076:DNA, Complementary / Q000378:metabolism; D020224:Expressed Sequence Tags; D018507:Gene Expression Regulation, Developmental; D018392:Genomic Imprinting; D005838:Genotype; D018398:Homeodomain Proteins / Q000235:genetics*; D006965:Hyperplasia; D007091:Image Processing, Computer-Assisted; D017403:In Situ Hybridization; D051379:Mice; D009154:Mutation; D009693:Nucleic Acid Hybridization; D020411:Oligonucleotide Array Sequence Analysis; D010641:Phenotype; D010920:Placenta / Q000378:metabolism* / Q000473:pathology*; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014157:Transcription Factors / Q000235:genetics*
chemical_list: D018076:DNA, Complementary; C107475:Esx1 protein, mouse; D018398:Homeodomain Proteins; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; D014157:Transcription Factors; D004247:DNA