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Different molecular mechanisms underlie placental overgrowth phenotypes caused by interspecies hybridization, cloning, and Esx1 mutation
Author(s) -
Singh Umashankar,
Fohn Laurel E.,
Wakayama Teruhiko,
Ohgane Jun,
Steinhoff Christine,
Lipkowitz Bettina,
Schulz Ralph,
Orth Annie,
Ropers H. Hilger,
Behringer Richard R.,
Tanaka Satoshi,
Shiota Kunio,
Yanagimachi Ryuzo,
Nuber Ulrike A.,
Fundele Reinald
Publication year - 2004
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20024
Subject(s) - biology , mutant , gene , cloning (programming) , genetics , phenotype , mutation , microbiology and biotechnology , molecular cloning , gene expression , computer science , programming language
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. Developmental Dynamics 230:149–164, 2004. © 2004 Wiley‐Liss, Inc.