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Restricted development of mouse triploid fetuses with disorganized expression of imprinted genes.

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/62347

Title: Restricted development of mouse triploid fetuses with disorganized expression of imprinted genes.
Authors: Yamazaki, Wataru Browse this author
Takahashi, Masashi Browse this author
Kawahara, Manabu Browse this author →KAKEN DB
Keywords: Fetal growth
Gene expression
Genomic imprinting
Triploid
Issue Date: Dec-2015
Publisher: Cambridge University Press
Journal Title: Zygote (Cambridge, England)
Volume: 23
Issue: 6
Start Page: 874
End Page: 884
Publisher DOI: 10.1017/S0967199414000550
PMID: 25318586
Abstract: Summary Eukaryotic species commonly contain a diploid complement of chromosomes. The diploid state appears to be advantageous for mammals because it enables sexual reproduction and facilitates genetic recombination. Nonetheless, the effects of DNA ploidy on mammalian ontogeny have yet to be understood. The present study shows phenotypic features and expression patterns of imprinted genes in tripronucleate diandric and digynic triploid (DAT and DGT) mouse fetuses on embryonic day 10.5 (E10.5). Measurement of crown-rump length revealed that the length of DGT fetuses (1.87 ± 0.13 mm; mean ± standard error of the mean) was much smaller than that of diploid fetuses (4.81 ± 0.05 mm). However, no significant difference was observed in the crown-rump length between diploid and DAT fetuses (3.86 ± 0.43 mm). In DGT fetuses, the expression level of paternally expressed genes, Igf2, Dlk1, Ndn, and Peg3, remained significantly reduced and that of maternally expressed genes, Igf2r and Grb10, increased. Additionally, in DAT fetuses, the Igf2 mRNA expression level was approximately twice that in diploid fetuses, as expected. These results provide the first demonstration that imprinted genes in mouse triploid fetuses show distinctive expression patterns independent of the number of parental-origin haploid sets. These data suggest that both DNA ploidy and asymmetrical functions of parental genomes separately influence mammalian ontogeny.
Rights: © Cambridge University Press 2015
Relation: http://journals.cambridge.org/action/displayJournal?jid=ZYG
Type: article (author version)
URI: http://hdl.handle.net/2115/62347
Appears in Collections:農学院・農学研究院 (Graduate School of Agriculture / Faculty of Agriculture) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 川原 学

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