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ToxSci Advance Access published online on October 16, 2008
Toxicological Sciences, doi:10.1093/toxsci/kfn209
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Published by Oxford University Press 2008.

CHROMOSOMAL MOSAICISM IN MOUSE TWO-CELL EMBRYOS AFTER PATERNAL EXPOSURE TO ACRYLAMIDE

Francesco Marchetti*,{dagger}, Jack Bishop{ddagger}, Xiu Lowe*,{dagger},¶ and Andrew J. Wyrobek*,{dagger}

* Biosciences Directorate, Lawrence Livermore National Laboratory, Livermore, CA 94550 {dagger} Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720 {ddagger} National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709 Department of Psychiatry, Kaiser Permanente Medical Group, Inc, Hayward, CA 94545

Send correspondence to: Dr. Francesco Marchetti, Life Sciences Division, MS74R0157, Lawrence Berkeley National Laboratory, 1 Cyclotron Rd, Berkeley CA 94720, Telephone: (510) 486-7352, Telefax: (510) 486-6691, e-mail: fmarchetti{at}lbl.gov.

Received July 18, 2008; revision received September 22, 2008; accepted September 28, 2008


  Abstract

Chromosomal mosaicism in human preimplantation embryos is a common cause of spontaneous abortions, however, our knowledge of its etiology is limited. We used multicolor fluorescence in situ hybridization (FISH) painting to investigate whether paternally-transmitted chromosomal aberrations result in mosaicism in mouse 2-cell embryos. Paternal exposure to acrylamide, an important industrial chemical also found in tobacco smoke and generated during the cooking process of starchy foods, produced significant increases in chromosomally defective 2-cell embryos, however, the effects were transient primarily affecting the postmeiotic stages of spermatogenesis. Comparisons with our previous study of zygotes demonstrated similar frequencies of chromosomally abnormal zygotes and 2-cell embryos suggesting that there was no apparent selection against numerical or structural chromosomal aberrations. However, the majority of affected 2-cell embryos were mosaics showing different chromosomal abnormalities in the two blastomeric metaphases. Analyses of chromosomal aberrations in zygotes and 2-cell embryos showed a tendency for loss of acentric fragments during the first mitotic division of embryogenesis, while both dicentrics and translocations apparently underwent proper segregation. These results suggest that embryonic development can proceed up to the end of the second cell cycle of development in the presence of abnormal paternal chromosomes and that even dicentrics can persist through cell division. The high incidence of chromosomally mosaic 2-cell embryos suggests that the first mitotic division of embryogenesis is prone to missegregation errors and that paternally-transmitted chromosomal abnromalities increase the risk of missegregation leading to embryonic mosaicism.

Key Words: acrylamide; in vivo; fluorescence in situ hybridization; spermatogenesis.


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