- THIS ARTICLE
- Full Text
- Full Text (PDF)
- Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Poirier, C.
- Articles by Bishop, C. E.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Poirier, C.
- Articles by Bishop, C. E.
Genetics, Vol. 168, 1557-1562, November 2004, Copyright © 2004
doi:10.1534/genetics.104.032177
A Complex Interaction of Imprinted and Maternal-Effect Genes Modifies Sex Determination in Odd Sex (Ods) Mice
Christophe Poirier*,
Yangjun Qin*,
Carolyn P. Adams*,
Yanett Anaya*,
Jonathan B. Singer
,
,
Annie E. Hill
,
Eric S. Lander
,
,**,
Joseph H. Nadeau
,
,
and
Colin E. Bishop*,
,1
* Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, Texas 77030

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030
Broad Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142
Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142
** Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142
Department of Genetics, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106

Center for Computational Genomics and Systems Biology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106

Department of Epidemiology and Biostatistics, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
1 Corresponding author: Department of Obstetrics and Gynecology, Smith Tower, Room 880, Baylor College of Medicine, 6550 Fannin St., Houston, TX 77030.
E-mail: bishop{at}bcm.tmc.edu
The transgenic insertional mouse mutation Odd Sex (Ods) represents a model for the long-range regulation of Sox9. The mutation causes complete female-to-male sex reversal by inducing a male-specific expression pattern of Sox9 in XX Ods/+ embryonic gonads. We previously described an A/J strain-specific suppressor of Ods termed Odsm1A. Here we show that phenotypic sex depends on a complex interaction between the suppressor and the transgene. Suppression can be achieved only if the transgene is transmitted paternally. In addition, the suppressor itself exhibits a maternal effect, suggesting that it may act on chromatin in the early embryo.
This article has been cited by other articles:
![]() |
S Pujar, K. Kothapalli, H. Goring, and V. Meyers-Wallen Linkage to CFA29 Detected in a Genome-Wide Linkage Screen of a Canine Pedigree Segregating Sry-Negative XX Sex Reversal J. Hered., August 3, 2007; (2007) esm028v2. [Abstract] [Full Text] [PDF] |
||||
![]() |
Q. Winger, J. Huang, H. J. Auman, M. Lewandoski, and T. Williams Analysis of Transcription Factor AP-2 Expression and Function During Mouse Preimplantation Development Biol Reprod, September 1, 2006; 75(3): 324 - 333. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. A. Gray, A. Wilson, P. J. Fortin, and R. D. Nicholls The putatively functional Mkrn1-p1 pseudogene is neither expressed nor imprinted, nor does it regulate its source gene in trans PNAS, August 8, 2006; 103(32): 12039 - 12044. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Kanai, R. Hiramatsu, S. Matoba, and T. Kidokoro From SRY to SOX9: Mammalian Testis Differentiation J. Biochem., July 1, 2005; 138(1): 13 - 19. [Abstract] [Full Text] [PDF] |
||||



