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Oral Presentation
Monday 18 November
20:45 - 21:00 HRS
X-INACTIVATION MEDIATES AN EFFECT ON MATERNAL RECOMBINATION AND MEIOTIC DRIVE
E. de la Casa-Esperon
Temple University
School of Medicine
Co-Authors: 1)
Loredo-Osti J C, 2) Pardo-Manuel de Villena
F, 4) Briscoe T L,
5) Malette J M, 6) Vaughan J E,
1) Morgan K, 8) Sapienza C
Institutions:
1) McGill University, 2) University of North Carolina F, 4) Temple
University School of Medicine, 5) Temple University School of Medicine,
6) Temple University School of Medicine, 7) McGill University, 8)
Temple University School of Medicine
Crosses between the DDK inbred mouse strain and other inbred strains and their F1 hybrids show two interesting phenomena: early embryonic lethality (“DDK syndrome”) and preferential segregation of chromosomes during female meiosis (meiotic drive at the second meiotic division). Components of both phenotypes have been mapped to the central region of chromosome 11. We now observe a third phenomenon: overall levels of meiotic recombination differ between females of identical (C57BL/6-Pgk1a x DDK)F1 genotype, and this variability correlates with their pattern of X-inactivation. Because meiotic drive is affected by recombination, a correlation is also observed between the levels of transmission ratio distortion at chromosome 11 and the patterns of X-inactivation of the F1 females. Our results indicate the presence of a locus/loci on the X chromosome that is involved in the control of recombination. This locus/loci is subject to X-inactivation and the expression of different alleles results in differences in levels of genome-wide recombination.
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