International Mammalian Genome Society

The 16th International Mouse Genome Conference (2002)

Plenary Presentations * Oral Presentations *
Poster Presentations: Complex Genetics and Disease Modifiers * Developmental Genetics * Functional Genomics * Gene Discovery * Genetic Manipulations to Alter Gene Function * Mouse Models: Human Disease and Pharmacogenetics * Sequence Annotation and Comparative Analysis of Genomes *
Attendees * Sponsors * Table of Contents * Photographs * Awards

POSTER 124 - CENPB-NULL MICE GENERATED BY HOMOZYGOUS BREEDING DISPLAY DECREASING REPRODUCTIVE PERFORMANCE DUE TO A LACK OF ENDOMETRIAL GLANDS

K Fowler
Murdoch Childrens Research Institute

1) Sibson M, 2) Reed S, 1) A Choo
1) Murdoch Childrens Research Institute 2) DAKO Australia

The observed small testis and uteri of Cenpb-null mice on R1 and W9.5 genetic backgrounds (Hudson et al, 1998; Fowler et al, 2000) is reminiscent of telomerse-deficient mice (mTR-/-) following intermating over a number of generations (Lee et al, 1998; Herrera et al, 1999a). Generation 6 mTR-/- intercrosses exhibited infertility due to embryonic lethality, defective spermatogenesis and apoptosis as well as decreased oocytes and a possible compromise in uterine structure and function. The worsening phenotype of the mTR-/- mice was linked to a reduction in telomere-length and chromosomal abnormalities. These observations together with a possible role for CENP-B as a transposase in genome evolution (Kipling and Warburton, 1997) has stimulated a similar ongoing breeding program in this study for Cenpb-null mice (R1-/- and W9.5-/-) examining testis-, uterus-, ovary- and litter-size over a number of generations. Unlike the mTR-/- mice that became infertile due to a number of phenotypic changes, the lack of reproductive performance in 10-week-old Cenpb-null mice appears to be mainly due to abnormal uterine pathology that was exacerbated by generations of Cenpb-null breeding. More specifically it was not the uterus size of 10-week-old R1-/- or W9.5-/- mice that decreased further with breeding from Cenpb-null mice but the number of endometrial glands within the uterus. Interestingly, it would appear that equivalent generation Cenpb-null females carried by a Cenpb-heterozygote dam surrounded in utero by heterozygous and wildtype littermates were not as susceptible to significant decreases in endometrial gland number at 10-week-old.