Human Molecular Genetics, Vol 8, 2489-2495, Copyright © 1999 by Oxford University Press
C Couldrey, MB Carlton, PM Nolan, WH Colledge and MJ Evans
Spermatogenesis is a complex developmental pro-cess involving cell division
and differentiation. Approximately half of all sterile males have defects
in spermatogenesis or sperm function. An insight into the molecular control
points regulating this process might help in treating male infertility.
Gene trapping in embryonic stem cells and the generation of transgenic mice
represents one route to identify genes expressed during spermatogenesis.
The trapped gene is tagged with a lacZ reporter gene so that the expression
pattern of the gene can be visualized by staining for beta-galactosidase
activity. We have screened transgenic mouse lines for expression of trapped
genes in the gonads. One such trap event was shown to be in the replacement
histone 3.3A gene ( H3.3A ). This gene was expressed ubiquitously during
embryonic development until 13.5 days post-coitum and in the adult heart,
kidney, brain, testes and ovaries. This mutation resulted in postnatal
death of 50% of homozygous mutants. Surviving mutants displayed reduced
growth rates when competing with wild-type siblings for food. Mutant mice
also had a neuro-muscular deficit and males displayed reduced copulatory
activity. When copulations did occur, these resulted in very few
pregnancies, suggesting that mutations in the H3.3A gene may contribute to
some cases of impaired fertility in man.
ARTICLES
A retroviral gene trap insertion into the histone 3.3A gene causes partial neonatal lethality, stunted growth, neuromuscular deficits and male sub-fertility in transgenic mice
Department of Physiology, University of Cambridge, Tennis Court Road, Cambridge CB2 3EG, UK,
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