To accommodate diverse personal needs in family planning, diverse contraceptive approaches are desirable. This goal requires identification of new contraceptive targets. Phenotype-driven mutagenesis is an unbiased approach to identify novel genes and functions in reproductive processes. The ReproGenomics Program at The Jackson Laboratory is a United States National Institutes of Health resource for production, identification and distribution of mutant mouse models of infertility that can be used for identification of potential targets for contraception. The strategy of this program is whole genome, random ENU mutagenesis, coupled with a phenotype screen for breeding failure as the only phenotype. A three-generation breeding scheme selects recessive mutations affecting reproductive functions. G3 males and females that fail to reproduce by natural mating to wild-type animals undergo secondary phenotype screens to assess gonad and accessory organ histology, hormone production, gamete production and gamete function in fertilization. The genetic transmission of the infertility trait in each family is confirmed and each mutation is genetically mapped to a defined chromosome region, facilitating identification of candidate genes from sequence and expression databases. Genes essential for fertility in both males and females and acting both meiotically and post-meiotically have been identified by this strategy. Phenotypes include male infertility with normal sperm count, but failure in fertilization of oocytes. Phenotype descriptions of each mutation are posted on the program website, . These unique reproductive mutant mouse resources will lead to new discoveries in andrology (and gynecology) research, as well as reproductive medicine. Dissection of gene function in known and newly discovered reproductive pathways will expand our focus to reveal novel targets for contraception.
[1]
M. Griswold,et al.
The Murine Testicular Transcriptome: Characterizing Gene Expression in the Testis During the Progression of Spermatogenesis1
,
2004,
Biology of reproduction.
[2]
M. Handel,et al.
New mouse genetic models for human contraceptive development
,
2004,
Cytogenetic and Genome Research.
[3]
M. Griswold,et al.
Androgen-Regulated Genes in the Murine Epididymis1
,
2004,
Biology of reproduction.
[4]
M. Justice,et al.
Mutations in a Novel Locus on Mouse Chromosome 11 Resulting in Male Infertility Associated with Defects in Microtubule Assembly and Sperm Tail Function1
,
2004,
Biology of reproduction.
[5]
N. Schultz,et al.
A multitude of genes expressed solely in meiotic or postmeiotic spermatogenic cells offers a myriad of contraceptive targets
,
2003,
Proceedings of the National Academy of Sciences of the United States of America.
[6]
M. Justice,et al.
The mutagenic action of N-ethyl-N-nitrosourea in the mouse
,
2000,
Mammalian Genome.
[7]
L. Reinholdt,et al.
Positional cloning and characterization of mouse mei8, a disrupted allele of the meiotic cohesin Rec8
,
2004,
Genesis.
[8]
E. Revenkova,et al.
Cohesin SMC1β is required for meiotic chromosome dynamics, sister chromatid cohesion and DNA recombination
,
2004,
Nature Cell Biology.
[9]
S. Nass,et al.
New frontiers in contraceptive research : a blueprint for action
,
2004
.