Abstract
The molecular mechanisms by which androgens act via the androgen receptor (AR) to maintain male fertility are poorly understood. Transgenic mice were produced expressing mutant ARs that can only (1) alter gene transcription through the classical response pathway (AR-C) or 2) activate kinase signaling cascades via the nonclassical pathway (AR-NC). AR-NC allowed completion of meiosis and the production of haploid germ cells. Expression of AR-C was sufficient to produce sperm and fertility. However, added AR-NC activity contributed to maintaining the blood-testis barrier, plus correct migration and orientation of maturing spermatids needed for fully efficient sperm production. AR-C activity is required for expression of cohesion and synaptonemal complex proteins that are essential for chromosome synapsis. AR-C supported partial development of prostate and coagulating glands, but full development required both pathways. Our results indicate that AR-C activity alone partially restores male fertility, but AR-NC is obligatory to maximize fertility.
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