Severe spermatogenic defects: an alteration in the distribution of stages of spermatogenesis. Mutation reduces the number of enlarged primary spermatocytes to approximately 10% the wild type level, resulting in a cluster of these cells close to the apical end of the testis. Mutation does not inhibit mitosis during spermatogenesis.
The male sterile phenotype is probably due to alteration of the cis-acting transcription regulatory sequence at the Trf site and this effect becomes more severe when a portion of the transposon is removed. The effects on Mcr expression (the second member of the Trf cluster) are the least likely explanation for the sterile phenotype. MED20 (the third member of the Trf cluster) may exhibit altered regulation explaining the defective male germ cells.