/Ectopic expression of Mst77Y alone is sufficient to cause nuclear decompaction. The Mst77Y genes have several interesting features. First, the gene locus contains 18 copies of Mst77F homolog, which originated from a single event of Mst77F translocation to the Y chromosome, followed by gene amplification. Second, many of the Mst77Y genes have mutations, which have resulted in changes in the position and number of critical arginine and lysine residues believed to be important for protamine function. Other mutations have resulted in premature truncations. Note that anti-Mst77Y antibody was generated by using multiple peptides from Mst77Y that are distinct from Mst77F to increase specificity. The peptides were also designed to be able to identify all copies of Mst77Y, which feature similar mutations. Because Mst77Y's mutations likely alter Mst77F's normal function, we hypothesized that Mst77Y genes may function as a dominant-negative form of Mst77F. Accordingly, Mst77Y's aberrantly high expression in modulo mutant may interfere with the process of normal histone-to-protamine transition. To test the possibility that the expression of Mst77Y causes the nuclear decompaction phenotype, we generated transgenic lines that express Mst77Y under a male germline-specific tubulin promoter. From the 18 copies of Mst77Y homologs present on the Y chromosome, we generated two lines expressing either Mst77Y-12 (a full-length version) or Mst77Y-3 (a truncated version due to premature stop codon). Strikingly, expression of either Mst77Y-3 or Mst77Y-12 recapitulated nuclear decompaction phenotype similar to that seen in modulo mutant. Notably, in contrast to the eventual decompaction of all spermatids seen in the modulo mutant, Mst77Y overexpression alone does not cause sterility. We speculate that this might be due to the added effect of the decreased incorporation of Mst77F and Protamine A/B, in addition to high Mst77Y incorporation, seen in the modulo mutant.