In conclusion, during the reprogramming of spermiogenesis, there was a finely orchestrated dissociation of types of CAFs, which might contribute directly to the closure of transcription. This process could erase the paternal epigenetic pattern and generate a relative na? ��ve chromatin. A much similar erasure program was also observed in the late oogenesis. Taken together, this reprogramming during gametogenesis would be essential for the installation of the zygotic developmental program after fertilization. At this moment, the regulation of this erasure procedure was mostly unknown. In another aspect, histone modifications dynamically modulate chromatin structure, conducting the chromatin binding of functional molecules. We wonder if the disassociation of CAFs is causally related to the changes of epigenome in spermatids. Generally, acetylation of histones, especially acetylated histone H3 and H4, are considered as markers of “open” configuration of chromatin. During mouse spermiogenesis, the substantial expression of AcH4 was observed in step 1�C8 round spermatids, followed by a global hyperacetylation in Step 9�C12 elongating spermatids. A similar hyperacetylation wave of histones was also found in the rat elongating spermatids. This characteristic phenomenon has long been understood as a prelude of histone replacement carried by transition proteins and protamine, by which the paternal genome packaged into a highly compact structure. In mouse elongating spermatids, the spatial distribution of acetylated H4 within the nuclei was tightly associated with the chromatin condensation. It should be noticed that, the time point of CAFs dissociation and transcription termination was just before the beginning of histone hyperacetylation. So the “erasure” in spermiogenesis was not a direct consequence of histone replacement, but related to that histone acetylation. In that case, disturbing the acetylation level might injure the programmed spermiogenesis. This view has been preliminarily proved by histone deacetylase BAY-60-7550 purchase inhibitor TSA treatment. However, we believe the execution of histone acetylase inhibitors, underlying an induced hypoacetylation status, should be more harmful to the spermatids. In this study, we treated primary mouse spermatids with HAT inhibitor Curcumin in vitro, evaluated its effects on cell viability, transcription activity and CAFs dynamics. Our data revealed that, a 
given dose of Curcumin could upregulate the spermatids apoptosis, as well as accelerated the erasure program happened to the CAFs and transcription, the mouse spermiogenesis was impaired by Curcumin treatment. Therefore, the BMS-907351 849217-68-1 potential reproductive toxicity of Curcumin, especially for its new preparations, should be carefully investigated. To explore the mechanism of male fertility, one of the biggest obstacles has been the lack of ideal models of the spermiogenesis, in vitro and in vivo. In this research, we applied a fluorescenceactivated cell sorting based on Hoechst33342 staining to purify the haploid spermatids. Most recently, haploid embryonic stem cell lines were established attributing to the similar ploidy sorting technique. Hoechst33342 is a living-cell permeant and relatively non-toxic. Verapamil has been used as an inhibitor of drug efflux pump proteins to block the efflux of Hoechst33342.