Figure 7.

Current models of SD action. (A) Sd–RanGAP directly binds Rsp repeats, disrupting chromatin condensation in Rsp^s-bearing spermatids causing spermatid dysfunction either as a consequence of disrupted nuclear transport or some other cellular function of RanGAP. (B) Sd–RanGAP disrupts nuclear transport globally, but Rsp^s-bearing spermatids are disproportionately sensitive to this disruption because large blocks of Rsp act as a sink for chromatin modifiers when their access to the nucleus is limited. (C) Rsp rasiRNAs, presumably required for postmeiotic chromatin condensation, are exported from the nucleus, where they form ribonucleoprotein (RNP) complexes; however, the RNP complexes fail to target chromatin modifiers to the genomic Rsp satellite because of some disrupted RanGAP, or ran-like, function (see text). Although the disruption is shown as a failure to reenter the nucleus due to disrupted transport, a disrupted Ran-GTP/Ran-GDP (or ran-like-GTP/ran-like-GDP) gradient could affect chromatin condensation more directly.