Sperm development involves the transformation of spermatids into mature cells that are capable of locating and fertilising the oocyte, and this process is dependent on external signals from somatic tissues. In Caenorhabditis elegans, sperm activation is regulated by SWM-1, a trypsin inhibitor-like protein that inhibits activation and opposes the activity of the serine protease TRY-5. However, how and where this interaction plays out in the context of the gonad has remained incompletely understood. Gillian Stanfield and colleagues now use a combination of reporter constructs, tagged knock-ins and genetic knockouts to address this problem. Consistent with its role in sperm activation, SWM-1 protein is found in the seminal vesicle lumen, in which it colocalises with TRY-5. But it is also found in the body cavity, and swm-1 transcription is limited to cells of the vas deferens and muscle cells lying outside of the gonad. Indeed, SWM-1 that is derived solely from the muscles localises to the seminal vesicle and rescues swm-1 mutant phenotypes. The ability of the gonad to take up proteins secreted into the body cavity by muscles (or other tissues) is not restricted to SWM-1, and this transfer can operate in both directions. Finally, SWM-1 is transferred as a component of seminal fluid after mating, and high levels of seminal fluid SWM-1 can decrease male fertility. Thus, a secreted signal travels from muscle to gonad to regulate sperm activation, and can also be transferred in seminal fluid to influence fertility.