Key result
Inactivating Drosophila myosuppressin neurons prolongs copulation while MsR2 loss cuts seminal fluid protein ~50%.
Why the study?
There is a paucity of information on how tightly coordinated neural and muscular activity achieves ejaculate formation and context-dependent modulation of seminal fluid investment in animals such as Drosophila melanogaster.
Myosuppressin signaling in the male accessory glands plays a role in controlling seminal fluid investment in the ejaculate, thereby increasing male reproductive fitness in Drosophila melanogaster.
Hypothesis-generating in Drosophila; leaves open any translational relevance to mammalian reproduction or cardiology.
In many animals, including insects, male competition can lead to longer copulation duration, greater ejaculate (sperm and seminal fluid, SF) investment and increased male reproductive success. In Drosophila melanogaster, sperm from the seminal vesicles (SV) is mixed in the anterior ejaculatory duct (aED) with SF from the male accessory glands (MAG). The formation of the ejaculate and the context-dependent modulation of SF investment necessitates tightly coordinated neural and muscular activity. There is, however, a paucity of information on how this is achieved. We have now identified a role for the neuropeptide, myosuppressin (Ms), signaling in the control of sperm and SF transfer to the female D. melanogaster. Ms is expressed in AbG neurons, as well as in an unpaired cell adjacent to the aED and a pair of rectal cells. Ms AbG neurons that innervate the MAG and aED are distinct from the serotonergic AbG (sAbG) neurons that promote ejaculation. Inactivating Ms neurons increased copulation duration and elevated the ejaculate holding period (EHP), while reducing oviposition in the mated female. Results indicate that Ms receptors (MsR1 and MsR2) are expressed in some of the sAbG neurons. Strong expression of MsR2 in the MAG muscle explains the Ms suppression of spontaneous contractions of the MAGs. Loss of a functional MsR2 leads to a 50% reduction of a SF protein in MAGs of virgin males. Taken together, our results suggest that Ms signaling in MAG plays a role in controlling SF investment in the ejaculate, thereby increasing male reproductive fitness.
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Seo et al. (2026) studied Male reproductive fitness. Inactivating myosuppressin (Ms) neurons / Loss of MsR2 was evaluated on Copulation duration, ejaculate holding period, and seminal fluid protein levels. Inactivating myosuppressin neurons in Drosophila increased copulation duration, while loss of functional MsR2 led to a 50% reduction of a seminal fluid protein in male accessory glands.
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