Abstract
Upon mating, regions of the female reproductive tract mature and alter their function [1-3], for example to facilitate storage of sperm or control the release of eggs [4-6]. The female's nervous system and neuromodulators play important roles in her responses to mating [7-13]. However, it is difficult to reconcile the reproductive tract's many changing but coordinated events with the small set of neuromodulators present [14-18]. We hypothesized that each part of the reproductive tract contains a characteristic combination of neuromodulators that confer unique identities on each region and that postmating changes in these combinations coordinate subsequent actions. We examined the presence, locations, and levels of neuromodulators and related molecules ("signaling molecules") in the reproductive tract of Drosophila melanogaster females before and after mating: the biogenic amine octopamine, which regulates ovulation rate in Drosophila and locusts [7, 14-20]; serotonin, which regulates muscle contraction in locust oviducts [21]; and the FMRF amide dromyosuppressin, which regulates contraction of Drosophila heart muscle [22] and may regulate muscle contractions in the reproductive tract, if it is expressed there. We find that separate aspects of mating (sperm, seminal proteins, and physical effects) independently modulate the release of signaling molecules. Each reproductive tract subregion displays a characteristic combination of signaling molecule release, resulting in a unique functional identity. These patterns, and thus functions, change reproducibly after mating. Thus, one event (mating) promotes new combinations of signaling molecules that endow different parts of the reproductive tract with unique temporal and spatial identities that facilitate many aspects of fertilization.
Original language | English |
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Pages (from-to) | 731-737 |
Number of pages | 7 |
Journal | Current Biology |
Volume | 24 |
Issue number | 7 |
DOIs | |
State | Published - 31 Mar 2014 |
Bibliographical note
Funding Information:We thank U. Tram, G. Findlay, D. Rubinstein, M. Goldberg, S. Goodwin, C. Rezával, B. LaFlamme, and anonymous reviewers for advice and comments on the manuscript, A. Hefetz for assistance with statistical analysis, and Z. Nir-Amitin for the graphics. We thank R. Hoy, J. Ewer, and R. Nichols for antibodies. This work was initiated under NSF grant 99-04824 and completed under NIH grant R01-HD038921 (both to M.F.W.), US-Israel BARD Fund research grant 3492 (to Y.H.), BSF grant 2009270 (to Y.H. and M. Siegal), and ISF grant numbers 51/12 and 1902/12 I-CORE (to Y.G.). We thank these agencies and a Lady Davis Fellowship (M.F.W.) for support.
Funding
We thank U. Tram, G. Findlay, D. Rubinstein, M. Goldberg, S. Goodwin, C. Rezával, B. LaFlamme, and anonymous reviewers for advice and comments on the manuscript, A. Hefetz for assistance with statistical analysis, and Z. Nir-Amitin for the graphics. We thank R. Hoy, J. Ewer, and R. Nichols for antibodies. This work was initiated under NSF grant 99-04824 and completed under NIH grant R01-HD038921 (both to M.F.W.), US-Israel BARD Fund research grant 3492 (to Y.H.), BSF grant 2009270 (to Y.H. and M. Siegal), and ISF grant numbers 51/12 and 1902/12 I-CORE (to Y.G.). We thank these agencies and a Lady Davis Fellowship (M.F.W.) for support.
Funders | Funder number |
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US-Israel BARD | 3492 |
National Science Foundation | 99-04824 |
National Institutes of Health | |
National Institute of Child Health and Human Development | R01HD038921 |
Bloom's Syndrome Foundation | 2009270 |
Iowa Science Foundation | 1902/12 I-CORE, 51/12 |