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Kim, Y.J., Bartalska, K., Audsley, N., Yamanaka, N., Yapici, N., Lee, J.Y., Kim, Y.C., Markovic, M., Isaac, E., Tanaka, Y., Dickson, B.J. (2010). MIPs are ancestral ligands for the sex peptide receptor.  Proc. Natl. Acad. Sci. U.S.A. 107(14): 6520--6525.
FlyBase ID
FBrf0210504
Publication Type
Research paper
Abstract

Upon mating, females of many animal species undergo dramatic changes in their behavior. In Drosophila melanogaster, postmating behaviors are triggered by sex peptide (SP), which is produced in the male seminal fluid and transferred to female during copulation. SP modulates female behaviors via sex peptide receptor (SPR) located in a small subset of internal sensory neurons that innervate the female uterus and project to the CNS. Although required for postmating responses only in these female sensory neurons, SPR is expressed broadly in the CNS of both sexes. Moreover, SPR is also encoded in the genomes of insects that lack obvious SP orthologs. These observations suggest that SPR may have additional ligands and functions. Here, we identify myoinhibitory peptides (MIPs) as a second family of SPR ligands that is conserved across a wide range of invertebrate species. MIPs are potent agonists for Drosophila, Aedes, and Aplysia SPRs in vitro, yet are unable to trigger postmating responses in vivo. In contrast to SP, MIPs are not produced in male reproductive organs, and are not required for postmating behaviors in Drosophila females. We conclude that MIPs are evolutionarily conserved ligands for SPR, which are likely to mediate functions other than the regulation of female reproductive behaviors.

PubMed ID
PubMed Central ID
PMC2851983 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Proc. Natl. Acad. Sci. U.S.A.
    Title
    Proceedings of the National Academy of Sciences of the United States of America
    Publication Year
    1915-
    ISBN/ISSN
    0027-8424
    Data From Reference
    Aberrations (1)
    Alleles (7)
    Gene Groups (1)
    Genes (6)
    Physical Interactions (2)
    Natural transposons (1)
    Transgenic Constructs (6)