@article{fdi:010080522,
  title = {{A} mating-induced reproductive gene promotes {A}nopheles tolerance to {P}lasmodium falciparum infection},
  author = {{M}arcenac, {P}. and {S}haw, {W}. {R}. and {K}akani, {E}. {G}. and {M}itchell, {S}. {N}. and {S}outh, {A}. and {W}erling, {K}. and {M}arrogi, {E}. and {A}bernathy, {D}. {G}. and {Y}erbanga, {R}. {S}. and {D}abire, {R}. {K}. and {D}iabate, {A}. and {L}ef{\`e}vre, {T}hierry and {C}atteruccia, {F}.},
  editor = {},
  language = {{ENG}},
  abstract = {{A}uthor summary {P}lasmodium falciparum, the deadliest form of human malaria, is transmitted when female {A}nopheles mosquitoes bite people and take a blood meal in order to develop eggs. {T}o date, it is still poorly understood whether {A}nopheles mosquitoes that get infected with {P}. falciparum suffer fitness costs. {H}ere, we find that the number of eggs produced by {A}nopheles gambiae and {A}nopheles stephensi females is not affected by {P}. falciparum infection, and that the mating status of the mosquitoes does not impact the parasite. {H}owever, in field experiments infecting a related species, {A}nopheles coluzzii, with {P}. falciparum using blood from donors in {B}urkina {F}aso, we find that interfering with the expression of a gene normally triggered by the sexual transfer of the steroid hormone 20-hydroxyecdysone induces increasing costs to egg development as females become more infected with {P}. falciparum, with no impacts on the parasite. {T}he results of our study suggest that pathways triggered by mating may help {A}nopheles prevent reproductive costs associated with {P}. falciparum infection, providing new insights into evolutionary strategies adopted by anophelines in the face of a longstanding association with {P}lasmodium parasites. {A}nopheles mosquitoes have transmitted {P}lasmodium parasites for millions of years, yet it remains unclear whether they suffer fitness costs to infection. {H}ere we report that the fecundity of virgin and mated females of two important vectors-{A}nopheles gambiae and {A}nopheles stephensi-is not affected by infection with {P}lasmodium falciparum, demonstrating that these human malaria parasites do not inflict this reproductive cost on their natural mosquito hosts. {A}dditionally, parasite development is not impacted by mating status. {H}owever, in field studies using different {P}. falciparum isolates in {A}nopheles coluzzii, we find that {M}ating-{I}nduced {S}timulator of {O}ogenesis ({MISO}), a female reproductive gene strongly induced after mating by the sexual transfer of the steroid hormone 20-hydroxyecdysone (20{E}), protects females from incurring fecundity costs to infection. {MISO}-silenced females produce fewer eggs as they become increasingly infected with {P}. falciparum, while parasite development is not impacted by this gene silencing. {I}nterestingly, previous work had shown that sexual transfer of 20{E} has specifically evolved in {C}ellia species of the {A}nopheles genus, driving the co-adaptation of {MISO}. {O}ur data therefore suggest that evolution of male-female sexual interactions may have promoted {A}nopheles tolerance to {P}. falciparum infection in the {C}ellia subgenus, which comprises the most important malaria vectors.},
  keywords = {{BURKINA} {FASO}},
  booktitle = {},
  journal = {{PL}o{S} {P}athogens},
  volume = {16},
  numero = {12},
  pages = {e1008908 [16 p.]},
  ISSN = {1553-7366},
  year = {2020},
  DOI = {10.1371/journal.ppat.1008908},
  URL = {https://www.documentation.ird.fr/hor/fdi:010080522},
}