@article{PAR00010610,
  title = {{AP}-1/{F}os-{TG}ase2 axis mediates wounding-induced {P}lasmodium falciparum killing in {A}nopheles gambiae},
  author = {{N}sango, {S}. {E}. and {P}ompon, {J}. and {X}ie, {T}. and {R}ademacher, {A}. and {F}raiture, {M}. and {T}homa, {M}. and {A}wono-{A}mbene, {P}. {H}. and {M}oyou, {R}. {S}. and {M}orlais, {I}sabelle and {L}evashina, {E}. {A}.},
  editor = {},
  language = {{ENG}},
  abstract = {{A}nopheline mosquitoes are the only vectors of human malaria worldwide. {I}t is now widely accepted that mosquito immune responses play a crucial role in restricting {P}lasmodium development within the vector; therefore, further dissection of the molecular mechanisms underlying these processes should inform new vector control strategies urgently needed to roll back the disease. {H}ere, using genome-wide transcriptional profiling, bioinformatics, and functional gene analysis, we identify a new axis of mosquito resistance to monoclonal {P}lasmodium falciparum infections that includes the {AP}-1 transcription factor {F}os and the transglutaminase 2 ({TG}ase2), a cross-linking enzyme with known roles in wound responses. {W}e demonstrate that {F}os regulates induction of {TG}ase2 expression after wounding but does not affect expression of the components of the well characterized complement-like system. {S}ilencing of {F}os or of {TG}ase2 aborts the wounding-induced mosquito killing of {P}. falciparum. {T}hese results reveal multiple signaling pathways that are required for efficient {P}lasmodium killing in {A}nopheles gambiae.},
  keywords = {},
  booktitle = {},
  journal = {{J}ournal of {B}iological {C}hemistry},
  volume = {288},
  numero = {22},
  pages = {16145--16154},
  ISSN = {0021-9258},
  year = {2013},
  DOI = {10.1074/jbc.{M}112.443267},
  URL = {https://www.documentation.ird.fr/hor/{PAR}00010610},
}