Knock-down of REL2, but not defensin A, augments Aedes aegypti susceptibility to Bacillus subtilis and Escherichia coli.
Some components of the Toll and Imd immune signaling pathways have remained conserved between Drosophila and mosquitoes, however, important differences in the way invading microorganisms activate these pathways in these organisms have started to be revealed. In the present study, we have attempted to silence the Aedes aegypti NF-kappaB-like factor REL2, which is analogous to Drosophila Relish, and analyze the effects on mosquito mortality upon infection with a Gram-negative and a Gram-positive bacterium, both containing a DAP-type peptidoglycan, and effects on embryo development. Moreover, we have silenced one of the antimicrobial peptides (AMPs) controlled by REL2, defensin A, a major AMP in A. aegypti, and compared the results on mosquito mortality upon bacterial infection to those obtained with REL2 silencing. Results show that REL2 is crucial for A. aegypti immunity upon infection with Escherichia coli and Bacillus subtilis, corroborating with previous studies on that REL2/Imd in mosquitoes is involved in a generalized antibacterial defense, differently than its analogous in Drosophila. However, defensin A silencing did not cause a significant increase in mortality in infected mosquitoes, indicating that this peptide is not essential in mosquito protection against the two bacteria and that other immune factors controlled by REL2 are playing this role. In regard to embryo development, REL2 knock-down did not cause any significant effect on: the number of laid eggs, number of developed pupae, percent of emerged adults, and ratio between emerged females versus males. A slight decrease in the number of hatched eggs (percent eclosion) was observed in REL2 knock-down mosquitoes, but these observations were inconclusive.
Magalhaes
T
T
Departamento de Entomologia, Centro de Pesquisas Aggeu Magalhães/FIOCRUZ, Av. Moraes Rego s/n, Cidade Universitária, Recife, PE, Brazil. teca@cpqam.fiocruz.br
Leandro
D C
DC
Ayres
C F J
CF
D000330:Aedes / Q000196:embryology / Q000254:growth & development / Q000276:immunology / Q000382:microbiology*; D000818:Animals; D001412:Bacillus subtilis / Q000502:physiology*; D023082:Defensins / Q000235:genetics* / Q000378:metabolism; D004926:Escherichia coli / Q000502:physiology*; D005260:Female; D020868:Gene Silencing; D054884:Host-Pathogen Interactions; D019476:Insect Proteins / Q000235:genetics / Q000378:metabolism; D008297:Male; D034622:RNA Interference; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014157:Transcription Factors / Q000235:genetics* / Q000378:metabolism
D023082:Defensins; D019476:Insect Proteins; D014157:Transcription Factors; C058181:insect defensin A