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Tetranychus urticae mites do not mount an induced immune response against bacteria

  • Articles in SCI Journals
  • Dec, 2017

Santos-Matos, G., Wybouw, N., Martins, N.E., Zélé, F., Riga, M., Leitão, A.B., Vontas, J., Grbić, M., Van Leeuwen, T., Magalhães, S. & Sucena, E. (2017) Tetranychus urticae mites do not mount an induced immune response against bacteria.

Proceedings of The Royal Society B-Biological Sciences, 284(1856), 20170401. DOI:10.1098/rspb.2017.0401 (IF2016 4,940; Q1 Biology)
Summary:

The genome of the spider mite Tetranychus urticae, a herbivore, is missing important elements of the canonical Drosophila immune pathways necessary to fight bacterial infections. However, it is not known whether spider mites can mount an immune response and survive bacterial infection. In other chelicerates, bacterial infection elicits a response mediated by immune effectors leading to the survival of infected organisms. In T. urticae, infection by either Escherichia coli or Bacillus megaterium did not elicit a response as assessed through genome-wide transcriptomic analysis. In line with this, spider mites died within days even upon injection with low doses of bacteria that are non-pathogenic to Drosophila. Moreover, bacterial populations grew exponentially inside the infected spider mites. By contrast, Sancassania berlesei, a litter-dwelling mite, controlled bacterial proliferation and resisted infections with both Gram-negative and Gram-positive bacteria lethal to T. urticae. This differential mortality between mite species was absent when mites were infected with heat-killed bacteria. Also, we found that spider mites harbour in their gut 1000-fold less bacteria than S. berlesei. We show that T. urticae has lost the capacity to mount an induced immune response against bacteria, in contrast to other mites and chelicerates but similarly to the phloem feeding aphid Acyrthosiphon pisum. Hence, our results reinforce the putative evolutionary link between ecological conditions regarding exposure to bacteria and the architecture of the immune response.


https://www.ncbi.nlm.nih.gov/pubmed/28592670