Functional analysis of RIP toxins from the Drosophila endosymbiont Spiroplasma poulsonii.
Animals
Bacterial Proteins
/ genetics
Bacterial Toxins
/ genetics
Drosophila melanogaster
/ microbiology
Embryo, Nonmammalian
/ microbiology
Female
Hemocytes
Hemolymph
/ microbiology
Host Microbial Interactions
Longevity
Male
Ribosome Inactivating Proteins
/ genetics
Spiroplasma
/ chemistry
Symbiosis
Drosophila
Endosymbiosis
Ribosome inactivating protein
Spiroplasma
Journal
BMC microbiology
ISSN: 1471-2180
Titre abrégé: BMC Microbiol
Pays: England
ID NLM: 100966981
Informations de publication
Date de publication:
20 02 2019
20 02 2019
Historique:
received:
09
07
2018
accepted:
31
01
2019
entrez:
22
2
2019
pubmed:
23
2
2019
medline:
18
12
2019
Statut:
epublish
Résumé
Insects frequently live in close relationship with symbiotic bacteria that carry out beneficial functions for their host, like protection against parasites and viruses. However, in some cases, the mutualistic nature of such associations is put into question because of detrimental phenotypes caused by the symbiont. One example is the association between the vertically transmitted facultative endosymbiont Spiroplasma poulsonii and its natural host Drosophila melanogaster. Whereas S. poulsonii protects its host against parasitoid wasps and nematodes by the action of toxins from the family of Ribosome Inactivating Proteins (RIPs), the presence of S. poulsonii has been reported to reduce host's life span and to kill male embryos by a toxin called Spaid. In this work, we investigate the harmful effects of Spiroplasma RIPs on Drosophila in the absence of parasite infection. We show that only two Spiroplasma RIPs (SpRIP1 and SpRIP2) among the five RIP genes encoded in the S. poulsonii genome are significantly expressed during the whole Drosophila life cycle. Heterologous expression of SpRIP1 and 2 in uninfected flies confirms their toxicity, as indicated by a reduction of Drosophila lifespan and hemocyte number. We also show that RIPs can cause the death of some embryos, including females. Our results indicate that RIPs released by S. poulsonii contribute to the reduction of host lifespan and embryo mortality. This suggests that SpRIPs may impact the insect-symbiont homeostasis beyond their protective function against parasites.
Sections du résumé
BACKGROUND
Insects frequently live in close relationship with symbiotic bacteria that carry out beneficial functions for their host, like protection against parasites and viruses. However, in some cases, the mutualistic nature of such associations is put into question because of detrimental phenotypes caused by the symbiont. One example is the association between the vertically transmitted facultative endosymbiont Spiroplasma poulsonii and its natural host Drosophila melanogaster. Whereas S. poulsonii protects its host against parasitoid wasps and nematodes by the action of toxins from the family of Ribosome Inactivating Proteins (RIPs), the presence of S. poulsonii has been reported to reduce host's life span and to kill male embryos by a toxin called Spaid. In this work, we investigate the harmful effects of Spiroplasma RIPs on Drosophila in the absence of parasite infection.
RESULTS
We show that only two Spiroplasma RIPs (SpRIP1 and SpRIP2) among the five RIP genes encoded in the S. poulsonii genome are significantly expressed during the whole Drosophila life cycle. Heterologous expression of SpRIP1 and 2 in uninfected flies confirms their toxicity, as indicated by a reduction of Drosophila lifespan and hemocyte number. We also show that RIPs can cause the death of some embryos, including females.
CONCLUSION
Our results indicate that RIPs released by S. poulsonii contribute to the reduction of host lifespan and embryo mortality. This suggests that SpRIPs may impact the insect-symbiont homeostasis beyond their protective function against parasites.
Identifiants
pubmed: 30786854
doi: 10.1186/s12866-019-1410-1
pii: 10.1186/s12866-019-1410-1
pmc: PMC6383259
doi:
Substances chimiques
Bacterial Proteins
0
Bacterial Toxins
0
Ribosome Inactivating Proteins
EC 3.2.2.22
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
46Subventions
Organisme : European Research Council
ID : 339970
Pays : International
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