Intra-lineage microevolution of Wolbachia leads to the emergence of new cytoplasmic incompatibility patterns

Alice Namias1, Annais Ngaku1, Patrick Makoundou1

  • 1ISEM, Université de Montpellier, CNRS, IRD, EPHE, Montpellier, France.

Plos Biology
|February 5, 2024
PubMed

Insights

Researchers observed a new mosquito mating incompatibility type in real time. This change was linked to the loss of specific Wolbachia bacterial genes, supporting the toxin-antidote model for reproductive incompatibility.

Area of Science:

  • * Molecular biology
  • * Evolutionary genetics
  • * Vector-borne disease research

Background:

  • * Culex pipiens mosquitoes are significant global vectors for arboviruses, filarial nematodes, and avian malaria.
  • * The endosymbiotic bacteria Wolbachia induce cytoplasmic incompatibility (CI) in these mosquitoes, affecting embryo viability.
  • * Wolbachia strains in Culex pipiens (wPip) exhibit complex CI patterns linked to variations in cidA and cidB genes.

Purpose of the Study:

  • * To investigate the real-time evolution of cytoplasmic incompatibility (CI) in Culex pipiens mosquitoes.
  • * To determine the genetic basis for changes in CI patterns and compatibility types.
  • * To validate the toxin-antidote (TA) model for CI in natural Wolbachia-host interactions.

Main Methods:

  • * Longitudinal study involving repeated crosses of Culex isofemale lines over 17 years.
  • * Genomic analysis of Wolbachia cid genes (cidA and cidB) in different mosquito lines.
  • * Comparative sequence analysis of toxin and antidote binding interfaces.

Main Results:

  • * Observed the emergence of a novel CI compatibility type in real time.
  • * Linked this new type to the loss of specific cidA gene copies in wPip genomes.
  • * Demonstrated that loss of certain cidA genes resulted in loss of compatibility, with evidence of recombination driving these changes.

Conclusions:

  • * The study provides strong in natura support for the toxin-antidote (TA) model of CI.
  • * Recombination, rather than point mutations, appears to be a key driver of rapid CI evolution in wPip.
  • * Understanding these genetic mechanisms is crucial for controlling vector populations and disease transmission.

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