ena-STUDY-Institute of Tropical Medicine-04-07-2018-10:24:12:232-7173
Mito-nuclear genomics challenges the theory of clonality in Trypanosoma congolense. Reply to Tibayrenc and Ayala.
We recently published the first genomic diversity study of Trypanosoma congolense, a major etiological agent of Animal African Trypanosomiasis. We demonstrated striking levels of SNP and indel diversity in the Eastern province of Zambia as a consequence of hybridization between divergent trypanosome lineages. We concluded that these and earlier findings in T. congolense challenge the Predominant Clonal Evolution (PCE) model. In a recent Comment, Tibayrenc and Ayala claim that there are many features in T. congolense supporting their theory of clonality. While we follow the reasoning of the authors, we also identify major limitations in their theory and interpretations that resulted in incorrect conclusions. First, we argue that each T. congolense subgroup should be analyzed independently as they may represent different (sub)species presumably as opposed to 'near-clades'. Second, the authors neglect major findings of two robust population genetic studies on Savannah T. congolense that  provide clear evidence of frequent recombination. Third, we reveal additional events of introgressive hybridization in T. congolense by analyzing the maxicircle coding region using Next Generation Sequencing analyses. Finally, we pinpoint two important misinterpretations by the authors and show that there are no spatially and temporally widespread clones in T. congolense. We stand by our earlier conclusions that the clonal framework is unlikely to accurately model the population structure of T. congolense. Other theoretical frameworks such as Maynard Smith's epidemic model may better represent the complex ancestry seen in T. congolense, where clones delimited in space and time seem to arise against a background of recombination.
We recently published the first genomic diversity study of Trypanosoma congolense, a major etiological agent of Animal African Trypanosomiasis. We demonstrated striking levels of SNP and indel diversity in the Eastern province of Zambia as a consequence of hybridization between divergent trypanosome lineages. We concluded that these and earlier findings in T. congolense challenge the Predominant Clonal Evolution (PCE) model. In a recent Comment, Tibayrenc and Ayala claim that there are many features in T. congolense supporting their theory of clonality. While we follow the reasoning of the authors, we also identify major limitations in their theory and interpretations that resulted in incorrect conclusions. First, we argue that each T. congolense subgroup should be analyzed independently as they may represent different (sub)species presumably as opposed to 'near-clades'. Second, the authors neglect major findings of two robust population genetic studies on Savannah T. congolense that  provide clear evidence of frequent recombination. Third, we reveal additional events of introgressive hybridization in T. congolense by analyzing the maxicircle coding region using Next Generation Sequencing analyses. Finally, we pinpoint two important misinterpretations by the authors and show that there are no spatially and temporally widespread clones in T. congolense. We stand by our earlier conclusions that the clonal framework is unlikely to accurately model the population structure of T. congolense. Other theoretical frameworks such as Maynard Smith's epidemic model may better represent the complex ancestry seen in T. congolense, where clones delimited in space and time seem to arise against a background of recombination.