@article{fdi:010044177,
  title = {{L}arge bottleneck size in {C}auliflower {M}osaic {V}irus populations during host plant colonization},
  author = {{M}onsion, {B}. and {F}roissart, {R}. and {M}ichalakis, {Y}annis and {B}lanc, {S}.},
  editor = {},
  language = {{ENG}},
  abstract = {{T}he effective size of populations ({N}e) determines whether selection or genetic drift is the predominant force shaping their genetic structure and evolution. {D}espite their high mutation rate and rapid evolution, this parameter is poorly documented experimentally in viruses, particularly plant viruses. {A}ll available studies, however, have demonstrated the existence of huge within-host demographic fluctuations, drastically reducing {N}e upon systemic invasion of different organs and tissues. {N}otably, extreme bottlenecks have been detected at the stage of systemic leaf colonization in all plant viral species investigated so far, sustaining the general idea that some unknown obstacle(s) imposes a barrier on the development of all plant viruses. {T}his idea has important implications, as it appoints genetic drift as a constant major force in plant virus evolution. {B}y co-inoculating several genetic variants of {C}auliflower mosaic virus into a large number of replicate host plants, and by monitoring their relative frequency within the viral population over the course of the host systemic infection, only minute stochastic variations were detected. {T}his allowed the estimation of the {C}a{MV} {N}e during colonization of successive leaves at several hundreds of viral genomes, a value about 100-fold higher than that reported for any other plant virus investigated so far, and indicated the very limited role played by genetic drift during plant systemic infection by this virus. {T}hese results suggest that the barriers that generate bottlenecks in some plant virus species might well not exist, or can be surmounted by other viruses, implying that severe bottlenecks during host colonization do not necessarily apply to all plant-infecting viruses.},
  keywords = {},
  booktitle = {},
  journal = {{P}los {P}athogens},
  volume = {4},
  numero = {10},
  pages = {e1000174},
  ISSN = {1553-7366},
  year = {2008},
  DOI = {10.1371/journal.ppat.1000174},
  URL = {https://www.documentation.ird.fr/hor/fdi:010044177},
}