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WITHIN‐ AND BETWEEN‐POPULATION VARIATION FOR WOLBACHIA‐INDUCED REPRODUCTIVE INCOMPATIBILITY IN A HAPLODIPLOID MITE
Author(s) -
Vala F.,
Weeks A.,
Claessen D.,
Breeuwer J. A. J.,
Sabelis M. W.
Publication year - 2002
Publication title -
evolution
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.84
H-Index - 199
eISSN - 1558-5646
pISSN - 0014-3820
DOI - 10.1111/j.0014-3820.2002.tb01447.x
Subject(s) - wolbachia , biology , cytoplasmic incompatibility , fecundity , population , haplodiploidy , mod , demography , host (biology) , sex ratio , genetics , zoology , offspring , pregnancy , artificial intelligence , sociology , computer science
Wolbachiapipientis is a bacterium that induces cytoplasmic incompatibility (CI), the phenomenon in which infected males are reproductively incompatible with uninfected females. CI spreads in a population of hosts because it reduces the fitness of uninfected females relative to infected females. CI encompasses two steps: modification (mod) of sperm of infected males and rescuing (resc) of these chromosomes by Wolbachia in the egg. Infections associated with CI have mod + resc + phenotypes. However, mod∼resc + phenotypes also exist; these do not result in CI. Assuming mod/resc phenotypes are properties of the symbiont, theory predicts that mod∼resc + infections can only spread in a host population where a mod + resc + infection already occurs. A mod∼resc + infection spreads if the cost it imposes on the infected females is lower than the cost inflicted by the resident (mod + resc + ) infection. Furthermore, introduction of a mod ‐ Wolbachia eventually drives infection to extinction. The uninfected population that results can be recolonized by a CI‐causing Wolbachia. Here, we investigated whether variability for induction of CI was present in two Tetranychus urticae populations. In one population all isofemale lines tested were mod ‐ . In the other, mod + resc + and mod∼resc + isofemale lines coexisted. We found no evidence for a cost difference to females expressing either type (mod + /∼). Infections in the two populations could not be distinguished based on sequences of two Wolbachia genes. We consider the possibility that mod ‐ is a host effect through a population dynamics model. A mod ‐ host allele leads to infection extinction in the absence of fecundity differences. Furthermore, the uninfected population that results is immune to reestablishment of the (same) CI‐causing Wolbachia.