Models for the Cytoplasmic Incompatibilty Sample Clauses

Models for the Cytoplasmic Incompatibilty. Regarding the mechanism of CI, we know that the host nuclear variation is not responsible for the success of a breeding (just to cite two of many evidences on this, see [29, 44]). We know also that in some species, for instance the parasitic wasp Nasoni vitripennis [14] and the fly Drosophila simulans [18], the breeding between infected males and uninfected females is jammed by the delay of the paternal chromosome in joining the maternal one and proceed with the development of the embryo. In general the mechanism behind the phenomenon of CI is not completely clear for some difficulties in terms of genetic tools. For instance, in the case of Wolbachia, there are difficulties in identifying involved genes [65]. However, there are methods involving phenotypic data only (i.e. which symbiont infects which host) that can give a satisfying primary idea on the number of genes involved (see under the Lock and Key Model and the Toxin and Antitoxin Model for further details). My research in the area is based on this phenotypic approach employing the Toxin and Antitoxin Model presented here under. We developed an algorithm which can help to cast light on the number of involved genetic factors starting from the observation of the patterns of successful breeds. In the rest of this section, we present some of the models used in the past and the current state of the art concerning the genetic and molecular mechanism behind CI. The Modification and Rescue Model