Biology Reference
In-Depth Information
14
Cytoplasmic Incompatibility
Kostas Bourtzis, Henk R. Braig, and Timothy L. Karr
CONTENTS
Wolbachia
-Induced CI....................................................................................................................226
The Mechanism of
Wolbachia
-Induced CI.............................................................................228
Genetics and Cell Biology of
-Induced CI............................................................230
Genetics of Growth Control in
Wolbachia
Drosophila
..................................................................233
-Induced CI ........................................................................235
Cell Biology of
Wolbachia
INTRODUCTION
Cytoplasmic incompatibility (CI) is the most widespread and one of the most prominent features
that
endosymbionts impose on their hosts. In this chapter, we try to demonstrate that
CI is not a peculiar phenotype of an obscure intracellular bacterium but a fundamental evolutionary
trait. The distribution and mechanisms of
Wolbachia
Wolbachia
-induced CI phenotypes are exempliÝed in the
model
. The genetics and cell biology of this hostÏpathogen interaction will offer a
better understanding of the early stages of fertilization and sterility.
Drosophila
CI SYSTEMS
CI is often seen as a mechanism that promotes the spread of the cytoplasmic factors causing it. This,
however, is not accomplished, as one might expect, by increasing the likelihood of transmission of
the cytoplasmic factors but rather by decreasing the proportion of progeny without those factors. CI
functions as a wide variety of post-segregational killing (PSK) mechanisms or post-disturbance cell-
killer systems that will kill whatever is not carrying the cytoplasmic factors. Since cells not having
obtained or having lost these cytoplasmic factors are punished for withdrawal of a dispensable genetic
element with no intrinsic adaptive value, these systems are also called addiction systems or modules.
