Interactions between Bacteria and the Centrosome

Finally, it remains possible that bacterial proteins might act on the centrosome directly to carry out their functions. Perhaps the most dramatic example of a bacterium which can interfere with centrosome function is Wolbachia, an endosymbiont which infects arthropods, and causes several reproductive defects in their hosts [112]. Wolbachia is also responsible for an unusual genetic puzzle which has been described in several different insects, that of cytoplasmic incompatibility (CI). This arises when sperm from infected male insects fertilize eggs from unin-fected females. The resulting embryos fail to develop normally, having severe defects in metaphase chromosome alignment which prevent the segregation of paternal chromosomes.

The most enigmatic feature of CI is the fact that crosses between infected males and infected females, and also those between uninfected males and infected females, are all viable. Early models suggested that Wolbachia somehow disrupts chromatin condensation or the correct formation of the mitotic spindle, and such arguments were favored by findings which showed that Wolbachia, like Chlamydia and Orientia, cluster around the centrosome in infected embryos.

Dramatic insights into the mechanism of CI have been obtained by following in real-time the dynamics of centrosomes and pronuclei during fertilization in the parasitoid wasp, Nasonia vitripennis. This showed that Wolbachia does not prevent transmission of paternal centrosomes to the embryo, and that centrosomes from infected males separate normally in preparation for the first mitotic division. However, the usual pattern of centrosomal inheritance was disrupted. In Nasonia, cen-trosomes are transmitted reciprocally, such that female embryos inherit the paternal centrosomes whereas male embryos inherit maternal centrosomes. In contrast, centrosomes derived from the sperm of Wolbachia-infected males were seen to dominate, even in male embryos in which the chromosomes which prevailed were all female. Also, the envelope of the pronucleus derived from infected males fails to break down in synchrony with the pronucleus of uninfected females, causing chromosome condensation and alignment on the metaphase plate to occur too late for successful, diploid mitosis [113].

Delayed nuclear envelope breakdown neatly explains why crosses involving infected females are always viable. Wolbachia are present during spermatogenesis, but the bacteria are shed during its final stages. In the egg, however, Wolbachia persists. If the bacterium acts by delaying the breakdown of the pronucleus, then bacteria in an infected egg may affect both the male and female pronuclei, and so both are delayed and asynchrony is avoided. Only if the male pronucleus is delayed by exposure to the bacterium, while the female pronucleus is unexposed, will asyn-chrony and CI follow. How Wolbachia disrupts the timing of nuclear envelope breakdown and the inheritance of centrosomes remains to be seen. The mitotic cyclin-

dependent kinase activity of Cdkl/cyclin B has been shown to play an important role in the onset of nuclear envelope breakdown, and so is a possible target [114]. Interestingly, cyclin B associates with the centrosome during interphase, and so would be in the vicinity of bacteria which accumulate at the MTOC [115]. If mitotic cyclins are indeed targeted by Wolbachia, this pathogen would join the ever-growing list of those which are able to re-engineer progression of the cell cycle.

0 0

Post a comment