Cytoplasmic Incompatibility - Insect Symbiosis - page 167

aberrant mitotic Ýgures and chromosomal fragmentation. Indeed, Callaini et al. (1996) reported
developmental anomalies at later stages of development that included segmentation defects,
suggesting that CI expression could affect various stages of development. Neither the nature of
these differences nor their origins during development are yet known. The analysis of CI in
Drosophila is further complicated by the fact that CI is never 100% penetrant, with egg lethality
in incompatible crosses varying from 60 to 90%. This is in stark contrast to CI in mosquitoes
and Nasonia , where the early CI phenotype is essentially 100% penetrant (Breeuwer and Werren,
1990, 1993). The phenotype of CI in this system is almost exclusively observed as diffuse
paternal chromatin and fragmentation during the Ýrst division (Reed and Werren, 1995).
Although a description of all Drosophila CI phenotypes is beyond the scope of this chapter,
sufÝce it to note that substantial variation in these phenotypes exists, suggesting that different
molecular mechanisms may be at work in these different species groups. Although no mecha-
nistic explanation for the variety of CI phenotyes observed in Drosophila has yet been put
forward, they do suggest that Wolbachia may operate by different mechanisms in different taxa.
If true, it may indicate that Wolbachia has evolved a variety of mechanisms in which to affect
host reproduction and CI expression.
Mechanistic Studies of CI in Nasonia
A signiÝcant advance in our understanding of the underlying mechanisms has come from recent
work in Nasonia that utilized real-time imaging and indirect immunoÞuorescence to visualize early
developmental events leading to the expression of CI and consequent egg lethality (Figure 14.4).
These results strongly supported a model whereby Wolbachia affects the timing of nuclear-envelope
breakdown (NEB) prior to the crucial Ýrst gonomeric division (Tram and Sullivan, 2002). Additional
studies by the same group further suggested that NEB delay was due to delayed activation of Cdk1,
a regulatory kinase whose activity is required for entry into mitosis.
These Ýrst molecular clues to the CI mechanism are consistent with a ÑkineticÒ model of CI
that suggested Wolbachia somehow affected the relative timing of the events following sperm entry
(Kose, 1995). The current work of Tram and Sullivan has provided a sound cell biological basis
for the phenomenon. It will be of great interest to determine whether other cell-cycle components
are affected by Wolbachia or whether similar mechanisms operate in diverse taxa.
FIGURE 14.4 (Color Ýgure follows p. 206.) Nuclear-envelope breakdown (NEB) assessed by time-lapsed
confocal microscopy of 0- to 1-h embryos injected with rhodamine-tubulin. When the nuclear envelope was
intact, the nucleus appeared as a black circle surrounded by a ring of red (rhodamine-tubulin). During NEB
rhodamine-tubulin invaded the nucleus (compare asterisks in upper and lower panels, t = 0 sec). The CI cross
nucleus remains relatively devoid of tubulin (indicated by dark regions of the intact nucleus), indicating delayed
NEB. (Insets) Schematized interpretation of NEB. [Adapted from Tram, U. and Sullivan, W. (2002). Science
296: 1124Ï1126.]