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Cytological analysis of cytoplasmic incompatibility induced byCardiniumsuggests convergent evolution with its distant cousinWolbachia
Author(s) -
Marco Gebiola,
Massimo Giorgini,
Suzanne E. Kelly,
Matthew R. Doremus,
Patrick M. Ferree,
Martha S. Hunter
Publication year - 2017
Publication title -
proceedings of the royal society b biological sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.342
H-Index - 253
eISSN - 1471-2954
pISSN - 0962-8452
DOI - 10.1098/rspb.2017.1433
Subject(s) - wolbachia , cytoplasmic incompatibility , biology , mitosis , genetics , ploidy , chromatin , nondisjunction , host (biology) , chromosome , aneuploidy , gene
Cytoplasmic incompatibility (CI) is a conditional sterility in numerous arthropods that is caused by inherited, intracellular bacteria such as Wolbachia Matings between males carrying CI-inducing Wolbachia and uninfected females, or between males and females infected with different Wolbachia strains, result in progeny that die during very early embryogenesis. Multiple studies in diploid ( Drosophila ) and haplodiploid ( Nasonia ) insects have shown that CI- Wolbachia cause a failure of the paternally derived chromatin from resolving into distinct chromosomes. This leads to the formation of chromatin bridges and other mitotic defects as early as the first mitotic division, and to early mitotic arrest. It is currently unknown if CI-inducing symbionts other than Wolbachia affect similar cellular processes. Here, we investigated CI caused by an unrelated bacterium, Cardinium , which naturally infects a parasitic wasp, Encarsia suzannae CI crosses in this host-symbiont system resulted in early mitotic defects including asynchrony of paternal and maternal chromosome sets as they enter mitosis, chromatin bridges and improper chromosome segregation that spanned across multiple mitotic divisions, triggering embryonic death through accumulated aneuploidy. We highlight small differences with CI- Wolbachia , which could be due to the underlying CI mechanism or host-specific effects. Our results suggest a convergence of CI-related cellular phenotypes between these two unrelated symbionts.

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