Biology subjects

Campbell, M. A.

Publications and source records attributed to Campbell, M. A..

3 recordsLinked to original sources

bioRxiv2018

Changes in endosymbiont complexity drive host-level compensatory adaptations in cicadas

For insects that depend on one or more bacterial endosymbionts for survival, it is critical that these bacteria are faithfully transmitted between insect generations. Cicadas harbor two essential bacterial endosymbionts, Sulcia muelleri and Hodgkinia cicadicola. In some cicada species, Hodgkinia has fragmented into multiple distinct cellular and genomic lineages that can differ in abundance by more than two orders of magnitude. This complexity presents a potential problem for the host cicada, because low-abundance-but-essential Hodgkinia lineages risk being lost during the symbiont transmission bottleneck from mother to egg. Here we show that all cicada eggs seem to receive the full complement of Hodgkinia lineages, and that in cicadas with more complex Hodgkinia this outcome is achieved by increasing the number of Hodgkinia cells transmitted by up to six-fold. We further show that cicada species with varying Hodgkinia complexity do not visibly alter their transmission mechanism at the resolution of cell biological structures. Together these data suggest that a major cicada adaptation to changes in endosymbiont complexity is an increase in the number of Hodgkinia cells transmitted to each egg. We hypothesize that the requirement to increase the symbiont titer is one of the costs associated with Hodgkinia fragmentation.

evolutionary biology↗

bioRxiv2018

Sequence variability, constraint and selection in the CD163 gene in pigs

BackgroundIn this paper, we investigate sequence variability, evolutionary constraint, and selection on the CD163 gene in pigs. The pig CD163 gene is required for infection by porcine reproductive and respiratory syndrome virus (PRRSV), a serious pathogen with major impact on pig production.\n\nResultsWe used targeted pooled sequencing of the exons of CD163 to detect sequence variants in 35,000 pigs of diverse genetic backgrounds and search for potential knock-out variants. We then used whole genome sequence data from three pig lines to calculate a variant intolerance score, which measures the tolerance of genes to protein coding variation, a selection test on protein coding variation over evolutionary time, and haplotype diversity statistics to detect recent selective sweeps during breeding.\n\nConclusionsWe performed a deep survey of sequence variation in the CD163 gene in domestic pigs. We found no potential knock-out variants. CD163 was moderately intolerant to variation, and showed evidence of positive selection in the lineage leading up to the pig, but no evidence of selective sweeps during breeding.

genomics↗

bioRxiv2017

Idiosyncratic genome degradation in a bacterial endosymbiont of periodical cicadas

When a free-living bacterium transitions to a host-beneficial endosymbiotic lifestyle, it almost invariably loses a large fraction of its genome [1, 2]. The resulting small genomes often become unusually stable in size, structure, and coding capacity [3-5]. Candidatus Hodgkinia cicadicola (Hodgkinia), a bacterial endosymbiont of cicadas, sometimes exemplifies this genomic stability. The Hodgkinia genome has remained completely co-linear in some cicadas diverged by tens of millions of years [6, 7]. But in the long-lived periodical cicada Magicicada tredecim, the Hodgkinia genome has split into dozens of tiny, gene-sparse genomic circles that sometimes reside in distinct Hodgkinia cells [8]. Previous data suggested that other Magicicada species harbor similarly complex Hodgkinia populations, but the timing, number of origins, and outcomes of the splitting process were unknown. Here, by sequencing Hodgkinia metagenomes from the remaining six Magicicada species and two sister species, we show that all Magicicada species harbor Hodgkinia populations of at least twenty genomic circles each. We find little synteny among the 256 Hodgkinia circles analyzed except between the most closely related species. Individual gene phylogenies show that Hodgkinia first split in the common ancestor of Magicicada and its closest known relatives, but that most splitting has occurred within Magicicada and has given rise to highly variable Hodgkinia gene dosages between cicada species. These data show that Hodgkinia genome degradation has proceeded down different paths in different Magicicada species, and support a model of genomic degradation that is stochastic in outcome and likely nonadaptive for the host. These patterns mirror the genomic instability seen in some mitochondria.

evolutionary biology↗