Biology subjects

Bordenstein, S. R.

Publications and source records attributed to Bordenstein, S. R..

4 recordsLinked to original sources

bioRxiv2018

Gut Microbiota Diversity across Ethnicities in the United States

Composed of hundreds of microbial species, the composition of the human gut microbiota can vary with chronic diseases underlying health disparities that disproportionally affect ethnic minorities. However, the influence of ethnicity on the gut microbiota remains largely unexplored and lacks reproducible generalizations across studies. By distilling associations between ethnicity and differences in two United States based 16S gut microbiota datasets including 1,673 individuals, we report 12 microbial genera and families that reproducibly vary by ethnicity. Interestingly, a majority of these microbial taxa, including the most heritable bacterial family, Christensenellaceae, overlap with genetically-associated taxa and form co-occurring clusters linked by similar fermentative and methanogenic metabolic processes. These results demonstrate recurrent associations between specific taxa in the gut microbiota and ethnicity, providing hypotheses for examining specific members of the gut microbiota as mediators of health disparities.

microbiology↗

bioRxiv2018

A single prophage WO gene rescues cytoplasmic incompatibility in Drosophila melanogaster

Wolbachia are maternally-inherited, intracellular bacteria at the forefront of vector control efforts to curb arbovirus transmission. In international field trials, the cytoplasmic incompatibility (CI) drive system of wMel Wolbachia is deployed to replace target vector populations, whereby a Wolbachia- induced modification of the sperm genome kills embryos. However, Wolbachia in the embryo rescue the sperm genome impairment, and therefore CI results in a strong fitness advantage for infected females that transmit the bacteria to offspring. The two genes responsible for the wMel-induced sperm modification of CI, cifA and cifB, were recently identified in the eukaryotic association module of prophage WO, but the genetic basis of rescue is unresolved. Here we use transgenic and cytological approaches to demonstrate that cifA independently rescues CI and nullifies embryonic death caused by wMel Wolbachia in Drosophila melanogaster. Discovery of cifA as the rescue gene and previously one of two CI induction genes establishes a new Two-by-One model that underpins the genetic basis of CI. Results highlight the central role of prophage WO in shaping Wolbachia phenotypes that are significant to arthropod evolution and vector control.\n\nSignificance StatementThe World Health Organization recommended pilot deployment of Wolbachia-infected mosquitoes to curb viral transmission to humans. Releases of mosquitoes are underway worldwide because Wolbachia can block replication of these pathogenic viruses and deterministically spread by a drive system termed cytoplasmic incompatibility (CI). Despite extensive research, the underlying genetic basis of CI remains only half-solved. We recently reported that two prophage WO genes recapitulate the modification component of CI in a released strain for vector control. Here we show that one of these genes underpins rescue of CI. Together, our results reveal the complete genetic basis of this selfish trait and pave the way for future studies exploring WO prophage genes as adjuncts or alternatives to current control efforts.

genetics↗

bioRxiv2018

A simple genetic basis for managing maternally transmitted symbionts

Maternal transmission of intracellular microbes is pivotal in establishing long-term, intimate symbioses. For germline microbes that exert negative reproductive effects on their hosts, selection can theoretically favor the spread of host genes that counteract the microbes harmful effects. Here, we leverage a major difference in bacterial (Wolbachia pipientis) titers between closely-related wasp species with forward genetic, transcriptomic, and cytological approaches to map two quantitative trait loci that suppress bacterial titers via a maternal effect. Fine mapping and knockdown experiments identify the gene Wolbachia density suppressor (Wds), which dominantly suppresses bacterial transmission from mother to embryo. Wds evolved by lineage-specific non-synonymous changes driven by positive selection. Collectively, our findings demonstrate that a genetically simple change arose by Darwinian selection in less than a million years to regulate maternally transmitted bacteria via a dominant, maternal effect gene.

evolutionary biology↗

bioRxiv2017

Evolutionary genetics of cytoplasmic incompatibility genes cifA and cifB in prophage WO of Wolbachia

The bacterial endosymbiont Wolbachia manipulates arthropod reproduction to facilitate its maternal spread through populations. The most common manipulation is cytoplasmic incompatibility (CI): Wolbachia-infected males produce modified sperm that cause embryonic mortality, unless rescued by eggs harboring the same Wolbachia. The genes underlying CI, cifA and cifB, were recently identified in the eukaryotic association module of Wolbachias prophage WO. Here, we use transcriptomic and genomic approaches to address three important evolutionary facets of these genes. First, we assess whether or not cifA and cifB comprise a classic toxin-antitoxin operon, and show they do not form an operon in strain wMel. They coevolve but exhibit strikingly distinct expression across host development. Second, we provide new domain and functional predictions across homologs within Wolbachia, and we show amino acid sequences vary substantially across the genus. Lastly, we investigate conservation of cifA and cifB and find degradation and loss of the genes is common in strains that no longer induce CI. Taken together, we find no evidence for the operon hypothesis in wMel, provide functional annotations that broaden the potential mechanisms of CI induction, illuminate recurrent erosion of cifA and cifB in non-CI strains, and advance an understanding of the most widespread form of reproductive parasitism.

evolutionary biology↗