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A single synonymous nucleotide change impacts the male-killing phenotype of prophage WO gene wmk

View ORCID ProfileJessamyn I. Perlmutter, Jane E. Meyers, View ORCID ProfileSeth R. Bordenstein
doi: https://doi.org/10.1101/2021.03.11.434916
Jessamyn I. Perlmutter
aDepartment of Biological Sciences, Vanderbilt University, Nashville, Tennessee, USA
bDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA
cVanderbilt Microbiome Innovation Center, Vanderbilt University, Nashville, Tennessee, USA
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  • ORCID record for Jessamyn I. Perlmutter
  • For correspondence: jessamyn.perlmutter@outlook.com s.bordenstein@vanderbilt.edu
Jane E. Meyers
aDepartment of Biological Sciences, Vanderbilt University, Nashville, Tennessee, USA
cVanderbilt Microbiome Innovation Center, Vanderbilt University, Nashville, Tennessee, USA
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Seth R. Bordenstein
aDepartment of Biological Sciences, Vanderbilt University, Nashville, Tennessee, USA
cVanderbilt Microbiome Innovation Center, Vanderbilt University, Nashville, Tennessee, USA
dDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, Tennessee, USA
eVanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University, Nashville, Tennessee, USA
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  • For correspondence: jessamyn.perlmutter@outlook.com s.bordenstein@vanderbilt.edu
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Abstract

Wolbachia are the most widespread bacterial endosymbionts in animals. Within arthropods, these maternally-transmitted bacteria can selfishly hijack host reproductive processes to increase the relative fitness of their transmitting females. One such form of reproductive parasitism called male killing, or the selective killing of infected males, is recapitulated to degrees by transgenic expression of the WO-mediated killing (wmk) gene. Here, we characterize the genotype-phenotype landscape of wmk-induced male killing in D. melanogaster using transgenic expression. While phylogenetically distant wmk homologs induce no sex-ratio bias, closely-related homologs exhibit complex phenotypes spanning no death, male death, or death of all hosts. We demonstrate that alternative start codons, synonymous codons, and notably a single synonymous nucleotide in wmk can ablate killing. These findings reveal previously unrecognized features of transgenic wmk-induced killing and establish new hypotheses for the impacts of post-transcriptional processes in male killing variation. We conclude that synonymous sequence changes are not necessarily silent in nested endosymbiotic interactions with life-or-death consequences.

Competing Interest Statement

Both J.I.P. and S.R.B. are inventors on a patent related to the transgenic use of wmk in vector control: US Patent 20210000092 16/982708.

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  • edited for shorter length and more clarity in text

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted October 13, 2021.
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A single synonymous nucleotide change impacts the male-killing phenotype of prophage WO gene wmk
Jessamyn I. Perlmutter, Jane E. Meyers, Seth R. Bordenstein
bioRxiv 2021.03.11.434916; doi: https://doi.org/10.1101/2021.03.11.434916
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A single synonymous nucleotide change impacts the male-killing phenotype of prophage WO gene wmk
Jessamyn I. Perlmutter, Jane E. Meyers, Seth R. Bordenstein
bioRxiv 2021.03.11.434916; doi: https://doi.org/10.1101/2021.03.11.434916

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