The GeneConvene Virtual Institute:
- An initiative of the GeneConvene Global Collaborative,
- Within the Foundation for the National Institutes of Health
- Aggregates, curates and shares knowledge to advance understanding of genetic biocontrol technologies, such as gene drive, as well as selfish genetic elements found throughout nature.
GeneConvene Virtual Institute eNewsletter
GeneConvene Global Collaborative Webinar Series:
Controlling Gene Drives
Webinars are recorded;
Register to attend and to receive link to recording or check HERE
September 22, 2021 11:00-12:30 EDT
Development of Gene Drives and a Method to Block Them in Anopheles gambiae
Dr. Chrysanthi Taxiarchi, Imperial College London.
September 29, 2021 11:00-12:30 EDT
Lessons Learned from Neutralizing Drives
Dr. Ethan Bier, University of California, San Diego.
October 6, 2021 11:00-12:30 EDT
Chemical approaches to control and enhance CRISPR-based technologies
Dr. Amit Choudhary, Harvard University.
GeneConvene Global Collaborative Webinar Series:
Invasive Species Management:
Informing Gene Drive Considerations
Webinars are recorded;
Register to attend and to receive link to recording or check HERE
October 13, 2021 11:00-12:30 EDT
Conservation in the Anthropocene:
Can community ecology help avoid unintended outcomes and improve conservation success?
Dr. Dean Pearson, USDA FS Rock Mountain Research Station.
October 27, 2021 11:00-12:30 EDT
Targeting Surveillance for Invasive Agricultural Pests and Diseases
Dr. Gericke Cook, USDA/APHIS Veterinary Services, Center for Epidemiology and Animal Health
Nov 10, 2021 11:00-12:30 EST
Monitoring gene drive vertebrates in the environment
Dr. Antoinette Piaggio, USDA/APHIS/Wildlife Services/
National Wildlife Research Center
The Latest About Gene Drive and Genetic Biocontrol
The GeneConvene Virtual Institute is built on a database of content in the categories shown in the tab labels below. Content coming into the Virtual Institute in these categories can be seen in each tab as well as all of the content in each of the categories, organized chronologically.
Featured Content
A single mutation weakens symbiont-induced reproductive manipulation through reductions in deubiquitylation efficiency
J. F. Beckmann, K. Van Vaerenberghe, D. E. Akwa and B. S. Cooper, Proceedings of the National Academy of Sciences, 118:e2113271118. 2021.
Wolbachia are maternally transmitted bacteria that infect most insects, making them the most common endosymbionts. Wolbachia achieved this status by manipulating host reproduction. For example, many Wolbachia cause cytoplasmic incompatibility (CI) that kills uninfected embryos. In females, Wolbachia can rescue CI, promoting their spread to high frequencies in host populations. CI strength varies in nature from weak to strong. Importantly, strong CI enables Wolbachia biocontrol strategies in mosquito systems, which protect millions of individuals from arboviruses. However, theory predicts that natural selection does not act to preserve genes that cause CI, suggesting mutations may disrupt it. We show that a single naturally observed mutation weakens CI by reducing deubiquitylation.
Summary of the ubiquitin system. In eukaryotes, the small protein modifier ubiquitin (Ub) can be covalently attached to a nucleophilic residue of its protein substrate by the combined actions of the E1 ubiquitin-activating enzyme, an E2 ubiquitin conjugating enzyme, and an E3 ubiquitin ligase in an ATP-dependent manner. Polyubiquitin chains can form when a ubiquitin is further modified by other ubiquitin molecules. Ubiquitin modification is reversed by the enzymatic activity of deubiquitylases (DUBs). Image from: Chen, H., Zhang, M., and Hochstrasser, M. (2020). The Biochemistry of Cytoplasmic Incompatibility Caused by Endosymbiotic Bacteria. Genes 11 doi: 10.3390/genes11080852.
These discoveries help elucidate the molecular basis of symbiont-induced reproductive manipulations.Animals interact with microbes that affect their performance and fitness, including endosymbionts that reside inside their cells. Maternally transmitted Wolbachia bacteria are the most common known endosymbionts, in large part because of their manipulation of host reproduction. For example, many Wolbachia cause cytoplasmic incompatibility (CI) that reduces host embryonic viability when Wolbachia-modified sperm fertilize uninfected eggs. Operons termed cifs control CI, and a single factor (cifA) rescues it, providing Wolbachia-infected females a fitness advantage. Despite CI’s prevalence in nature, theory indicates that natural selection does not act to maintain CI, which varies widely in strength. Here, we investigate the genetic and functional basis of CI-strength variation observed among sister Wolbachia that infect Drosophila melanogaster subgroup hosts. We cloned, Sanger sequenced, and expressed cif repertoires from weak CI–causing wYak in Drosophila yakuba, revealing mutations suspected to weaken CI relative to model wMel in D. melanogaster. A single valine-to-leucine mutation within the deubiquitylating (DUB) domain of the wYak cifB homolog (cidB) ablates a CI-like phenotype in yeast. The same mutation reduces both DUB efficiency in vitro and transgenic CI strength in the fly, each by about twofold. Our results map hypomorphic transgenic CI to reduced DUB activity and indicate that deubiquitylation is central to CI induction in cid systems. We also characterize effects of other genetic variation distinguishing wMel-like cifs. Importantly, CI strength determines Wolbachia prevalence in natural systems and directly influences the efficacy of Wolbachia biocontrol strategies in transinfected mosquito systems. These approaches rely on strong CI to reduce human disease.All study data are included in the article and/or supporting information.
More related to this:
The toxin–antidote model of cytoplasmic incompatibility: Genetics and evolutionary implications
The Biochemistry of Cytoplasmic Incompatibility Caused by Endosymbiotic Bacteria
Converting female mosquitoes to non-biting males with implications for mosquito control
One prophage WO gene rescues cytoplasmic incompatibility in Drosophila melanogaster
