A multiplexed, confinable CRISPR/Cas9 gene drive can propagate in caged Aedes aegypti populations

Michelle A. E. Anderson, Estela Gonzalez, Matthew P. Edgington, Joshua X. D. Ang, Deepak-Kumar Purusothaman, Lewis Shackleford, Katherine Nevard, Sebald A. N. Verkuijl, Timothy Harvey-Samuel, Philip T. Leftwich, Kevin Esvelt and Luke Alphey ()
Additional contact information
Michelle A. E. Anderson: Arthropod Genetics, The Pirbright Institute
Estela Gonzalez: Arthropod Genetics, The Pirbright Institute
Matthew P. Edgington: Arthropod Genetics, The Pirbright Institute
Joshua X. D. Ang: Arthropod Genetics, The Pirbright Institute
Deepak-Kumar Purusothaman: Arthropod Genetics, The Pirbright Institute
Lewis Shackleford: Arthropod Genetics, The Pirbright Institute
Katherine Nevard: Arthropod Genetics, The Pirbright Institute
Sebald A. N. Verkuijl: Arthropod Genetics, The Pirbright Institute
Timothy Harvey-Samuel: Arthropod Genetics, The Pirbright Institute
Philip T. Leftwich: Arthropod Genetics, The Pirbright Institute
Kevin Esvelt: Massachusetts Institute of Technology
Luke Alphey: Arthropod Genetics, The Pirbright Institute

Nature Communications, 2024, vol. 15, issue 1, 1-13

Abstract: Abstract Aedes aegypti is the main vector of several major pathogens including dengue, Zika and chikungunya viruses. Classical mosquito control strategies utilizing insecticides are threatened by rising resistance. This has stimulated interest in new genetic systems such as gene drivesHere, we test the regulatory sequences from the Ae. aegypti benign gonial cell neoplasm (bgcn) homolog to express Cas9 and a separate multiplexing sgRNA-expressing cassette inserted into the Ae. aegypti kynurenine 3-monooxygenase (kmo) gene. When combined, these two elements provide highly effective germline cutting at the kmo locus and act as a gene drive. Our target genetic element drives through a cage trial population such that carrier frequency of the element increases from 50% to up to 89% of the population despite significant fitness costs to kmo insertions. Deep sequencing suggests that the multiplexing design could mitigate resistance allele formation in our gene drive system.

Date: 2024
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-024-44956-2 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-44956-2

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-024-44956-2

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().