Abstract:
:We have studied the mode of action of the insecticide spirotetramat in the nematode Caenorhabditis elegans. A combination of symptomology, forward genetics and genome editing show that spirotetramat acts on acetyl-CoA carboxylase (ACC) in C. elegans, as it does in insects. We found C. elegans embryos exposed to spirotetramat show a cell division defect which closely resembles the phenotype of loss-of-function mutations in the gene pod-2, which encodes ACC. We then identified two mutations in the carboxyl transferase domain of pod-2 (ACC) which confer resistance and were confirmed using CRISPR/Cas9. One of these mutations substitutes an invertebrate-specific amino acid with one ubiquitous in other taxa; this residue may, therefore, be a determinant of the selectivity of spirotetramat for invertebrates. Such a mutation may also be the target of selection for resistance in the field. Our study is a further demonstration of the utility of C. elegans in studying bioactive chemicals.
journal_name
Pestic Biochem Physioljournal_title
Pesticide biochemistry and physiologyauthors
Guest M,Kriek N,Flemming AJdoi
10.1016/j.pestbp.2020.104604subject
Has Abstractpub_date
2020-10-01 00:00:00pages
104604eissn
0048-3575issn
1095-9939pii
S0048-3575(20)30099-7journal_volume
169pub_type
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