Investigating the Mechanism of Metabolic Resistance to Tribenuron-Methyl in Capsella bursa-pastoris (L.) Medik. by Full-Length Transcriptome Assembly Combined with RNA-Seq

Capsella bursa-pastoris (L.) Medik.
has evolved resistance to ALS-inhibiting herbicides on a large scale.
Previous studies primarily focused on the target-site resistance (TSR),
and the non-TSR (NTSR) is not well characterized. In this study, pre-treatment
with the cytochrome P450 monooxygenase (P450) inhibitor malathion
clearly reduced the tribenuron-methyl resistance in the resistant
(R) population. After tribenuron-methyl treatment, the glutathione S-transferase (GST) activity of R plants was significantly
higher than that of susceptible (S) plants. The higher tribenuron-methyl
metabolism in R plants was also confirmed by using LC–MS/MS
analysis. Isoform sequencing (Iso-Seq) combined with RNA sequencing
(RNA-Seq) was used to identify candidate genes involved in non-target
metabolic resistance in this population. A total of 37 differentially
expressed genes were identified, 11 of them constitutively upregulated
in R plants, including three P450s, one GST, two glycosyltransferases,
two ATP-binding cassette transporters, one oxidase, and two peroxidases.
This study confirmed the metabolic tribenuron-methyl resistance in C. bursa-pastoris, and the transcriptome data obtained
by Iso-Seq combined with RNA-Seq provide gene resources for understanding
the molecular mechanism of NTSR in C. bursa-pastoris.