Subgenome dominance of ALS target site mutations impacts herbicide resistance in allohexaploid Echinochloa crus-galli
Cutti, L.; Turra, G. M.; Machado, F. M.; Sulzbach, E.; Angonese, P. S.; Markus, C.; Gaines, T. A.; Merotto, A.
Show abstract
Herbicide target site resistance in polyploid species is more complex than diploids due to potential subgenome interactions and gene dosage of mutations. The objective of this study was to identify the level of resistance and cross-resistance patterns of ALS mutations located in the different subgenomes of allohexaploid Echinochloa crus-galli. E. crus-galli populations were screened and dose-response curves were performed with ALS-inhibitors from different chemical groups. The ALS genes of each subgenome (A, B, and C) were sequenced. Copy number variation, global relative expression, and the specific relative expression of ALS gene from each subgenome were performed. Out of 100 populations, 32% were resistant only to imazethapyr, and 48% were cross-resistant to all ALS-inhibitors. The mutations Ala122Thr, Ala205Asn, and Ser653Asn confer resistance only to imazethapyr, while Trp574Leu confers resistance to all four herbicides tested. ALS mutations were most frequent in subgenome A, but ALS from subgenome C had the highest expression. The biotype SAOJER-01 had Trp574Leu mutation in subgenome C and was 22 times more resistant to imazethapyr and penoxsulam than CAMAQ-01, which had the same Trp574Leu mutation in subgenome A with no differences in herbicide metabolism rate. The ALS genes from subgenomes A and C contribute approximately 13% and 50% respectively to the total ALS transcripts. The higher contribution of subgenome C to the total ALS transcripts pool combined with the Trp574Leu resistance mutation makes the biotype SAOJER-01 more resistant to herbicides than CAMAQ-01. This is the first study showing the effect of subgenome gene expression level on the herbicide resistance level in a polyploid weed species. In addition, while imazethapyr did not control any biotype with an ALS mutation, the other ALS-inhibitor herbicides were able to control biotypes carrying Ala122Thr, Ala205Asn, and Ser653Asn, which reinforces the utility of these herbicides in weed and resistance management.
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