ArticlePest management science2025
A point mutation in IAA34 confers resistance to the auxin herbicide 2,4-D in Sisymbrium orientale.
Article in Pest management science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- A deletion upstream of the degron of AcIAA27 leads to auxinic herbicide resistance in Arctotheca calendula.Pest management science · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSisymbrium orientale has evolved resistance to 2,4-D in Australia due to a 27 bp deletion in SoIAA2. However, one population of Sisymbrium orientale resistant to 2,4-D (R1) did not contain the SoIAA2
resultsR1 is resistant to 2,4-D, 2-methyl-4-chlorophenoxyacetic acid (MCPA), and fluroxypyr with increased tolerance to dicamba, triclopyr and picloram. The 2,4-D resistance level for R1 is lower than resistant populations containing a 27 bp deletion in IAA2. 2,4-D resistance in R1 was due to a single dominant gene. Pretreatment of R1 with the P450 inhibitor malathion did not reduce resistance to 2,4-D. We identified a point mutation, Leu 175 Pro, in SoIAA34 in R1, but not in three susceptible (S) populations. This mutation was present (either homozygous or heterozygous) in all 2,4-D resistant plants in a segregating F2 population generated from a cross between S and R1 plants. Transgenic Arabidopsis plants expressing SoIAA34-R had significantly greater root length and dry mass than the wild-type (WT) or transgenic Arabidopsis plants carrying SoIAA34-S under 2,4-D treatment.
conclusionWe confirmed resistance to 2,4-D in the R1 population was controlled by a single dominant locus. Further, we verified that the Leu 175 Pro mutation in SoIAA34 is responsible for the 2,4-D resistance in R1. © 2025 The Author(s). Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.