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Indaziflam herbicidal action: a potent auxin signaling inhibitor
Author(s) -
Behnami Sara,
Bonetta Dario
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.02719
Subject(s) - physcomitrella patens , auxin , mutant , mutagenesis , arabidopsis , arabidopsis thaliana , biology , microbiology and biotechnology , chemistry , biochemistry , gene
Cellulose biosynthesis is a common feature of land plants. Therefore, cellulose biosynthesis inhibitors (CBIs) are useful tools in decoding fundamental aspects of cellulose biosynthesis. Here, we characterize the herbicide indaziflam, which has a unique mode of action for resistance management and appears to prevent plant growth by inhibiting cellulose biosynthesis and causes radial swelling and ectopic lignification; typical responses to treatment with CBIs. Previous work has demonstrated that Arabidopsis thaliana mutants that are indaziflam resistant can be identified through forward genetic screening. Since indaziflam is also active in the moss Physcomitrella patens , we took advantage of this system to attempt to understand the mode of action of indaziflam. Using UV‐induced mutagenesis, we generated mutants in Physcomitrella patens that were resistant to 30μM of indaziflam ( izr ), interestingly among the izr mutants; some were cross‐resistant to synthetic auxin 2,4‐D and NAA, which is predicted that indaziflam affects multiple pathways required for plant growth and development, since auxin affects the production and remodeling of plant cell wall either directly or indirectly. The izr mutants displayed a phenotype similar to that of auxin treated wild type plants, with small, undifferentiated, and leafless filaments, so we tested their responses to exogenous auxin, and it appears mutants were insensitive to synthetic auxin and started differentiation of chloronema to caulonemal filaments and gametophore development. To positionally clone the causative mutations, we have generated segregating populations by crossing the izr mutants with the Villersexel (Vx) wild type using a protoplast fusion technique. Our screen was designed to select mutant lines with indaziflam and auxin resistance; as a result, it establishes how critical elements within the indaziflam mode of action can refine auxin repressor activity, and have the long‐term developmental outcome. As a herbicide, indaziflam could potentially be used for weed management and eliminate the effects of these invasive grasses. Support or Funding Information NSERC (The Natural Sciences and Engineering Research Council of Canada)