AI Article Synopsis

  • Researchers identified 93 mutant families of flax with abnormal lignin development in their bast fibers, naming them the Linum usitatissimum lbf mutants, which offer new insights into how flax regulates lignin production.
  • The lbf1 mutant demonstrated a significant increase of 350% in lignin content in outer stem tissues with bast fibers, while inner tissues remained unchanged, indicating a targeted response in fiber cells.
  • Analyses revealed that this ectopic lignification is linked to enhanced expression of genes associated with lignin biosynthesis and oxidative processes, suggesting a complex regulatory mechanism in flax bast fiber development.

Article Abstract

Histochemical screening of a flax ethyl methanesulfonate population led to the identification of 93 independent M2 mutant families showing ectopic lignification in the secondary cell wall of stem bast fibers. We named this core collection the Linum usitatissimum (flax) lbf mutants for lignified bast fibers and believe that this population represents a novel biological resource for investigating how bast fiber plants regulate lignin biosynthesis. As a proof of concept, we characterized the lbf1 mutant and showed that the lignin content increased by 350% in outer stem tissues containing bast fibers but was unchanged in inner stem tissues containing xylem. Chemical and NMR analyses indicated that bast fiber ectopic lignin was highly condensed and rich in G-units. Liquid chromatography-mass spectrometry profiling showed large modifications in the oligolignol pool of lbf1 inner- and outer-stem tissues that could be related to ectopic lignification. Immunological and chemical analyses revealed that lbf1 mutants also showed changes to other cell wall polymers. Whole-genome transcriptomics suggested that ectopic lignification of flax bast fibers could be caused by increased transcript accumulation of (1) the cinnamoyl-CoA reductase, cinnamyl alcohol dehydrogenase, and caffeic acid O-methyltransferase monolignol biosynthesis genes, (2) several lignin-associated peroxidase genes, and (3) genes coding for respiratory burst oxidase homolog NADPH-oxidases necessary to increase H2O2 supply.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4277216PMC
http://dx.doi.org/10.1105/tpc.114.130443DOI Listing

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