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Title: Ectopic Defense Gene Expression Is Associated with Growth Defects in Medicago truncatula Lignin Pathway Mutants

Journal Article · · Plant Physiology (Bethesda)
DOI:https://doi.org/10.1104/pp.19.00533· OSTI ID:1559395
ORCiD logo [1];  [2];  [3];  [4]; ORCiD logo [5]; ORCiD logo [5]; ORCiD logo [6]; ORCiD logo [6];  [7]; ORCiD logo [8]
  1. BioDiscovery Institute and Department of Biological Sciences, University of North Texas, Denton, Texas 76201, Center for Bioenergy Innovation, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831
  2. Samuel Roberts Noble Foundation, Ardmore, Oklahoma 73401
  3. Department of Biochemistry and MU Metabolomics Center, University of Missouri, Columbia, Missouri 65201
  4. BioDiscovery Institute and Department of Biological Sciences, University of North Texas, Denton, Texas 76201, Bioenergy Sciences Center, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831
  5. Center for Bioenergy Innovation, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831, Bioenergy Sciences Center, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831, BioSciences Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831
  6. Samuel Roberts Noble Foundation, Ardmore, Oklahoma 73401, University of Texas at San Antonio, San Antonio, Texas 78249
  7. Samuel Roberts Noble Foundation, Ardmore, Oklahoma 73401, Department of Biochemistry and MU Metabolomics Center, University of Missouri, Columbia, Missouri 65201
  8. BioDiscovery Institute and Department of Biological Sciences, University of North Texas, Denton, Texas 76201, Center for Bioenergy Innovation, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831, Bioenergy Sciences Center, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831

Lignin provides crucial mechanical support for plant cell walls but decreases the digestibility of forage crops and increases the recalcitrance of biofuel crops. Attempts to modify lignin content and/or composition by genetic modification often result in negative growth effects. Although several studies have attempted to address the basis for such effects in individual transgenic lines, no common mechanism linking lignin modification with perturbations in plant growth and development has yet been identified. To address whether a common mechanism exists, we have studied transposon insertion mutants resulting in independent loss of function of five enzymes of the monolignol pathway, as well as one double mutant, in the model legume Medicago truncatula. These plants exhibit growth phenotypes from essentially wild-type to severely retarded. Extensive phenotypic, transcriptomic, and metabolomics analyses, including structural characterization of differentially expressed compounds, revealed diverse phenotypic consequences of lignin pathway perturbation that were perceived early in plant development, but were not predicted by lignin content or composition alone. Notable phenotypes among the mutants with severe growth impairment were increased trichome numbers, accumulation of a variety of triterpene saponins, and extensive but differential ectopic expression of defense response genes. No currently proposed model explains the observed phenotypes across all lines. We report that re-allocation of resources into defense pathways is linked to the severity of the final growth phenotype in monolignol pathway mutants of Medicago, although it remains unclear as to whether this is a cause or an effect of the growth impairment.

Research Organization:
Oak Ridge National Laboratory (ORNL), Oak Ridge, TN (United States)
Sponsoring Organization:
USDOE Office of Science (SC), Biological and Environmental Research (BER); National Science Foundation (NSF)
Grant/Contract Number:
AC05-00OR22725
OSTI ID:
1559395
Alternate ID(s):
OSTI ID: 1545187
Journal Information:
Plant Physiology (Bethesda), Journal Name: Plant Physiology (Bethesda) Vol. 181 Journal Issue: 1; ISSN 0032-0889
Publisher:
Oxford University PressCopyright Statement
Country of Publication:
United States
Language:
English
Citation Metrics:
Cited by: 25 works
Citation information provided by
Web of Science

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