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Title: A Phytochrome B-Independent Pathway Restricts Growth at High Levels of Jasmonate Defense

Journal Article · · Plant Physiology (Bethesda)
DOI:https://doi.org/10.1104/pp.19.01335· OSTI ID:1608185
ORCiD logo [1]; ORCiD logo [2]; ORCiD logo [1]; ORCiD logo [3]; ORCiD logo [4]; ORCiD logo [5]
  1. Department of Energy-Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824
  2. Department of Energy-Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824, Department of Plant Biology, Michigan State University, East Lansing, Michigan 48824
  3. Department of Energy-Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824, Plant Resilience Institute, Michigan State University, East Lansing, Michigan 42284
  4. Department of Energy-Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824, Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan 48824
  5. Department of Energy-Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824, Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan 48824, Plant Resilience Institute, Michigan State University, East Lansing, Michigan 42284

The plant hormone jasmonate (JA) promotes resistance to biotic stress by stimulating the degradation of JASMONATE ZIMDOMAIN (JAZ) proteins, which relieves repression on MYC transcription factors that execute defense programs. JA-triggered depletion of JAZ proteins in Arabidopsis (Arabidopsis thaliana) is also associated with reduced growth and seed production, but the mechanisms underlying these pleiotropic growth effects remain unclear. Here, we investigated this question using an Arabidopsis JAZ-deficient mutant (jazD; jaz1–jaz7, jaz9, jaz10, and jaz13) that exhibits high levels of defense and strong growth inhibition. Genetic suppressor screens for mutations that uncouple growth-defense tradeoffs in the jazD mutant identified nine independent causal mutations in the red-light receptor phytochrome B (phyB). Unlike the ability of the phyB mutations to completely uncouple the mild growth-defense phenotypes in a jaz mutant (jazQ) defective in JAZ1, JAZ3, JAZ4, JAZ9, and JAZ10, phyB null alleles only weakly alleviated the growth and reproductive defects in the jazD mutant. phyB-independent growth restriction of the jazD mutant was tightly correlated with upregulation of the Trp biosynthetic pathway but not with changes in central carbon metabolism. Interestingly, jazD and jazD phyB plants were insensitive to a chemical inhibitor of Trp biosynthesis, which is a phenotype previously observed in plants expressing hyperactive MYC transcription factors that cannot bind JAZ repressors. These data provide evidence that the mechanisms underlying JA-mediated growth-defense balance depend on the level of defense, and they further establish an association between growth inhibition at high levels of defense and dysregulation of Trp biosynthesis.

Research Organization:
Michigan State Univ., East Lansing, MI (United States). MSU-DOE Plant Research Laboratory
Sponsoring Organization:
USDOE Office of Science (SC), Basic Energy Sciences (BES)
Grant/Contract Number:
FG02-91ER20021
OSTI ID:
1608185
Alternate ID(s):
OSTI ID: 1735822
Journal Information:
Plant Physiology (Bethesda), Journal Name: Plant Physiology (Bethesda) Vol. 183 Journal Issue: 2; ISSN 0032-0889
Publisher:
American Society of Plant BiologistsCopyright Statement
Country of Publication:
United States
Language:
English
Citation Metrics:
Cited by: 39 works
Citation information provided by
Web of Science

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