Plant fatty acids (FAs) and lipids are essential in storing energy and act as structural components for cell membranes and signaling molecules for plant growth and stress responses. Acyl Carrier Proteins (ACPs) are small acidic proteins that covalently bind the fatty acyl intermediates during the elongation of FAs. The Arabidopsis thaliana ACP family has eight members. Through reverse genetic, molecular, and biochemical approaches, we have discovered that ACP1 localizes to the chloroplast and limits the magnitude of pattern-triggered immunity (PTI) against the bacterial pathogen Pseudomonas syringae pathovar tomato (Pto). The mutant acp1 plants have reduced levels of linolenic acid (18:3), which is the primary precursor for the biosynthesis of the phytohormone jasmonic acid (JA), and a corresponding decrease in the abundance of JA. Consistent with the known antagonistic relationship between JA and salicylic acid (SA), acp1 mutant plants also accumulate higher level of SA and display the corresponding shifts in JA- and SA-regulated transcriptional outputs. Moreover, the methyl JA and linolenic acid treatments cause an apparently enhanced decrease of resistance against Pto in acp1 mutants than that in wild-type plants. The ability of ACP1 to prevent this hormone imbalance likely underlies its negative impact on PTI in plant defense. Thus, ACP1 links FA metabolism to stress hormone homeostasis to be negatively involved in PTI in Arabidopsis plant defense.
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Reply to the ‘Comment on “Tensional homeostasis at different length scales” by J. Humphrey and C. Cyron, Soft Matter , 2022, 18 , DOI: 10.1039/D1SM01151K’
Drs Humphrey and Cyron wrote a commentary regarding our review article entitled “Tensional homeostasis at different length scales” that was published in Soft Matter , 2020, 16 , 6946–6963. These authors brought up some valid concerns to which we would like to respond. Their first concern is related to our remark regarding equations that we used to describe homeostasis in blood vessels, where we stated that those equations were limited only to linearly elastic materials. We were wrong, and we agree with the authors that these equations hold for all cylindrical vessels regardless of their material properties. Their second concern is related to tensional homeostasis at the subcellular level. Drs Humphrey and Cyron disagree with our substantiated claim that tensional homeostasis breaks down at the level of focal adhesions (FAs) of a living cell. In our reply, we provided several pieces of evidence that demonstrate that tensional homeostasis depends upon FA size, FA maturity and FA force dynamics and thus, tensional homeostasis cannot hold in all FAs across a cell. In summary, we are grateful for the opportunity to reply to the commentary of Drs Humphrey and Cyron. Moreover, we are excited that this topic has become an important focus in the biomechanics and mechanobiology communities, and we feel strongly that critical feedback is necessary to move this field forward.
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- Award ID(s):
- 1910401
- NSF-PAR ID:
- 10318581
- Date Published:
- Journal Name:
- Soft Matter
- Volume:
- 18
- Issue:
- 3
- ISSN:
- 1744-683X
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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- Free Publicly Accessible Full Text
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Accepted Manuscript1.0
- Journal Article:
- https://doi.org/10.1039/d1sm01495a
