The modification of proteins by the attachment of fatty acids is a targeting tactic involved in mechanisms of both plant immunity and bacterial pathogenesis. The plant plasma membrane (PM) is a key battleground in the war against disease-causing microbes. This membrane is armed with an array of sensor proteins that function as a surveillance system to detect invading pathogens. Several of these sensor proteins are directed to the plasma membrane through the covalent addition of fatty acids, a process termed fatty acylation. Phytopathogens secrete effector proteins into the plant cell to subvert these surveillance mechanisms, rendering the host susceptible to infection. The targeting of effectors to specific locales within plant cells, particularly the internal face of the host PM, is critical for their virulence function. Several bacterial effectors hijack the host fatty acylation machinery to be modified and directed to this contested locale. To find and fight these fatty acylated effectors the plant leverages lipid-modified intracellular sensors. This review provides examples featuring how fatty acylation is a battle tactic used by both combatants in the molecular arms race between plants and pathogens. Also highlighted is the exploitation of a specific form of host-mediated fatty acid modification, which appears to be exclusively employed by phytopathogenic effector proteins.
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http://dx.doi.org/10.1093/jxb/erv059 | DOI Listing |
Transl Cancer Res
December 2024
Department of Pathology, Faculty of Medicine, Hunan University of Chinese Medicine, Changsha, China.
Background: In cuproptosis, excess copper ions induce cell death via fatty acylation in the tricarboxylic acid (TCA) cycle. However, the effects of cuproptosis-TCA-related long non-coding RNAs (lncRNAs) on the clinical prognosis of non-small cell lung cancer (NSCLC) and the associated tumor microenvironment remain unclear. The purpose of this study is to use cuproptosis-TCA related lncRNAs to predict the prognosis of NSCLC.
View Article and Find Full Text PDFJ Endocrinol
January 2025
N Inagaki, Department of Diabetes, Endocrinology and Nutrition, Kyoto University, Kyoto, Japan.
Glucagon-like peptide 1 (GLP-1) receptor agonists (GLP-1 RAs) are widely used as antidiabetic and anti-obesity agents. Although conventional GLP-1 RAs such as liraglutide and semaglutide are acylated with fatty acids to delay their degradation by dipeptidylpeptidase-4 (DPP-4), the manufacturing process is challenging. We previously developed selectively lipidated GLP-1 peptides at their only tryptophan residue (peptide A having one 8-amino-3,6-dioxaoctanoic acid (miniPEG) linker and peptide B having three miniPEG linkers).
View Article and Find Full Text PDFJ Lipid Res
January 2025
Laboratory of Molecular Pharmacology, Biosignal Research Center, Kobe University, Kobe, 657-8501, Japan. Electronic address:
At least 10% of proteins constituting the human proteome are subject to S-acylation by a long-chain fatty acid, thioesterified to a Cys thiol side chain. Fatty S-acylation (prototypically, S-palmitoylation) operates across eukaryotic phylogeny and cell type. S-palmitoylation is carried out in mammalian cells by a family of 23-24 dedicated zDHHC palmitoyl transferase enzymes, and mutation of zDHHCs is associated with a number of human pathophysiologies.
View Article and Find Full Text PDFPlants (Basel)
January 2025
School of Pharmacy and BioMolecular Sciences, Liverpool John Moores University, Byram Street, Liverpool L3 3AF, UK.
Protein S-acyl transferases (PATs) are a family of enzymes that catalyze protein S-acylation, a post-translational lipid modification involved in protein membrane targeting, trafficking, stability, and protein-protein interaction. S-acylation plays important roles in plant growth, development, and stress responses. Here, we report the genome-wide analysis of the family genes in the woodland strawberry (), a model plant for studying the economically important Rosaceae family.
View Article and Find Full Text PDFChem Phys Lipids
January 2025
College & Hospital of Stomatology, Anhui Medical University, Key Lab. of Oral Diseases Research of Anhui Province, No.81, Meishan Road, Shushan District, Hefei 230032, China. Electronic address:
Dental fluorosis, as a common chronic fluoride toxicity oral disease, is mainly caused by long-term excessive intake of fluoride, which seriously affects the aesthetics and function of patients' teeth. In recent years, with the rapid development of metabolomics technology, lipidomics, as an important means to study the changes in lipid metabolism in organisms, has shown great potential in revealing the mechanisms of disease development. As a major component of cell membranes and a signaling molecule, metabolic disorders of lipids are closely related to a variety of diseases, but the specific mechanism of action in dental fluorosis is still unclear.
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