Research roundup: ubiquitination, autophagy-driven lipid shifts, and BRAF in synaptic pain signaling

Plant Physiology reports on proteome and ubiquitination profiling of sweet orange leaves infected with Candidatus Liberibacter asiaticus. The study combined ubiquitinated‑peptide immunoaffinity enrichment with 4D label‑free quantitative proteomics and found broad proteome remodeling with a strong global increase in protein ubiquitination. A predominant set of proteins showed reduced abundance together with increased ubiquitination, including proteins tied to chloroplast function, redox homeostasis, and primary metabolism. The degradation machinery was also modified, with ubiquitination of proteasome subunits and indications of enhanced proteasome‑dependent protein turnover. Physiological analyses linked these changes to suppression of hydrogen peroxide scavenging, reduced catalase abundance with increased catalase ubiquitination, and higher hydrogen peroxide levels. Actin emerged as a major target: actin proteins had enhanced ubiquitination and degradation, actin filaments were disrupted, and the CsACT7 isoform underwent 26S proteasome‑dependent degradation. Mutation of seven CLas‑upregulated lysines on CsACT7 stabilized the protein and reduced CLas accumulation in citrus hairy‑root assays reported by the authors. These observations are limited to the reported experimental systems and do not by themselves indicate wider agricultural outcomes.

A second Plant Physiology paper characterizes lipid remodeling and autophagy during potato purple top (PPT) phytoplasma infection in tomato. The authors observed increased ATG8 lipidation and autophagosome formation at endoplasmic reticulum stress sites, and redistribution of lipid droplets toward phytoplasma cells. Lipidomics revealed declines in chloroplast galactolipids and phospholipids concurrent with a rise in triacylglycerol (TAG), interpreted as accelerated membrane turnover and neutral lipid sequestration. Transmission electron microscopy showed frequent proximity between lipid droplets and phytoplasmas. Chemical inhibition of autophagy with 3‑methyladenine blocked lipid droplet breakdown, altered ER organization, and reduced phytoplasma titers in the reported experiments, supporting a role for host autophagy in phytoplasma proliferation under the study conditions. Complementary genome analysis identified a conserved phytoplasma alpha/beta hydrolase (PPT‑lipase) predicted to resemble monoacylglycerol lipases; in vivo assays in yeast and Nicotiana benthamiana reported reduction of neutral lipids by PPT‑lipase and loss of activity when catalytic triad residues were mutated. The authors note that PPT‑lipase lacks a predicted signal peptide and likely acts intracellularly within phytoplasma cells. These results derive from specific plant models and heterologous assays and should be interpreted in that experimental context.

A Science Signaling report addresses mechanisms of sustained NMDA receptor hyperactivity in the spinal dorsal horn after nerve injury. The study identifies BRAF as a regulator that translocates from dorsal root ganglia to spinal cord synaptosomes after injury and is associated with increased phosphorylation of downstream kinases MEK and ERK. The authors describe enhanced interaction of NMDARs with the BRAF/MEK/ERK module in both rat and human spinal cord samples analyzed. Pharmacological inhibition or genetic deletion of BRAF in mouse DRG neurons reversed injury‑associated NMDAR phosphorylation, synaptic trafficking changes, and pre‑ and postsynaptic hyperactivity reported by the investigators. In mouse models, lack of BRAF or treatment with pathway inhibitors was associated with a shorter or less severe period of pain hypersensitivity compared with wild type, whereas expression of a constitutively active BRAF mutant in DRG neurons induced sustained nociceptive hypersensitivity that was blocked in the experiments by NMDAR antagonists, gabapentin, or an α2δ‑1 C‑terminal‑interfering peptide. The paper frames BRAF as a potential mechanistic target for further investigation, but these findings are preclinical and pertain to the experimental systems described.