Ornamental plants can survive stress while losing the traits that determine their commercial value. Post-translational modifications (PTMs) connect environmental and developmental signals to protein activity, localisation, and lifetime, offering a regulatory link between stress perception and horticultural performance. This review examines phosphorylation, ubiquitination, and lysine acylation across four areas of ornamental research: membrane regulation in rose immunity, cold-responsive crotonylation and enzyme function in chrysanthemum, senescence and acyl metabolism in petunia, and photosynthetic responses in Rhododendron. A non-exhaustive structured audit of ten selected profiling records describes analytical confidence and functional scope separately, identifying opportunities to integrate proteome measurements, refine site assignments, and connect discovery datasets to native-species experiments. Targeted chrysanthemum studies illustrate the complementary contributions of biochemical residue assays and native genetic tests. Model-plant evidence for SUMOylation, cysteine-redox modifications, S-acylation, N- and O-glycosylation, protein methylation, and limited proteolysis extends the framework to additional regulatory layers. Direct causal links between specific covalent modifications and ornamental quality remain limited. We propose a research agenda combining matched analytical streams, time-resolved measurements, and controlled native perturbations, with flower opening, petal integrity, colour, scent, and vase life as explicit outcomes. Connecting PTM dynamics to protein function, recovery, and quality trade-offs can strengthen the mechanistic basis for improving stress resilience in ornamental plants.

Hydraulic perturbations are among the earliest plant-wide consequences of drought, salinity and wounding, yet they are often treated as passive outcomes rather than as biologically interpreted inputs. This review distinguishes hydraulic state, hydraulic perturbation and hydraulic signal, and evaluates how organ-scale pressure and water-potential changes are converted into local membrane tension, wall strain, turgor and water-flux cues. We propose, as a testable model rather than an established mechanism, a distributed architecture comprising OSCA/TMEM63 and other mechanosensitive channels, cell-wall integrity pathways, aquaporin-mediated conductance control and vacuolar buffering. Evidence for the individual components is substantial, but evidence that they act together within a single physiological event is still limited. These layers are reciprocally coupled to Ca²⁺, ROS, electrical, hormonal and peptide networks. Hydraulic cues are fast, and they differ in amplitude, direction, rise time, duration, recovery and anatomical route, so they are not informationally inert. Specificity nevertheless appears to emerge from the integration of the hydraulic waveform with tissue state and coincident ionic, electrical and biochemical inputs rather than from any single variable. We compare drought, salinity and wounding; clarify the roles of roots, vasculature, bundle sheath, mesophyll and guard cells; and outline experiments that combine calibrated physical perturbations with live reporters, tissue-specific genetics and hydromechanical modeling. The key frontier is no longer to document that pressure changes occur. It is to identify the variables directly sensed, to separate instructive from permissive roles, and to test whether dynamic decoding traits improve crop resilience at acceptable carbon and growth cost.

Heat stress is a major constraint on plant growth and productivity, and excessive accumulation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), especially hydrogen peroxide (H₂O₂), is a primary cause of heat-induced cellular damage. Photorespiration becomes accelerated at high temperature and generates the toxic metabolite 2-phosphoglycolate (2PG), whose accumulation is prevented by the first photorespiratory enzyme 2-phosphoglycolate phosphatase (PGLP1). Here, we identify the auxilin-like J-domain protein JAC1 (AT1G75100) as a positive regulator of thermotolerance in Arabidopsis thaliana (A. thaliana). JAC1 transcripts were rapidly induced by heat treatment, and loss-of-function jac1 mutants (jac1-1 and jac1-2) were hypersensitive to long-term heat stress (38 °C, 7 d), whereas three independent JAC1 overexpression lines (#2, #4, #5) exhibited enhanced survival. Consistent with a role in ROS homeostasis, heat-treated jac1 mutants showed stronger DAB staining, consistent with higher apparent H₂O₂ levels, whereas JAC1 overexpression lines showed weaker staining. Although PGLP1 abundance (mRNA and protein) was unchanged among genotypes, heat treatment (38 °C, 12 h) caused a marked reduction in leaf PGLP1 enzymatic activity in jac1 mutants and a significant increase in JAC1 overexpression lines, leading to corresponding changes in 2PG content. PGLP1 sulfenylation, a H₂O₂-dependent post-translational modification that inhibits PGLP1, was detectable only after heat and was enhanced in jac1 mutants but suppressed in JAC1 overexpression lines. Genetic manipulation of PGLP1 supported that PGLP1 functions downstream of JAC1: overexpressing PGLP1 in jac1-1 rescued heat sensitivity, whereas knocking down PGLP1 in the JAC1 overexpression background reversed thermotolerance. Together, our results support a model in which JAC1 maintains heat-induced H₂O₂ homeostasis, thereby limiting PGLP1 sulfenylation, sustaining PGLP1 activity and preventing toxic 2PG accumulation during heat stress.