Hydrogen sulfide (H₂S) serves as an important gaseous signaling molecule that is involved in intra- and intercellular signal transduction in plant–environment interactions. In plants, H₂S is formed in sulfate/cysteine reduction pathways. The activation of endogenous H₂S and its exogenous application has been found to be highly effective in ameliorating a wide variety of stress conditions in plants. The H₂S interferes with the cellular redox regulatory network and prevents the degradation of proteins from oxidative stress via post-translational modifications (PTMs). H₂S-mediated persulfidation allows the rapid response of proteins in signaling networks to environmental stimuli. In addition, regulatory crosstalk of H₂S with other gaseous signals and plant growth regulators enable the activation of multiple signaling cascades that drive cellular adaptation. In this review, we summarize and discuss the current understanding of the molecular mechanisms of H₂S-induced cellular adjustments and the interactions between H₂S and various signaling pathways in plants, emphasizing the recent progress in our understanding of the effects of H₂S on the PTMs of proteins. We also discuss future directions that would advance our understanding of H₂S interactions to ultimately mitigate the impacts of environmental stresses in the plants.

In plants, heteromeric acetyl-CoA carboxylase (hetACCase) initiates de novo fatty acid synthesis (FAS) by generating malonyl-CoA in the first committed step of this process. hetACCase activity is precisely regulated to meet the cellular demand for acyl chains during the plant life cycle. In this study, we performed a systematic co-expression analysis of hetACCase and its regulators in Arabidopsis (Arabidopsis thaliana) to better understand the regulatory mechanism of hetACCase. Our analysis uncovered REGULATOR OF FATTY ACID SYNTHESIS 1 (RFS1), whose expression is positively correlated with that of other regulators of hetACCase. The RFS gene family encodes two plastid inner envelope membrane proteins with undiscovered roles. Further analysis revealed that RFS1 co-localizes and directly interacts with CARBOXYLTRANSFERASE INTERACTOR 1 (CTI1). CRISPR/Cas9-mediated knockouts of RFSs exhibit enhanced hetACCase activity, higher FAS rates, and increased fatty acid contents, with particularly marked accumulation of absolute triacylglycerol levels in leaves, similar to cti mutants. The mutations of rfs and cti alter the plastid membrane distribution pattern of α-carboxyltransferase, leading to reduced hetACCase activity on the membrane, which could potentially be the original mechanism through which RFSs restrain hetACCase activity. Thus, we reveal a unique regulatory module that regulates de novo FAS and a genetic locus that may contribute to breeding of improved oil crops.

Lipid droplets (LDs) have emerged as dynamic organelles central to plant lipid metabolism, stress adaptation, and energy homeostasis. This review synthesizes recent advances in understanding LD biogenesis and degradation in plants, highlighting conserved and divergent mechanisms relative to other eukaryotes. LD formation originates in the endoplasmic reticulum (ER), where neutral lipids synthesized by diacylglycerol acyltransferases (DGAT) and phospholipid: diacylglycerol acyltransferases (PDAT) accumulate into lens-like structures. These structures bud into the cytosol via ER machinery, including SEIPIN complexes, vesicle-associated membrane proteins, and LD-associated protein-interacting protein which regulate LD size and abundance. Degradation occurs through two major pathways: lipolysis, mainly mediated by the patatin-like lipase SUGAR-DEPENDENT1, and lipophagy, where AUTOPHAGY-RELATED proteins deliver LDs for breakdown. LDs also function as stress-responsive hubs, accumulating under abiotic stresses and during pathogen interactions, where they participate in membrane remodeling and antimicrobial defense. Extensive studies in major oilseed crops reveal that expressions of multiple genes involved in LD turnover are significantly induced under various abiotic stresses and phytohormone treatments. These genetic components operate autonomously or synergistically (e.g. DGAT and PDAT) within the TAG biosynthesis and LD metabolic pathways, effecting concurrent enhancements in stress resilience and oil production under suboptimal growth conditions. Critical knowledge gaps persist, including the interplay between lipolysis and lipophagy, the integration of energy-related signaling pathways in LD turnover, and stress-modulated post-translational control of LD proteome. Deciphering these mechanisms will advance our understanding towards LD biology.

P4B (2-phenyl-1-[4-(6-(piperidin-1-yl) pyridazin-3-yl) piperazin-1-yl] butan-1-one) is a novel cellulose biosynthesis inhibitor (CBI) discovered in a screen for molecules to identify inhibitors of Arabidopsis (Arabidopsis thaliana) seedling growth. Growth and cellulose synthesis inhibition by P4B were greatly reduced in a novel mutant for the cellulose synthase catalytic subunit gene CESA3 (cesa3^pbr1). Cross-tolerance to P4B was also observed for isoxaben-resistant (ixr) cesa3 mutants ixr1-1 and ixr1-2. P4B has an original mode of action as compared with most other CBIs. Indeed, short-term treatments with P4B did not affect the velocity of cellulose synthase complexes (CSCs) but led to a decrease in CSC density in the plasma membrane without affecting their accumulation in microtubule-associated compartments. This was observed in the wild type but not in a cesa3^pbr1 background. This reduced density correlated with a reduced delivery rate of CSCs to the plasma membrane but also with changes in cortical microtubule dynamics and orientation. At longer timescales, however, the responses to P4B treatments resembled those to other CBIs, including the inhibition of CSC motility, reduced growth anisotropy, interference with the assembly of an extensible wall, pectin demethylesterification, and ectopic lignin and callose accumulation. Together, the data suggest that P4B either directly targets CESA3 or affects another cellular function related to CSC plasma membrane delivery and/or microtubule dynamics that is bypassed specifically by mutations in CESA3.

Lijuan Zhou, Yajin Ye; A genetic pathway for naturally colored cotton production, Plant Physiology, , kiac168, https://doi.org/10.1093/plphys/kiac168

Two mitogen-activated protein kinase (MAPK) cascades with MPK4 and MPK3/MPK6 as the bottommost kinases are key to plant growth/development and immune signaling. Disruption of the MPK4 cascade leads to severe dwarfism and autoimmunity, complicating the study of MPK4 in plant growth/development and immunity. In this study, we successfully rescued the Arabidopsis (Arabidopsis thaliana) mpk4 mutant using a chemical-sensitized MPK4 variant, MPK4^YG, creating a conditional activity-null mpk4 mutant named MPK4SR (genotype: P_MPK4:MPK4^YG mpk4) that could be used to examine the functions of MPK4 in plant growth/development and immunity. We discovered that the duration of the loss of MPK4 activity is important to plant immune responses. Short-term loss of MPK4 activity did not impact flg22-induced ROS burst or resistance against Pseudomonas syringae (Pst). Enhanced Pst resistance was only observed in the MPK4SR plants with stunted growth following prolonged inhibition of MPK4 activity. Transcriptome analyses in plants with short-term loss of MPK4 activity revealed a vital role of MPK4 in regulating several housekeeping processes, including mitosis, transcription initiation, and cell wall macromolecule catabolism. Furthermore, the constitutive weak activation of MPK4^GA in the MPK4CA plants (genotype: P_MPK4:MPK4^GA mpk4) led to early flowering and premature senescence, which was associated with its compromised resistance against Pst. These findings suggest that MPK4 plays important roles in plant growth and development and in maintaining the delicate balance between growth/development and immune adaptation in plants.