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van der Meer, T.

Publications and source records attributed to van der Meer, T..

3 recordsLinked to original sources

Phytosulfokine signaling modulates salt stress responses and cell wall remodeling in Arabidopsis

Salinity severely impairs plant growth and development. Increasing evidence suggests that the cell wall (CW) plays a central role in salt stress acclimation, not only as a structural barrier but also as a dynamic sensor that activates downstream stress signaling pathways. To identify extracellular factors involved in cell wall remodeling and integrity signaling during salt stress, we performed a comparative proteomic analysis of the Arabidopsis seedling apoplast. Among the proteins that accumulated under salt stress, we focused on three members of the Subtilisin-Like Protease family (SBT1.1, SBT1.6, and SBT5.3), which have previously been implicated in the processing of signaling peptides and CW-associated proteins. Functional analyses revealed that sbt1.1 and sbt5.3 mutants exhibit enhanced lignin deposition under salt stress, suggesting altered CW remodeling during stress application. Given the established role of SBT1.1 in processing PHYTOSULFOKINE (PSK) peptides, we investigated the involvement of PSK signaling in salt stress responses. Mutants lacking the two PSK RECEPTORS (pskr1 pskr2) displayed reduced growth and increased lignification under salt treatment. Exogenous application of PSK attenuated salt-induced responses, including MITOGEN ACTIVATED PROTEIN KINASE 6 (MPK6) phosphorylation, salt stress marker gene expression, and lignin accumulation, ultimately promoting root elongation under salt stress. Furthermore, PSK treatment mitigated salt-induced changes in CW composition. In cell wall integrity (CWI) mutants, PSK treatment failed to restore wild-type root growth under salt stress and induced a pronounced root bending phenotype in fer-4, indicating that CWI signaling influences PSK-mediated root growth responses. Together, these results support a role for PSK signaling in modulating CW-associated responses to salinity stress in Arabidopsis.

plant biology↗

Supervised machine learning versus expert assessment of ultrastructural changes in wild-type and OGT knockout macrophages

Automated transmission electron microscopy (TEM) generates large datasets that challenge traditional qualitative analysis of cellular ultrastructure. Quantitative assessment of structural differences between different samples remains difficult due to structural variability in thin sections of organelles. Here we applied supervised machine learning (sML) to segment, quantify and compare cellular structures -including nuclei, chromatin, mitochondria, rough endoplasmic reticulum, and endocytic vesicles- in large TEM images of wild-type macrophages versus those with altered cellular physiology due to deficiency in O-GlcNAc Transferase (OGT). sML revealed that OGT knockout macrophages are larger and more oval, with increased euchromatin, nucleoli size, and relative mitochondrial and rER surface areas. Comparison with six TEM experts showed sML provides more objective and sensitive quantification of subtle differences, while expert consensus is only achieved for larger structural variations. These findings demonstrate that sML enhances quantitative TEM analysis and complements human expertise in ultrastructural studies.

cell biology↗

O-GlcNAcylation drives macrophage IL-4 responsiveness and tissue residency through metabolic and cell cycle calibration

The metabolic requirements for macrophage IL-4 polarization remain contentious, while immunometabolic studies of tissue resident macrophages are still sparse. Hexosamine biosynthesis has gained attention regarding its immune regulatory potential via downstream O-GlcNAcylation. Here we identify protein O-GlcNAcylation as a requirement for IL-4 polarization in vitro and proliferative expansion in vivo during cytokine challenge or infection. We further show that O-GlcNAcylation is critical for controlling tissue residency. By enforcing metabolic and cell cycle quiescence during differentiation, O-GlcNAcylation is needed for adult monocytes to establish a long-live residency program. In this context, its absence leads to perpetual DNA vulnerability and damage via reactive oxygen species, resulting in a senescent-like state poised for cell death. Conversely, long-lived populations instead require O-GlcNAcylation for self-renewal and inflammatory expansion. Our findings altogether suggest O-GlcNAcylation, fueled by hexosamine biosynthesis, serves as a central metabolic rheostat for resident macrophage formation and maintenance during homeostasis and disease.

immunology↗