@article{yadav_primary_2026,
	title = {The primary beta-galactosidase {BGAL10} modulates pavement cell shape acquisition in {Arabidopsis}},
	issn = {0022-0957},
	url = {https://doi.org/10.1093/jxb/erag320},
	doi = {10.1093/jxb/erag320},
	abstract = {Cell shape acquisition is a fundamental biological process that allows cells to establish and maintain morphologies adapted to their specialised functions while preserving tissue integrity. In plants, this process is strongly influenced by the presence of the cell wall, a dynamic extracellular network of polysaccharides and proteins that surrounds the plasma membrane and physically connects neighbouring cells. By constraining and directing cellular expansion, the cell wall plays a central role in controlling cell shape. In Arabidopsis leaves, epidermal pavement cells adopt a characteristic jigsaw-puzzle–like morphology through the formation of interdigitating lobes and necks, providing a powerful model system for dissecting the mechanisms underlying complex plant cell shape acquisition. Here, we demonstrate the involvement of the glycoside hydrolase BETA-GALACTOSIDASE 10 (BGAL10) in pavement cell morphogenesis. Using high-resolution time-series imaging, we analysed cell growth dynamics alongside the spatial expression and subcellular localisation of BGAL10, revealing a prominent role for BGAL10 in mature cells, particularly at curved regions of the cell wall along pavement cell lobes. Furthermore, Brillouin microscopy revealed altered mechanical properties in the bgal10-1 mutant, most notably at lobe–indentation interfaces and cell junctions. Together, our results indicate that BGAL10 fine-tunes lobe outgrowth, likely through modification of the hemicellulose matrix, thereby regulating cell wall extensibility and mechanical stress distribution during pavement cell shape acquisition.},
	urldate = {2026-07-07},
	journal = {Journal of Experimental Botany},
	author = {Yadav, Sandeep and Kumar, Vinod and Heymans, Adrien and Sabooni, Nasrin and Jobert, François and Lin, Mengzhuo and Grones, Peter and Bacete, Laura and Robert, Stéphanie},
	month = jul,
	year = {2026},
	pages = {erag320},
}

Cell shape acquisition is a fundamental biological process that allows cells to establish and maintain morphologies adapted to their specialised functions while preserving tissue integrity. In plants, this process is strongly influenced by the presence of the cell wall, a dynamic extracellular network of polysaccharides and proteins that surrounds the plasma membrane and physically connects neighbouring cells. By constraining and directing cellular expansion, the cell wall plays a central role in controlling cell shape. In Arabidopsis leaves, epidermal pavement cells adopt a characteristic jigsaw-puzzle–like morphology through the formation of interdigitating lobes and necks, providing a powerful model system for dissecting the mechanisms underlying complex plant cell shape acquisition. Here, we demonstrate the involvement of the glycoside hydrolase BETA-GALACTOSIDASE 10 (BGAL10) in pavement cell morphogenesis. Using high-resolution time-series imaging, we analysed cell growth dynamics alongside the spatial expression and subcellular localisation of BGAL10, revealing a prominent role for BGAL10 in mature cells, particularly at curved regions of the cell wall along pavement cell lobes. Furthermore, Brillouin microscopy revealed altered mechanical properties in the bgal10-1 mutant, most notably at lobe–indentation interfaces and cell junctions. Together, our results indicate that BGAL10 fine-tunes lobe outgrowth, likely through modification of the hemicellulose matrix, thereby regulating cell wall extensibility and mechanical stress distribution during pavement cell shape acquisition.

@article{hussain_progression_2026,
	title = {The progression of leaf senescence is gated by the cytosolic arginine pool},
	copyright = {2026 The Author(s)},
	issn = {2055-0278},
	url = {https://www.nature.com/articles/s41477-026-02328-2},
	doi = {10.1038/s41477-026-02328-2},
	abstract = {Leaf senescence aims to degrade cellular components to recover valuable nutrients and reallocate them to other organs1. Once this remobilization is complete, cells undergo a vacuolar-type of programmed cell death2, ultimately leading to the death of the entire organ. But how do cells from a senescing leaf ‘know’ when to die? If the cell death process per se is initiated too early, remobilization may not be completed, rendering it futile. This suggests the presence of a ‘sensing’ mechanism that coordinates the remobilization phase with the onset of cell death during leaf senescence. Here, using Arabidopsis thaliana functional stay-green mutants, we show that senescing cells are wired to metabolically dissipate the cytosolic arginine pool, which otherwise represses the progression of leaf senescence. We propose a model in which a senescing cell uses this pool as a proxy for the completion of nitrogen remobilization and to accurately time the subsequent induction of cell death.},
	language = {en},
	urldate = {2026-07-07},
	journal = {Nature Plants},
	publisher = {Nature Publishing Group},
	author = {Hussain, Shah and Boussardon, Clément and Keech, Olivier},
	month = jun,
	year = {2026},
	keywords = {Abiotic, Cell fate},
	pages = {1--9},
}

Leaf senescence aims to degrade cellular components to recover valuable nutrients and reallocate them to other organs1. Once this remobilization is complete, cells undergo a vacuolar-type of programmed cell death2, ultimately leading to the death of the entire organ. But how do cells from a senescing leaf ‘know’ when to die? If the cell death process per se is initiated too early, remobilization may not be completed, rendering it futile. This suggests the presence of a ‘sensing’ mechanism that coordinates the remobilization phase with the onset of cell death during leaf senescence. Here, using Arabidopsis thaliana functional stay-green mutants, we show that senescing cells are wired to metabolically dissipate the cytosolic arginine pool, which otherwise represses the progression of leaf senescence. We propose a model in which a senescing cell uses this pool as a proxy for the completion of nitrogen remobilization and to accurately time the subsequent induction of cell death.

@article{bladh_role_2026,
	title = {The role of mucosal {IgA} in protection against influenza {A} {H1N1} virus infection in a real-world setting},
	volume = {129},
	issn = {2352-3964},
	url = {https://www.sciencedirect.com/science/article/pii/S2352396426002422},
	doi = {10.1016/j.ebiom.2026.106359},
	abstract = {Background
Parenteral vaccines against influenza virus prevent severe disease but provide limited protection against infection, likely due to limited induction of mucosal immunity. However, direct clinical evidence for mucosal antibody-mediated protection against influenza virus infection in humans has been lacking. The aim of this study was to evaluate the role of antigen-specific mucosal IgA as a correlate of protection against influenza virus infection. We investigated H1-specific nasal IgA and serum IgG and the effect on influenza virus infection, with corresponding SARS-CoV-2 data from the same cohort as an internal comparator.
Methods
Using a prospective cohort study design, we analysed paired antigen-specific serum IgG and nasal IgA responses at baseline, after influenza A (H1N1) virus and SARS-CoV-2 infections, and after intramuscular influenza and SARS-CoV-2 vaccination. We then evaluated associations between baseline antibody levels, vaccination, and the risk of subsequent influenza A (H1N1) virus infection or SARS-CoV-2 infections in a 4-month home-based qPCR screening in Stockholm, Sweden (2023–2024). A Poisson regression model with a log offset for time at risk was used to evaluate if baseline antigen-specific nasal IgA or serum IgG levels or recent vaccination was associated with protection against infection. Antibody quantification was performed using a highly sensitive electrochemiluminescence immunoassay (Meso Scale Diagnostics, USA) optimised for mucosal sampling.
Findings
A total of 926 study participants were enrolled. After influenza A (H1N1) virus infection, H1-specific nasal IgA and serum IgG increased (p = 0.007 and p {\textless} 0.001 respectively), while vaccination boosted serum IgG (p = 0.006) but not nasal IgA. Baseline nasal H1-specific IgA were lower in H1N1-infected individuals (p = 0.024), and notably, baseline nasal H1-specific IgA above median was associated with reduced H1N1 infection risk (IRR 0.23, 95\% CI 0.05–0.75, p = 0.026), while serum IgG and recent vaccination were not (IRR 2.03, 0.70–6.62, p = 0.206 and IRR 1.06, 0.38–3.03, p = 0.917, respectively). Moreover, each two-fold increase in baseline nasal H1-specific IgA levels was associated with a significantly lower infection risk (IRR 0.69, 95\% CI 0.51–0.92; p = 0.014). Similar findings were observed for SARS-CoV-2 for mucosal IgA, whereas baseline serum spike-specific IgG above the median was also associated with reduced risk of infection.
Interpretation
Leveraging fit-for-purpose sampling, a validated and highly sensitive assay, and a large real-world cohort, we directly link mucosal IgA to protection against influenza virus infection. While currently employed vaccines provide robust protection against severe disease and hospital admissions, these findings highlight the need for novel approaches generating robust mucosal protection against infection per se, and the need to incorporate mucosal endpoints into next-generation vaccine development aiming for infection-blocking immunity.
Funding
This work was funded by the European Research Council (101164772 - D-MAP), the Swedish Society for Medical Research (SSMF CG-24-0191-B-H-01), the Knut and Alice Wallenberg Foundation (KAW 2024.0108), and the SciLifeLab Pandemic Laboratory Preparedness Program.},
	urldate = {2026-07-07},
	journal = {eBioMedicine},
	author = {Bladh, Oscar and Pongrácz, Tamás and Aguilera, Katherina and Berkell, Matilda and Marking, Ulrika and Greilert Norin, Nina and Rihani, Ali and Alm, Jessica J. and Krammer, Florian and Åberg, Mikael and Thålin, Charlotte},
	month = jul,
	year = {2026},
	keywords = {Correlate of protection, Infection, Influenza A, Mucosal antibodies, SARS-CoV-2, Vaccines},
	pages = {106359},
}

Background Parenteral vaccines against influenza virus prevent severe disease but provide limited protection against infection, likely due to limited induction of mucosal immunity. However, direct clinical evidence for mucosal antibody-mediated protection against influenza virus infection in humans has been lacking. The aim of this study was to evaluate the role of antigen-specific mucosal IgA as a correlate of protection against influenza virus infection. We investigated H1-specific nasal IgA and serum IgG and the effect on influenza virus infection, with corresponding SARS-CoV-2 data from the same cohort as an internal comparator. Methods Using a prospective cohort study design, we analysed paired antigen-specific serum IgG and nasal IgA responses at baseline, after influenza A (H1N1) virus and SARS-CoV-2 infections, and after intramuscular influenza and SARS-CoV-2 vaccination. We then evaluated associations between baseline antibody levels, vaccination, and the risk of subsequent influenza A (H1N1) virus infection or SARS-CoV-2 infections in a 4-month home-based qPCR screening in Stockholm, Sweden (2023–2024). A Poisson regression model with a log offset for time at risk was used to evaluate if baseline antigen-specific nasal IgA or serum IgG levels or recent vaccination was associated with protection against infection. Antibody quantification was performed using a highly sensitive electrochemiluminescence immunoassay (Meso Scale Diagnostics, USA) optimised for mucosal sampling. Findings A total of 926 study participants were enrolled. After influenza A (H1N1) virus infection, H1-specific nasal IgA and serum IgG increased (p = 0.007 and p \textless 0.001 respectively), while vaccination boosted serum IgG (p = 0.006) but not nasal IgA. Baseline nasal H1-specific IgA were lower in H1N1-infected individuals (p = 0.024), and notably, baseline nasal H1-specific IgA above median was associated with reduced H1N1 infection risk (IRR 0.23, 95% CI 0.05–0.75, p = 0.026), while serum IgG and recent vaccination were not (IRR 2.03, 0.70–6.62, p = 0.206 and IRR 1.06, 0.38–3.03, p = 0.917, respectively). Moreover, each two-fold increase in baseline nasal H1-specific IgA levels was associated with a significantly lower infection risk (IRR 0.69, 95% CI 0.51–0.92; p = 0.014). Similar findings were observed for SARS-CoV-2 for mucosal IgA, whereas baseline serum spike-specific IgG above the median was also associated with reduced risk of infection. Interpretation Leveraging fit-for-purpose sampling, a validated and highly sensitive assay, and a large real-world cohort, we directly link mucosal IgA to protection against influenza virus infection. While currently employed vaccines provide robust protection against severe disease and hospital admissions, these findings highlight the need for novel approaches generating robust mucosal protection against infection per se, and the need to incorporate mucosal endpoints into next-generation vaccine development aiming for infection-blocking immunity. Funding This work was funded by the European Research Council (101164772 - D-MAP), the Swedish Society for Medical Research (SSMF CG-24-0191-B-H-01), the Knut and Alice Wallenberg Foundation (KAW 2024.0108), and the SciLifeLab Pandemic Laboratory Preparedness Program.

@article{laudon_increasing_2026,
	title = {Increasing temporal variations in growth of {Swedish} forests call for better mechanistic insights},
	volume = {618},
	issn = {0378-1127},
	url = {https://www.sciencedirect.com/science/article/pii/S0378112726004949},
	doi = {10.1016/j.foreco.2026.123996},
	abstract = {In recent decades, Swedish forests have experienced increasing variability of annual growth rate both in amplitude and frequency, jeopardizing national contribution to EU targets for carbon sequestration and climate change mitigation during periods of time. We postulate a set of hypotheses that with variable strengths can help explain and evaluate five major phases of growth variability observed the last three decades. We suggest that each phase needs to be understood based on its unique combinations of long-term monotonic trends and short-term extreme events, both that directly and indirectly influence growth rate. While the mechanistic understanding underlying this variability remains elusive, our set of hypotheses suggest that we need to move beyond traditional correlative approaches and instead combine observational data with process-based studies, large scale experiments, and modelling to will help support the development of adaptive management strategies to ensure forest resilience.},
	urldate = {2026-06-26},
	journal = {Forest Ecology and Management},
	author = {Laudon, Hjalmar and Näsholm, Torgny and Fridman, Jonas and Mensah, Alex Appiah and Lim, Hyungwoo and Jämtgård, Sandra and Nilsson, Ove},
	month = oct,
	year = {2026},
	keywords = {Adaptive forest management, Climate change, Forest production, Inter-annual variability, Nordic forests, Swedish National Forest Inventory},
	pages = {123996},
}

In recent decades, Swedish forests have experienced increasing variability of annual growth rate both in amplitude and frequency, jeopardizing national contribution to EU targets for carbon sequestration and climate change mitigation during periods of time. We postulate a set of hypotheses that with variable strengths can help explain and evaluate five major phases of growth variability observed the last three decades. We suggest that each phase needs to be understood based on its unique combinations of long-term monotonic trends and short-term extreme events, both that directly and indirectly influence growth rate. While the mechanistic understanding underlying this variability remains elusive, our set of hypotheses suggest that we need to move beyond traditional correlative approaches and instead combine observational data with process-based studies, large scale experiments, and modelling to will help support the development of adaptive management strategies to ensure forest resilience.

@article{jeong_phenotyping_2026,
	title = {Phenotyping seasonal photosynthetic energy-partitioning states in temperate evergreen conifers using hyperspectral imaging},
	volume = {8},
	issn = {2643-6515},
	url = {https://www.sciencedirect.com/science/article/pii/S2643651526000786},
	doi = {10.1016/j.plaphe.2026.100241},
	abstract = {Evergreen conifers retain needles and photosynthetic capacity during winter despite prolonged exposure to freezing temperatures and high irradiance, yet it remains unclear which aspects of this seasonal photosynthetic regulation can be reliably detected using passive optical sensing. Here, we phenotype seasonal photosynthetic energy-partitioning states in two temperate evergreen conifers, Pinus densiflora and Pinus koraiensis, by integrating chlorophyll (Chl) fluorescence imaging, pigment analyses, photosynthetic oxygen evolution, and hyperspectral reflectance imaging. Across three years, Chl fluorescence parameters (e.g., Fv/Fm, YPSII, YNPQ, and YNR) indicated reduced PSII photochemical efficiency and increased energy dissipation during winter, accompanied by changes in carotenoid-to-chlorophyll (Car/Chl) ratio, xanthophyll cycle de-epoxidation (DEPS), and photosynthetic oxygen evolution. Despite reduced PSII photochemical efficiency, photosynthetic oxygen evolution and pigment pools remained comparatively stable, indicating that reductions in PSII photochemistry were not accompanied by proportional declines in whole-leaf photosynthetic capacity. These seasonal physiological states were consistently reflected in hyperspectral vegetation indices. Photochemical Reflectance Index (PRI) showed correlations with both regulated (r = 0.57) and non-regulated light energy dissipation (r = −0.67), consistent with its sensitivity to Car/Chl ratio (r = −0.87) and DEPS (r = −0.85). Indices including Fluorescence Curvature Index (FCI) and Ratio Analysis of Reflectance Spectra chlorophyll b (RARSb) showed consistent seasonal correlations with photosynthetic oxygen evolution (r = −0.68 and −0.68), while also reflecting variation in pigment composition (e.g., Chl content; r = 0.73 and 0.78). Drone-based hyperspectral imaging further indicated that these needle-level physiological patterns were detected at the canopy level under the conditions examined. Indices such as FCI exhibited clear seasonal profiles, with separation between summer and winter values. By framing seasonal photosynthetic regulation as a phenotyping problem rather than a mechanistic one, this study provides a data-supported proof-of-concept framework for non-invasive, scalable monitoring of evergreen forests using hyperspectral sensing.},
	number = {3},
	urldate = {2026-06-26},
	journal = {Plant Phenomics},
	author = {Jeong, Seok-Won and Choi, Myoung-Goo and Kim, Young-Won and Kim, Jaewook and Hurry, Vaughan and Ivanov, Alexander G. and Chow, Wah Soon and Park, Youn-Il},
	month = sep,
	year = {2026},
	keywords = {Chlorophyll fluorescence, Cold acclimation, Hyperspectral vegetation indices, PSII energy partitioning, Temperate conifers},
	pages = {100241},
}

Evergreen conifers retain needles and photosynthetic capacity during winter despite prolonged exposure to freezing temperatures and high irradiance, yet it remains unclear which aspects of this seasonal photosynthetic regulation can be reliably detected using passive optical sensing. Here, we phenotype seasonal photosynthetic energy-partitioning states in two temperate evergreen conifers, Pinus densiflora and Pinus koraiensis, by integrating chlorophyll (Chl) fluorescence imaging, pigment analyses, photosynthetic oxygen evolution, and hyperspectral reflectance imaging. Across three years, Chl fluorescence parameters (e.g., Fv/Fm, YPSII, YNPQ, and YNR) indicated reduced PSII photochemical efficiency and increased energy dissipation during winter, accompanied by changes in carotenoid-to-chlorophyll (Car/Chl) ratio, xanthophyll cycle de-epoxidation (DEPS), and photosynthetic oxygen evolution. Despite reduced PSII photochemical efficiency, photosynthetic oxygen evolution and pigment pools remained comparatively stable, indicating that reductions in PSII photochemistry were not accompanied by proportional declines in whole-leaf photosynthetic capacity. These seasonal physiological states were consistently reflected in hyperspectral vegetation indices. Photochemical Reflectance Index (PRI) showed correlations with both regulated (r = 0.57) and non-regulated light energy dissipation (r = −0.67), consistent with its sensitivity to Car/Chl ratio (r = −0.87) and DEPS (r = −0.85). Indices including Fluorescence Curvature Index (FCI) and Ratio Analysis of Reflectance Spectra chlorophyll b (RARSb) showed consistent seasonal correlations with photosynthetic oxygen evolution (r = −0.68 and −0.68), while also reflecting variation in pigment composition (e.g., Chl content; r = 0.73 and 0.78). Drone-based hyperspectral imaging further indicated that these needle-level physiological patterns were detected at the canopy level under the conditions examined. Indices such as FCI exhibited clear seasonal profiles, with separation between summer and winter values. By framing seasonal photosynthetic regulation as a phenotyping problem rather than a mechanistic one, this study provides a data-supported proof-of-concept framework for non-invasive, scalable monitoring of evergreen forests using hyperspectral sensing.