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Rowland, L.

Publications and source records attributed to Rowland, L..

15 recordsLinked to original sources

Beyond air-seeding: Dynamic, multiphase interactionsreveal a two-step mechanism of embolism propagation inangiosperm xylem

BackgroundThe mechanism underlying drought-induced embolism in angiosperm xylem has been attributed to air-seeding. This concept describes the bulk flow of gas from embolised to neighbouring conduits through the penetration of gas-liquid menisci across pores in interconduit pit membranes. While there is compelling evidence for the spatial propagation of embolism, air-seeding rests on various simplifying assumptions. Among others, air-seeding presumes that xylem sap has physical properties comparable to pure water, that pit membranes can be approximated as structures with simple pores, and that embolism occurs whenever a gas-liquid interface crosses a pit membrane. ScopeRecent experimental and theoretical work demonstrates that the biophysical conditions and processes governing gas-liquid interactions at interconduit pit membranes are fundamentally more dynamic and complex than assumed by air-seeding. These phenomena include: (1) gas movement through constriction pore networks, (2) insoluble, polar lipids at conduit surfaces and interfaces, (3) dynamic surface tension of xylem sap that depends on the local packing density of interfacial lipids, (4) bubble snap-off dynamics within pit membranes, (5) surfactant-stabilized nanobubbles in sap that is oversaturated with dissolved gas, and (6) electrostatic interactions between charged interfaces. Importantly, embolism propagation involves bubble generation and embolism formation as distinct, temporarily and spatially separated processes. Embolism formation occurs when nanobubbles become unstable, whereas nanobubbles below critical stability thresholds can remain stable in sap-filled conduits. ConclusionsTogether, these findings reconfirm that pit membranes function as safety valves enabling water transport according to the cohesion-tension theory, and provide mechanistic insights into embolism propagation. They address the question why plants do not suffer constant embolism formation despite negative xylem pressures. We conclude that a revised framework explicitly accounting for the 3D structure of pit membranes, and multiphase, dynamic processes operating within them are required to explain the biophysics underlying water transport and embolism resistance in angiosperm xylem.

plant biology↗

Obesity-Driven Lung Lipidome Remodeling Suppresses NK Cell Activation and Antiviral Immunity to Influenza Infection

Obesity is a major risk factor for severe influenza A virus (IAV) infection, however, the innate immune mechanisms underlying this increased vulnerability remain unclear. Here, we identify significant defects in natural killer (NK) cell antiviral responses in mice with diet-induced obesity. In lean mice, NK cells are critical for protection as NK cell depletion during IAV infection led to increased lung viral load, morbidity, and mortality. In contrast, in obese mice NK cell depletion had minimal impact on viral replication or survival. Notably, IAV infection in obese mice recapitulated the phenotype observed in NK cell-depleted lean mice, indicating that obesity is associated with preexisting NK cell dysfunction. Following IAV infection, obese NK cells in the lung were functionally impaired with diminished activation (CD69+), cytokine production (IFN-{gamma}), and cytolytic activity (Granzyme B) accompanied by defects in the mTOR signaling pathway and reduced glycolytic and oxidative metabolism. Bulk and spatial lipidomics revealed obesity and infection-driven remodeling of the lung lipidome. We observed increased triglyceride accumulation, abundance of long-chain free fatty acids, and a shift toward monounsaturated phospholipid species, reshaping the lung microenvironment that coincides with NK cell metabolic dysfunction. Consistent with this lipid-rich environment, obese NK cells sustained high expression of the lipid transporter CD36 post-IAV infection and accumulation of intracellular lipids (LipidTOX+), consistent with mechanisms known to suppress NK cell function. Notably, short-term weight loss (4 weeks) was sufficient to restore NK cell metabolism, antiviral function, and survival following IAV infection. These findings uncover a lipid-associated mechanism regulating NK cell function and show it plays a critical role in defense against infection and that it is dysfunctional in obesity. We suggest that targeting immunometabolism could lead to new antiviral therapies and potentially improve vaccine efficacy, especially in high-risk populations such as obesity. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=101 SRC="FIGDIR/small/710186v1_ufig1.gif" ALT="Figure 1"> View larger version (42K): org.highwire.dtl.DTLVardef@313263org.highwire.dtl.DTLVardef@1e31111org.highwire.dtl.DTLVardef@758ba6org.highwire.dtl.DTLVardef@12372d0_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

Brazil Seed Transfer Zones: Supporting Seed Sourcing for Climate-Resilient Ecosystem Restoration

O_LIEcosystem restoration is key to jointly address the biodiversity, climate, and social inequality crises. In Brazil, large-scale seed-based restoration is gaining momentum, but a national framework to match seed sources with planting sites is still lacking, undermining long-term success. C_LIO_LIWe developed the first Seed Transfer Zones (STZs) for Brazil using 25 environmental variables. We assessed restoration supply and demand within each STZ and projected the zones into the future under contrasting climate change scenarios. C_LIO_LIWe identified 48 STZs, distributed across Brazils six major vegetation regions (Amazon, Cerrado, Atlantic Forest, Caatinga, Pantanal, and Pampa). Overlaying the STZs with data on seed collection capacity and restoration opportunities revealed priority regions where seed supply is unlikely to meet demand (e.g., Cerrado). Future climate projections also indicate substantial reshaping of STZs, with 51-88% of Brazils land area expected to experience mismatches between current and future seed zones. C_LIO_LIThe creation of Brazils first STZs provides a scalable framework to guide seed sourcing for restoration, aligning supply with demand, and future-proofing projects to deliver lasting benefits for biodiversity, climate, and society. C_LI Societal Impact StatementTens of millions of hectares of degraded land in Brazil are in need of ecosystem restoration to achieve national and global biodiversity and climate goals. Sowing genetically diverse native seeds is key to restoring degraded lands to climate-resilient landscapes, but we still lack guidance on how to effectively match seed sources to restoration sites across broad geographic scales, within the context of a changing climate. We addressed this by identifying 48 Seed Transfer Zones (STZs) based on current and expected future climatic conditions. These zones will help ensure that the right seeds are used in the right places, enabling more effective and climate-smart restoration for nature and people.

ecology↗

Thermogenic adipocytes alleviate hepatic steatosis and insulin resistance via macrophage cytokine secretion in obese mice

The Nrip1 gene encodes the protein Rip140, which suppresses nuclear receptors that regulate energy metabolism. Here we show adipocyte-selective deficiency of Nrip1 (AdNrip1KO) in mice causes a striking expansion of alternatively activated, M2-like macrophages within subcutaneous inguinal adipose tissue (iWAT) in addition to the appearance of thermogenic adipocytes expressing uncoupling protein 1 (UCP1). AdNrip1KO mice are less cold sensitive but showed no differences in whole body energy expenditure or food intake compared to control mice at 22 {degrees}C. Strikingly, AdNrip1KO mice on HFD display markedly attenuated hepatic steatosis and insulin resistance compared to control mice on HFD. Secreted factors that might mediate this crosstalk from adipose tissue to liver were searched for by iWAT RNAseq. Unexpectedly, upregulation of genes associated with cytokines and cytokine receptor signaling were the most highly correlated with adipocyte-selective Nrip1 loss in obese mice. Furthermore, the top upregulated genes that encode secreted proteins in AdNrip1KO iWAT are most highly expressed in macrophages, not adipocytes. This list included the IL-1b antagonist IL-1rn, known to attenuate hepatic steatosis and insulin resistance. Indeed, the IL-1rn protein in AdNrip1KO mice was found to circulate at levels we previously reported strongly attenuates hepatic steatosis and glucose tolerance in obese mice. Taken together, these results suggest a paradigm for metabolic crosstalk from thermogenic adipose tissue to liver that is mediated by IL-1rn and potentially other factors secreted from M2-like macrophages within beige adipose tissues. Graphic Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=123 SRC="FIGDIR/small/667482v1_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@15fb086org.highwire.dtl.DTLVardef@13e6689org.highwire.dtl.DTLVardef@1bde77borg.highwire.dtl.DTLVardef@a83f2e_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIAdipocyte Nrip1 deficiency (AdNrip1KO) strongly promotes adipose browning C_LIO_LIMouse AdNrip1KO polarizes adipose tissue macrophages towards M2-like C_LIO_LIAdNrip1KO reduces the hepatic fat and insulin resistance of obese mice C_LIO_LIAdNrip1KO adipose tissue macrophages secrete IL-1rn, known to mitigate hepatic fat and insulin resistance C_LI

physiology↗

Enhanced cell aggregation in the Chlamydomonas reinhardtii rbo1 mutant in response to multifactorial stress combination

Global change factors associated with climate change and increased pollution are subjecting plants, microbes, and different ecosystems to conditions of multifactorial stress combination (MFSC). While recent studies centered on the effects of MFSC on different plants and ecosystems, much less is known about how these conditions impact unicellular organisms. Here, we report on the physiological and proteomic responses of wild type and respiratory burst oxidase homolog 1 (rbo1) mutant cells of Chlamydomonas reinhardtii to a MFSC of 5 different abiotic stresses. While several similarities were found between plant and C. reinhardtii responses to MFSC, our work revealed that MFSC induces aggregation in the unicellular organism C. reinhardtii. We further show that MFSC induced aggregation is enhanced in the rbo1 mutant and can be triggered by H2O2. As aggregation typically leads to reduced growth, respiration and/or photosynthesis, enhanced aggregation of unicellular organisms in different ecosystems subjected to MFSC could explain part of the negative impacts of MFSC on the services they provide. Our findings shed new light on the response of unicellular organisms to MFSC and suggest that one of the main drivers leading to multicellularity during evolution was early conditions of MFSC under an oxygenated environment.

plant biology↗

Unraveling the molecular mechanism underlying the anticancer activity of CISD2/NAF-144-67

We recently reported on the development of a unique cancer-targeting peptide called NAF-144-67 (derived from CISD2/NAF-1). NAF-144-67 selectively permeates the plasma membrane (PM) of cancer cells, but not healthy cells, causing the activation of apoptotic and ferroptotic cell death pathways specifically in cancer cells. NAF-144-67 also targets and shrinks human breast and ovarian cancer tumors in a xenograft mice model system without any apparent side effects. Although the specific permeation of NAF-144-67 through cancer cell PMs was studied, and its cancer killing effects validated in vitro and in vivo, little is known about how NAF-144-67 exerts its biological activity once it enters cancer cells. Here, we report that NAF-144-67 targets the CISD2/NAF-1 protein of cancer cells and disrupts its homodimeric structure. We further reveal that a peptide derived from the same domain of the human CISD1 (mitoNEET; mNT19-42) protein, a close family member to CISD2, has no killing activity towards cancer cells, and that dimers of NAF-144-67 (at two different orientations) have higher anticancer activity compared to monomeric NAF-144-67. Our findings shed new light on the biological activity of NAF-144-67 and bring it closer to becoming a potential new anticancer drug.

cancer biology↗

Thermal acclimation of stem respiration reduces global carbon burden

Stem respiration is a key driver of carbon flux from ecosystems to the atmosphere, yet its response to global warming remains poorly constrained. In particular it has been proposed that stem respiration acclimates to changing temperatures, which could have large implications for carbon cycling under climate change, but no theory exists to predict acclimated respiration rates. Here, we hypothesized that stem respiration is physiologically linked to transpiration in order to maintain hydraulic continuity. We then use that linkage, combined with Eco-evolutionary optimality theory, to develop a theoretical prediction of the temperature sensitivity of both acclimated and instantaneous stem respiration. Leveraging an extensive global dataset, we observe temperature sensitivities of stem respiration across geographical and seasonal variations that are consistent with this prediction. Our findings reveal that stem respiration contributes approximately a quarter of the global above-ground auto-trophic respiration, with an estimated annual emission of around 11.20 {+/-} 5.88 Pg C--comparable to total anthropogenic emissions. Importantly, incorporating thermal acclimation of stem respiration into projections significantly reduces predicted land ecosystem carbon emissions by 4.41 and 9.56 Pg C under the SSP126 and SSP585 scenarios, respectively, for the 21st century.

ecology↗

Global variation in the ratio of sapwood to leaf area explained by optimality principles

The sapwood area supporting a given leaf area (vH) reflects a coordinated coupling between carbon uptake, water transport and loss at a whole plant level. Worldwide variation in vH reflects diverse plants strategies adapt to prevailing environments, and impact the evolution of global carbon and water cycles. Why such a variation has not been convincingly explained yet, thus hinder its representation in Earth System Models. Here we hypothesize that optimal vH tends to mediate between plant hydraulics and leaf photosynthesis so that leaf water loss matches water supply. By compiling and testing against two extensive datasets, we show that our hypothesis explains nearly 60% of vH variation responding to light, vapour pressure deficit, temperature, and sapwood conductance in a quantitively predictable manner. Sapwood conductance or warming-enhanced hydraulic efficiency reduces the demand on sapwood area for a given total leaf area and, whereas brightening and air dryness enhance photosynthetic capacities consequently increasing the demand. This knowledge can enrich Earth System Models where carbon allocation and water hydraulics play key roles in predicting future climate-carbon feedback.

ecology↗

Propagation of a rapid cell-to-cell H2O2 signal over long distances in a monolayer of cardiomyocyte cells

Cell-to-cell communication plays a cardinal role in the biology of multicellular organisms. H2O2 is an important cell-to-cell signaling molecule involved in the response of mammalian cells to wounding and other stimuli. We previously identified a signaling pathway that transmits wound-induced cell-to-cell H2O2 signals within minutes over long distances, measured in centimeters, in a monolayer of cardiomyocytes. Here we report that this long-distance H2O2 signaling pathway is accompanied by enhanced accumulation of cytosolic H2O2 and altered redox state in cells along its path. We further show that it requires the production of superoxide, as well as the function of gap junctions, and that it is accompanied by changes in the abundance of hundreds of proteins in cells along its path. Our findings highlight the existence of a unique and rapid long-distance H2O2 signaling pathway that could play an important role in different inflammatory responses, wound responses/healing, cardiovascular disease, and/or other conditions. HighlightsO_LIWounding induces an H2O2 cell-to-cell signal in a monolayer of cardiomyocytes. C_LIO_LIThe cell-to-cell signal requires H2O2 and O2{middle dot}- accumulation along its path. C_LIO_LIThe signal propagates over several centimeters changing the redox state of cells. C_LIO_LIChanges in the abundance of hundreds of proteins accompanies the signal. C_LIO_LIThe cell-to-cell signal requires paracrine and juxtacrine signaling. C_LI Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=70 SRC="FIGDIR/small/572374v1_ufig1.gif" ALT="Figure 1"> View larger version (18K): org.highwire.dtl.DTLVardef@3b3806org.highwire.dtl.DTLVardef@1db37fcorg.highwire.dtl.DTLVardef@138bdd7org.highwire.dtl.DTLVardef@377402_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

CISD3 is required for Complex I function, mitochondrial integrity, and skeletal muscle maintenance

Mitochondria play a central role in muscle metabolism and function. In skeletal muscles, a unique family of iron-sulfur proteins, termed CISD proteins, support mitochondrial function. The abundance of these proteins declines with aging leading to muscle degeneration. Although the function of the outer mitochondrial proteins CISD1 and CISD2 has been defined, the role of the inner mitochondrial protein CISD3, is currently unknown. Here we show that CISD3 deficiency in mice results in muscle atrophy that shares proteomic features with Duchenne Muscular Dystrophy. We further reveal that CISD3 deficiency impairs the function and structure of skeletal muscle mitochondria, and that CISD3 interacts with, and donates its clusters to, Complex I respiratory chain subunit NDUFV2. These findings reveal that CISD3 is important for supporting the biogenesis and function of Complex I, essential for muscle maintenance and function. Interventions that target CISD3 could therefore impact muscle degeneration syndromes, aging, and related conditions.

cell biology↗

ROS are evolutionary conserved cell-to-cell signals

Cell-to-cell communication is fundamental to multicellular organisms and unicellular organisms living in a microbiome. A unique cell-to-cell communication mechanism that uses reactive oxygen species (ROS) as a signal (termed the ROS wave) was recently identified in flowering plants. Here we report that a ROS-mediated cell-to-cell signaling process, like the ROS wave, can be found in ferns, mosses, unicellular algae, amoeba, mammalian cells, and isolated hearts. We further show that this process can be triggered by a localized stress treatment or H2O2 application and blocked by inhibition of NADPH oxidases, and that in unicellular algae, it communicates important stress-response signals between cells. Taken together, our findings suggest that cell-to-cell ROS signaling evolved before unicellular and multicellular organisms diverged. The finding of a ROS wave-like signaling process in mammalian cells further contributes to our understanding of different diseases and could impact the development of new drugs that target cancer or heart disease.

plant biology↗

Paradoxical activation of SREBP1c and de novo lipogenesis by hepatocyte-selective ACLY depletion in obese mice.

Hepatic steatosis associated with high fat diets, obesity and type 2 diabetes is thought to be the major driver of severe liver inflammation, fibrosis, and cirrhosis. Cytosolic acetyl-coenzyme A (AcCoA), a central metabolite and substrate for de novo lipogenesis (DNL), is produced from citrate by ATP-citrate lyase (ACLY) and from acetate through AcCoA synthase short chain family member 2 (ACSS2). However, the relative contributions of these two enzymes to hepatic AcCoA pools and DNL rates in response to high fat feeding is unknown. We report here that hepatocyte-selective depletion of either ACSS2 or ACLY caused similar 50% decreases in liver AcCoA levels in obese mice, showing that both pathways contribute to generation of this DNL substrate. Unexpectedly however, the hepatocyte ACLY depletion in obese mice paradoxically increased total DNL flux measured by D2O incorporation into palmitate, while in contrast ACSS2 depletion had no effect. The increase in liver DNL upon ACLY depletion was associated with increased expression of nuclear sterol regulatory element-binding protein 1c (SREBP1c) and of its target DNL enzymes. This upregulated DNL enzyme expression explains the increased rate of palmitate synthesis in ACLY depleted livers. Furthermore, this increased flux through DNL may also contribute to the observed depletion of AcCoA levels due to its increased conversion to Malonyl CoA (MalCoA) and palmitate. Together, these data indicate that in HFD fed obese mice, hepatic DNL is not limited by its immediate substrates AcCoA or MalCoA, but rather by activities of DNL enzymes.

molecular biology↗

Fiber-parenchyma trade-off underlies changes in tropical forest structure and xylem architecture across a soil water gradient

O_LIWood anatomical traits can underpin tropical forest structural and functional changes across soil water gradients and therefore could improve our mechanistic understanding of how plants adapt to environmental change. C_LIO_LIWe assessed how the variation in the forest maximum height (Hmax), stem diameter, and wood density (WD) is associated with variation in xylem traits (area of fibers and parenchyma, conductive area [CondA, sum of all vessels lumens], vessel lumen area [VLA], vessel density [VD], and vessel wall reinforcement [VWR]) across 42 plots of a Brazilian Atlantic Forest habitat that span strong soil water gradients. C_LIO_LIWe found that in wetter communities, greater height and lower WD were associated with greater parenchyma area (capacitance), and lower fibers, VD, VWR. Contrastingly, in drier communities, lower height was associated with higher fiber area (xylem reinforcement), WD, VD, and VWR, while parenchyma area and vessels are reduced. C_LIO_LITree communities vary from conservative resource-use and structurally dependent hydraulic safety (Fibers) to acquisitive resource-use and capacitance dependent hydraulic safety (parenchyma). Such a fiber-parenchyma trade-off (FPT) underlies the variation in tree height across a soil water gradient. Wood anatomy is fundamental to understanding and predicting the impacts of environmental change on forest structure. C_LI

ecology↗

New insights into large tropical tree mass and structure from direct harvest and terrestrial lidar

A large portion of the terrestrial vegetation carbon stock is stored in the above-ground biomass (AGB) of tropical forests, but the exact amount remains uncertain, partly due to the lack of measurements. To date, accessible peer-reviewed data are available for just 10 large tropical trees in the Amazon that have been harvested and directly measured entirely via weighing. Here, we harvested four large tropical rainforest trees (stem diameter: 0.6-1.2m, height: 30-46m, AGB: 3960-18 584 kg) in intact old-growth forest in East Amazonia, and measured above-ground green mass, moisture content and woody tissue density. We first present rare ecological insights provided by these data, including unsystematic intra-tree variations in density, with both height and radius. We also found the majority of AGB was usually found in the crown, but varied from 42-62%. We then compare non-destructive approaches for estimating the AGB of these trees, using both classical allometry, and new lidar-based methods. Terrestrial lidar point clouds were collected pre-harvest, on which we fitted cylinders to model woody structure, enabling retrieval of volume-derived AGB. Estimates from this approach were more accurate than allometric counterparts (mean tree-scale relative error: 3% vs. 15%), and error decreased when up-scaling to the cumulative AGB of the four trees (1% vs. 15%). Further, whilst allometric error increased four-fold with tree size over the diameter range, lidar error remained constant. This suggests error in these lidar-derived estimates is random and additive. Were these results transferable across forest scenes, terrestrial lidar methods would reduce uncertainty in stand-scale AGB estimates, and therefore advance our understanding of the role of tropical forests in the global carbon cycle.

ecology↗

Single Cell RNA Profiling Reveals Adipocyte to Macrophage Signaling Sufficient to Enhance Thermogenesis

The "browning" of inguinal white adipose tissue (iWAT) through increased abundance of thermogenic beige/brite adipocytes is induced by cold exposure and many other perturbations in association with beneficial systemic metabolic effects. Adipose browning is reported to require activation of sympathetic nerve fibers (SNF), aided by alternately activated macrophages within iWAT. Here we demonstrate the first example of a non-cell autonomous pathway for iWAT browning that is fully independent of SNF activity. Thus, the strong induction of thermogenic adipocytes prompted by deletion of adipocyte fatty acid synthase (iAdFASNKO mice) was unaffected by denervation or the deletion of SNF modulator Neuregulin-4. However, browning of iWAT in iAdFASNKO mice does require adipocyte cAMP/protein kinase A signaling, as it was blocked in adipocyte- selective Fasn/Gs double KO mice. Single-cell transcriptomic analysis of iAdFASNKO mouse adipose stromal cells revealed increased macrophages displaying gene expression signatures of the alternately activated type. Mechanistically, depletion of such phagocytic immune cells in iAdFASNKO mice fully abrogated appearance of thermogenic adipocytes in iWAT. Altogether, these findings reveal an unexpected pathway of cAMP/PKA-dependent iWAT browning that is initiated by adipocyte signals and caused by macrophage-like cells independent of sympathetic neuron involvement.

physiology↗