Biology subjects

Caldeira, M.

Publications and source records attributed to Caldeira, M..

5 recordsLinked to original sources

bioRxiv2026

Intra-annual precipitation variability mutes or magnifies the impact of wet and dry years on plant biomass.

As the atmosphere warms, both the amount and timing of precipitation are changing, but how those two trends interact to influence plant growth remains unresolved. Using 5-15 years of data from 48 globally distributed grassland sites, we quantified how the temporal distribution of precipitation within the year (evenness) interacts with annual precipitation amount and nutrient limitation to influence plant biomass. Annual precipitation anomalies had a large influence on plant biomass when intra-annual precipitation was more evenly distributed (frequent small events) and little impact when less even (infrequent large events). This relationship was consistent across aridity gradients and nutrient limitations and strongest in systems with warm wet seasons. Our work shows that the response of plant systems to changes in annual precipitation amount are largely dependent on how evenly it is temporally distributed.

ecology↗

bioRxiv2025

Lipid droplet dysmetabolism affects cell homeostasis in an in vitro model of Alzheimer disease

Lipid droplets (LD) are dynamic organelles involved in neutral lipid storage, energy homeostasis, and can prevent lipotoxicity and oxidative distress. LD dysmetabolism has been considered a pathological hallmark in neurodegenerative disorders, including Alzheimers disease (AD). In this study, we investigated the alterations in LD metabolism and their impact on mitochondria-associated membranes (MAM) in an in vitro model of AD, namely the mouse neuroblastoma cell (N2A) line overexpressing the amyloid precursor protein with the familial Swedish mutation (APPswe). In APPswe cells, we found depletion of LD associated with an accumulation of free fatty acids that can be related with the observed LD degradation by chaperone-mediated autophagy. In these cells we also found decreased levels of seipin, which might contribute to triacylglycerol accumulation. These lipid alterations are associated with increased levels of ROS and lipid peroxidation in APPswe cells. The pharmacological modulation of DGAT1, that mediates triacylglycerol synthesis, normalized LD size and improved ER-mitochondria contacts and mitochondrial function in APPswe cells. In summary, these observations suggest the involvement of altered LD metabolism in AD pathophysiology, which impact on MAM and mitochondria function leading to cell dyshomeostasis. Our findings also support the idea that LD are relevant therapeutic targets in AD. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=111 SRC="FIGDIR/small/658644v1_ufig1.gif" ALT="Figure 1"> View larger version (41K): org.highwire.dtl.DTLVardef@de3fc6org.highwire.dtl.DTLVardef@12d1f2forg.highwire.dtl.DTLVardef@15a5185org.highwire.dtl.DTLVardef@9e1655_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2025

Short- and long-term effects of uterine disease on oocyte developmental capacity in postpartum dairy cows

The hypothesis was that early postpartum uterine disease would reduce the developmental capacity of oocytes thus contributing to the reduced fertility of dairy cows with uterine disease. Dairy cows were diagnosed healthy or with metritis at 7 to 10 d postpartum. The reproductive tract was collected at approximately 1 mo (Exp. 1) or approximately 80 or 165 d (Exp. 2) postpartum for the collection of cumulus-oocyte complexes (COC). The COC were matured, co- incubated with sperm for fertilization, and cultured to the blastocyst stage (8 d) in vitro. For Exp.1, the disease diagnosis (healthy or metritis) did not affect the number of collected COC or the subsequent embryo development to the blastocyst stage. The presence of purulent material in the uterine lumen (endometritis) at time of oocyte collection, however, was associated with a reduced cleavage rate evaluated 3 d following fertilization. For Exp. 2, there was no effect of disease diagnosis (healthy or metritis) on the number of COC or their subsequent development. Reduced cleavage rates were observed in COC retrieved from cows slaughtered at 80 d postpartum, but not at 165 d postpartum, and this reduction was associated with a vaginal microbiome indicative of uterine disease at 4 to 5 wk postpartum. Regression analyses that included plasma haptoglobin or energy metabolite concentrations or uterine bacterial genera abundance did not explain a large percentage of the variation in oocyte development in vitro. We conclude that there is an effect of uterine disease at one month postpartum on the oocyte and its capacity for development (Exp. 1) and this effect may be present at 80 d postpartum (Exp. 2). In later postpartum cows (165 d postpartum; Exp. 2) there was no effect of uterine disease on in vitro oocyte development. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=141 SRC="FIGDIR/small/636469v1_ufig1.gif" ALT="Figure 1"> View larger version (44K): org.highwire.dtl.DTLVardef@7ab5d7org.highwire.dtl.DTLVardef@3845e3org.highwire.dtl.DTLVardef@743f52org.highwire.dtl.DTLVardef@1e95c38_HPS_FORMAT_FIGEXP M_FIG C_FIG HIGHLIGHTSO_LIOocytes collected at 1 month postpartum from dairy cows with endometritis (purulent uterine lumen) had a lower cleavage rate following in vitro fertilization when compared with oocytes collected from healthy cows (Exp. 1). C_LIO_LIOocytes collected at approximately 80 d postpartum from dairy cows with evidence of uterine disease at 4 to 5 wk postpartum had a lower cleavage rate following in vitro fertilization but this disease-associated difference was not observed when oocytes were collected from cows later postpartum (approximately 165 d postpartum; Exp. 2). C_LIO_LIRegardless of the study (Exp. 1 or 2), uterine disease primarily affected the percentage of oocytes that cleaved after fertilization. C_LIO_LIStatistical associations between circulating metabolites or relative abundance of uterine bacteria were either not significant or explained only a small percentage of the variation in the in vitro embryo development in either experiment. C_LI

physiology↗

bioRxiv2024

Mitochondria drive microglial NRLP3 inflammasome activation via TSPO

Uncontrolled microglial response is core to neuroinflammatory brain diseases. The correlation between the mitochondrial protein TSPO and inflammation has so far failed to explain whether TSPO positively or negatively regulates microglial function. The recent evidence on the species specificity of TSPO in microglia demands a deeper understanding of the protein biology in these brain-resident macrophages. To this end, we have here enrolled a murine model of microglial cells showing that TSPO is required for the priming of mitochondria to inflammation and a conduit for its escalation. Namely, in response to inflammatory cues TSPO is stabilised on the mitochondria where it binds and sequesters NOD-like receptor (NLR) protein (i), represses the PARK2-mediated mitophagy (ii) and engages the retrograde communication with the nucleus via the accumulation of the Nf-kB to promote the expression of pro-inflammatory genes (iii). Notably, the TSPO sustained inflammatory response drives cellular demise and ultimately leads to excitotoxicity (iv). Our findings advance the current knowledge of TSPO widening the understanding of mitochondria in inflammation and indicating a target for their regulation.

cell biology↗

bioRxiv2021

Multiple resource limitations explain biomass-precipitation relationships in grasslands

Interannual variability in grassland primary production is strongly driven by precipitation, nutrient availability and herbivory, but there is no general consensus on the mechanisms linking these variables. If grassland biomass is limited by the single most limiting resource at a given time, then we expect that nutrient addition will not affect biomass production at arid sites. We conducted a distributed experiment manipulating nutrients and herbivores at 44 grassland sites in 8 regions around the world, spanning a broad range in aridity. We estimated the effects of 5-11 years of nutrient addition and herbivore exclusion treatments on precipitation sensitivity of biomass (proportional change in biomass relative to proportional change in rainfall among years), and the biomass in the driest year (to measure treatment effects when water was most limiting) at each site. Grazer exclusion did not interact with nutrients to influence driest year biomass or sensitivity. Nutrient addition increased driest year biomass by 74% and sensitivity by 0.12 (proportional units), and that effect did not change across the range of aridity spanned by our sites. Grazer exclusion did not interact with nutrients to influence sensitivity or driest year biomass. At almost half of our sites, the previous year's rainfall explained as much variation in biomass as current year precipitation. Overall, our distributed fertilization experiment detected co-limitation between nutrients and water governing grasslands, with biomass sensitivity to precipitation being limited by nutrient availability irrespective of site aridity and herbivory. Our findings refute the classical ideas that grassland plant performance is limited by the single most limiting resource at a site. This suggests that nutrient eutrophication will destabilize grassland ecosystems through increased sensitivity to precipitation variation.

ecology↗