Biology subjects

Mo, L.

Publications and source records attributed to Mo, L..

15 recordsLinked to original sources

bioRxiv2026

A pretrained unified model enables cellular functional profile prediction and multi-objective virtual drug screening

Cells are characterized by molecular states, coordinated molecular interactions, regulatory programs, and responses to perturbations. Systematic mapping of these cellular functional profiles across biological contexts remains experimentally costly and fragmented. Here we present InsilicoCell, a pretrained multi-modal, multi-task model that unifies prediction of cellular functional profiles spanning molecular states, molecular interactions, and perturbation-induced responses. Built on a supervised transformer architecture and pretrained on more than 88 million measurements across seven tasks, including drug sensitivity, drug-induced gene expression, and drug-protein binding, InsilicoCell learns a shared representation that links molecular profiles to cellular phenotypes, improves performance over task-specific models, and generalizes to unseen entities, contexts, and conditions. InsilicoCell extends beyond cell line systems to patient, spatial and single-cell settings, and enables multi-objective virtual drug screening. It identifies novel candidate compounds with experimental validation, including c-Myc activity inhibitors, antifibrotic agents and stemness-inducing compounds. Together, InsilicoCell provides a scalable framework for predictive cellular biology and therapeutic discovery.

bioinformatics↗

bioRxiv2026

TLR7 Signaling Regulates Embryonic Hematopoietic Stem Cell Development by Sensing microRNA-146a in Vertebrates

The specification of hematopoietic stem cells (HSCs) is tightly regulated by multiple transcription factors and signaling pathways. Inflammatory signaling is pivotal for embryonic HSC development, but the mechanisms that activate it in vivo remain poorly understood. Here, we show that Toll-like receptor 7 (TLR7) is essential for the emergence of embryonic HSC in both zebrafish and mouse embryos. TLR7 deficiency reduces HSC numbers but not primitive or definitive progenitors. Conversely, the TLR7 agonist R848 enhances embryonic HSC development. Mechanistically, TLR7 signaling acts through interferon regulatory factor 5 (IRF5) to induce the expression of inflammatory cytokines, which subsequently activate Notch signaling to promote HSC emergence through a non-cell-autonomous mechanism. Notably, we identify microRNA-146a (miR-146a) as a potential endogenous activator of TLR7, inducing inflammatory signaling and promoting HSC development. Pharmacological treatment with miR-146a significantly increases HSC numbers in zebrafish embryos. Together, our findings reveal a crucial role for miR-146a-TLR7-IRF5 signaling axis in HSC emergence, providing insights into the endogenous factors that drive tonic inflammatory signaling during normal hematopoiesis and suggesting the translational potential of TLR7 agonists and miR-146a for stem-cell-based therapeutics. Significance StatementThe embryonic origin of hematopoietic stem cells (HSCs) requires inflammatory signals, but the endogenous factor that triggers this process remains elusive. We identify microRNA-146a (miR-146a) as a natural activator of Toll-like Receptor 7 (TLR7) signaling, which is essential for HSC emergence. This miR-146a-TLR7 axis functions through IRF5 and inflammatory cytokines to activate the Notch signaling, specifically promoting embryonic HSC development. Our work addresses the critical question of endogenous ligands that mediate tonic inflammatory signaling in normal hematopoiesis, uncovers novel crosstalk between miRNAs and innate immunity in HSC specification, and identifies promising candidates for stem cell-based therapeutics.

developmental biology↗

bioRxiv2025

Developmental constraints mediate the summer solstice reversal of climate effects on European beech bud set

Accurate projections of temperate tree growing seasons under climate change require representing developmental constraints that determine tree resource allocation. Recent work has identified a phenological "switch point" after the summer solstice (21 June), with pre-solstice warming advancing autumn phenology and post-solstice warming delaying it. Here, we propose this switch is flexible and occurs at the compensatory point between the antagonistic effects of early-season development and late-season temperature. We performed trans-solstice climate manipulation experiments on potted European beech (Fagus sylvatica) saplings to test (i) how spring leaf-out timing and June-August temperatures influence end-of-season timing (bud set and leaf senescence [50% loss of leaf chlorophyll content]), and (ii) whether daytime and nighttime temperatures before and after the solstice have different effects, given that trees primarily grow at night. Bud set and leaf senescence responses were tightly coupled (R2 = 0.49), with bud responses being generally stronger. Each day delay in spring leaf-out delayed bud set by 0.24 {+/-} 0.06 days and senescence by 0.22 {+/-} 0.08 days. Post-solstice full-day cooling in July delayed autumn phenology in late-leafing individuals (bud set +4.9 {+/-} 2.6 days; senescence +3.1 {+/-} 2.8 days) but had negligible impact on early-leafing trees (bud set +1.4 {+/-} 2.6 days; leaf senescence +2.2 {+/-} 2.8 days). Conversely, August full-day cooling advanced both stages. Daytime cooling before the solstice had no effect, while after the solstice it advanced autumn phenology. Nighttime cooling always delayed bud set. These findings support the Solstice-as-Phenology-Switch model and highlight the central role of developmental progression in constraining growing seasons. Faster early-season development -especially under nighttime warming- moves trees past the switch earlier, increasing sensitivity to late-season cooling and thereby triggering earlier autumn phenology. To improve growing season length projections, phenology models should account for these developmentally-mediated and diel-specific temperature responses.

ecology↗

bioRxiv2025

A Theory of Heterosis

Heterosis refers to the superior performance of a hybrid over its parents. It is the basis for hybrid breeding particularly for maize and rice. Genetically it is due to interactions between alleles of quantitative trait loci (QTL) (dominance and epistasis). Despite enormous interest and efforts to study the genetic basis of heterosis, the relative contribution of dominance vs. epistasis to heterosis is still not clear. This is because most published studies estimate QTL effects in pieces, not able to put them together to assess the overall pattern adequately. We propose a theoretical framework that focuses on the inference of the relationship between genome and traits that includes the identification of multiple QTL and estimation of the whole set of QTL (additive, dominant, and epistatic) effects. Used for heterosis, it gives a clear genetic definition and interpretation of heterosis. We applied the theory and methods to a large maize dataset with a factorial design of many male and female inbred lines and their hybrid crosses. Heterosis of ear weight in maize is primarily due to QTL dominant effects, many are over-dominant. The contribution to heterosis due to epistasis is small and diffused. For comparison, we also analyzed a rice dataset that is an F2-type population derived from a cross between two inbred lines. The result indicates that dominance is still the main contributor to heterosis, and epistasis contribution is small. Article SummaryWe propose a general theoretical framework to analyze and interpret quantitative trait genetic variation in a population through the identification of quantitative trait loci (QTL) and the estimation of QTL effects including interactions. Applied to a large genomic study in maize, we produce direct estimation of genetic contribution to heterosis--QTL dominance and epistasis and compare them to the observed heterosis. The evidence is clear that the heterosis of ear weight in maize is primarily due to QTL dominance. The contribution to heterosis due to QTL epistasis is relatively small and diffused.

genetics↗

bioRxiv2024

Spatial frequency channels mediate a visual metric for human spatial perception

An intriguing mystery concerning spatial vision is that the perceived spatial property information of the same stimulus varies in different contexts. While previous findings are suggestive of an adaptable mental ruler by which the raw retinal signals are flexibly scaled according to the prevailing context, whether and how such a putative mental ruler is utilized by the visual brain remain largely unknown. We hypothesized that the putative mental ruler was represented by multiple differently-tuned spatial frequency (SF) channels. A finer division of the ruler, signaled by dominance of the high-SF channels, is translated to a wider-spread topography of neural activation via concentration of neuronal receptive fields, causing perceptual inflation. Combining psychophysics and fMRI, we found that modulation of SF channels caused a systematic distortion in perceived separation, a representative fundamental spatial property, and a global displacement of population receptive fields (pRF) in primary visual cortex. Computational modeling further showed that both the perceptual distortion and the global pRF displacement were functionally coupled with the magnitude of SF channel modulation. Our findings reveal, for the first time, an adjustable mental ruler that commonly governs the perception of spatial property information in different contexts, and suggest a cognitive scaling system based on SF channel reweighting and displacement of neuronal RFs.

neuroscience↗

bioRxiv2024

Causal discovery in biodiversity-mediated social-ecological systems

Global biodiversity loss and climate change exacerbate feedbacks within social-ecological systems, i.e., between ecosystems, their services and well-being of human societies. Our ability to mediate these feedbacks is hampered by incomplete understanding of the underlying causal links, which could benefit from interdisciplinary approaches to discover theoretical or empirical links from heterogeneous data characteristic of social-ecological studies. We propose a novel framework connecting literature-based causal knowledge with data-driven inference of causality. We test this framework for the highly biodiverse island of Borneo by conducting a systematic literature review of 7473 studies over 170 years, and a causal inference analysis for three conceptual causal diagrams connecting global change, socio-economics, ecosystem services, and biodiversity-ecosystem function using a set of 227 spatially explicit variables. We find that, while natural or social processes have been mostly studied independently, a set of studies already documents causal links across social-ecological domains for processes related to deforestation, food or energy. Causal discovery unveiled consistent negative causal links between global change, social-economic landscape, and biodiversity-ecosystem function, and positive causal links between global change and socio-economics, and these links were robust to indicator selection and addition. We detected few and weak links between social-economic landscape, global change, and ecosystem services. When comparing the data-driven inferred causal links to those documented by the literature, we find that links between biodiversity and ecosystem function with global change, and links between social-economic landscape and ecosystem services were also consistent, and causal analysis uncovered new (potential) causal links not yet described in the literature. Significance StatementAddressing climate change and biodiversity loss in the Anthropocene requires us to recognize that human societies and ecological systems are inherently interconnected in complex adaptive systems. Causal understanding in social-ecological systems enables understanding system dynamics and response to pressures and shocks. While promising, few studies have studied these systems using a combination of big literature which provides the state-of-the-knowledge and big data that provides the underlying information for causal discovery. With this framework, we can specify and rigorously test, causal links in biodiversity-mediated social-ecological processes under global change and examine potential interventions that lead to much needed sustainable outcomes.

ecology↗

bioRxiv2024

Opposing Motor Memories in the Direct and Indirect Pathways of the Basal Ganglia

Loss of dopamine neurons causes motor deterioration in Parkinsons disease patients. We have previously reported that in addition to acute motor impairment, the impaired motor behavior is encoded into long-term memory in an experience-dependent and task-specific manner, a phenomenon we refer to as aberrant inhibitory motor learning. Although normal motor learning and aberrant inhibitory learning oppose each other and this is manifested in apparent motor performance, in the present study, we found that normal motor memory acquired prior to aberrant inhibitory learning remains preserved in the brain, suggesting the existence of independent storage. To investigate the neuronal circuits underlying these two opposing memories, we took advantage of the RNA-binding protein YTHDF1, an m6A RNA methylation reader involved in the regulation of protein synthesis and learning/memory. Conditional deletion of Ythdf1 in either D1 or D2 receptor-expressing neurons revealed that normal motor memory is stored in the D1 (direct) pathway of the basal ganglia, while inhibitory memory is stored in the D2 (indirect) pathway. Furthermore, fiber photometry recordings of GCaMP signals from striatal D1 (dSPN) and D2 (iSPN) receptor-expressing neurons support the preservation of normal memory in the direct pathway after aberrant inhibitory learning, with activities of dSPN predictive of motor performance. Finally, a computational model based on activities of motor cortical neurons, dSPN and iSPN neurons, and their interactions through the basal ganglia loops supports the above observations. These findings have important implications for novel approaches in treating Parkinsons disease by reactivating preserved normal memory, and in treating hyperkinetic movement disorders such as chorea or tics by erasing aberrant motor memories.

neuroscience↗

bioRxiv2024

Neonatal sensitivity to vocal emotions: A milestone at 37 weeks of gestational age

Emotional responsiveness in neonates, particularly their ability to discern vocal emotions, plays an evolutionarily adaptive role in human communication and adaptive behaviors. The developmental trajectory of emotional sensitivity in neonates is crucial for understanding the foundations of early social-emotional functioning. However, the precise onset of this sensitivity and its relationship with gestational age (GA) remain subjects of investigation. In a study involving 120 healthy neonates categorized into six groups based on their GA (ranging from 35 and 40 weeks), we explored their emotional responses to vocal stimuli. These stimuli encompassed disyllables with happy and neutral prosodies, alongside acoustically matched nonvocal control sounds. The assessments occurred during natural sleep states using the odd-ball paradigm and event-related potentials. The results reveal a distinct developmental change at 37 weeks GA, marking the point at which neonates exhibit heightened perceptual acuity for emotional vocal expressions. This newfound ability is substantiated by the presence of the mismatch response, akin to an initial form of adult mismatch negativity, elicited in response to positive emotional vocal prosody. Notably, this perceptual shifts specificity becomes evident when no such discrimination is observed in acoustically matched control sounds. Neonates born before 37 weeks GA do not display this level of discrimination ability. This developmental change has important implications for our understanding of early social-emotional development, highlighting the role of gestational age in shaping early perceptual abilities. Moreover, while these findings introduce the potential for a valuable screening tool for conditions like autism, characterized by atypical social-emotional functions, it is important to note that the current data are not yet robust enough to fully support this application. This study makes a substantial contribution to the broader field of developmental neuroscience and holds promise for future research on early intervention in neurodevelopmental disorders. Significance statementThis study illuminates a key developmental change, pinpointing the emergence of heightened emotional perceptual acuity at 37 weeks of gestational age. Employing rigorous methods, we reveal that neonates at this stage exhibit remarkable discrimination abilities for emotional vocal prosody, a vital turning point in early social-emotional functioning. These findings emphasize the pivotal role of gestational age in shaping neonatal perception and provides a potential pathway for early screening of neurodevelopmental disorders, particularly autism. This insight holds profound implications for understanding the foundations of early social-emotional development in humans, offering a potential tool for early intervention in neurodevelopmental disorders, thereby enhancing child health and well-being.

neuroscience↗

bioRxiv2021

Global trade-offs in tree functional traits

AO_SCPLOWBSTRACTC_SCPLOWDue to massive energetic investments in woody support structures, trees are subject to unique physiological, mechanical, and ecological pressures not experienced by herbaceous plants. When considering trait relationships across the entire plant kingdom, plant trait frameworks typically must omit traits unique to large woody species, thereby limiting our understanding of how these distinct ecological pressures shape trait relationships in trees. Here, by considering 18 functional traits--reflecting leaf economics, wood structure, tree size, reproduction, and below-ground allocation--we quantify the major axes of variation governing trait expression of trees worldwide. We show that trait variation within and across angiosperms and gymnosperms is captured by two independent processes: one reflecting tree size and competition for light, the other reflecting leaf photosynthetic capacity and nutrient economies. By exploring multidimensional relationships across clusters of traits, we further identify a representative set of seven traits which captures the majority of variation in form and function in trees: maximum tree height, stem conduit diameter, specific leaf area, seed mass, bark thickness, root depth, and wood density. Collectively, this work informs future trait-based research into the functional biogeography of trees, and contributes to our fundamental understanding of the ecological and evolutionary controls on forest biodiversity and productivity worldwide.

ecology↗

bioRxiv2021

Interannual climate variability data improves niche estimates in species distribution models

AimClimate is an essential element of species niche estimates in many current ecological applications such as species distribution models (SDMs). Climate predictors are often used in the form of long-term mean values. Yet, climate can also be described as spatial or temporal variability for variables like temperature or precipitation. Such variability, spatial or temporal, offers additional insights into niche properties. Here, we test to what degree spatial variability and long-term temporal variability in temperature and precipitation improve SDM predictions globally. LocationGlobal. Time period1979-2013 Major taxa studiesMammal, Amphibians, Reptiles MethodsWe use three different SDM algorithms, and a set of 833 amphibian, 779 reptile, and 2211 mammal species to quantify the effect of spatial and temporal climate variability in SDMs. All SDMs were cross-validated and accessed for their performance using the Area under the Curve (AUC) and the True Skill Statistic (TSS). ResultsMean performance of SDMs with climatic means as predictors was TSS=0.71 and AUC=0.90. The inclusion of spatial variability offers a significant gain in SDM performance (mean TSS=0.74, mean AUC=0.92), as does the inclusion of temporal variability (mean TSS=0.80, mean AUC=0.94). Including both spatial and temporal variability in SDMs shows similarly high TSS and AUC scores. Main conclusionsAccounting for temporal rather than spatial variability in climate improved the SDM prediction especially in exotherm groups such as amphibians and reptiles, while for endotermic mammals no such improvement was observed. These results indicate that more detailed information about temporal climate variability offers a highly promising avenue for improving niche estimates and calls for a new set of standard bioclimatic predictors in SDM research.

ecology↗

bioRxiv2021

A vimentin-targeting oral compound with host-directed antiviral and anti-inflammatory actions addresses multiple features of COVID-19 and related diseases

Damage in COVID-19 results from both the SARS-CoV-2 virus and its triggered overreactive host immune responses. Therapeutic agents that focus solely on reducing viral load or hyperinflammation fail to provide satisfying outcomes in all cases. Although viral and cellular factors have been extensively profiled to identify potential anti-COVID targets, new drugs with significant efficacy remain to be developed. Here, we report the potent preclinical efficacy of ALD-R491, a vimentin-targeting small molecule compound, in treating COVID-19 through its host-directed antiviral and anti-inflammatory actions. We found that by altering the physical properties of vimentin filaments, ALD-491 affected general cellular processes as well as specific cellular functions relevant to SARS-CoV-2 infection. Specifically, ALD-R491 reduced endocytosis, endosomal trafficking, and exosomal release, thus impeding the entry and egress of the virus; increased the microcidal capacity of macrophages, thus facilitating the pathogen clearance; and enhanced the activity of regulatory T cells, therefore suppressing the overreactive immune responses. In cultured cells, ALD-R491 potently inhibited the SARS-CoV-2 spike protein and human ACE2-mediated pseudoviral infection. In aged mice with ongoing, productive SARS-CoV-2 infection, ALD-R491 reduced disease symptoms as well as lung damage. In rats, ALD-R491 also reduced bleomycin-induced lung injury and fibrosis. Our results indicate a unique mechanism and significant therapeutic potential for ALD-R491 against COVID-19. We anticipate that ALD-R491, an oral, fast-acting, and non-toxic agent targeting the cellular protein with multipart actions, will be convenient, safe, and broadly effective, regardless of viral mutations, for patients with early- or late-stage disease, post-COVID complications and other related diseases. IMPORTANCEWith the Delta variant currently fueling a resurgence of new infections in the fully-vaccinated population, developing an effective therapeutic drug is especially critical and urgent in fighting COVID-19. In contrast to the many efforts to repurpose existing drugs or address only one aspect of COVID-19, we are developing a novel agent with first-in-class mechanism-of-actions that address both the viral infection and the overactive immune system in the pathogenesis of the disease. Unlike virus-directed therapeutics that may lose efficacy due to viral mutations and immunosuppressants that require ideal timing to be effective, this agent, with its unique host-directed antiviral and anti-inflammatory actions, can work against all variants of the virus, be effective during all stages of the disease, and even resolve post-disease damage and complications. A further development of the compound will provide an important tool in the fight against COVID-19, its complications, as well as future outbreaks of new viruses.

pharmacology and toxicology↗

bioRxiv2020

IL4-driven microglia modulate stress resilience through BDNF-dependent neurogenesis

Adult neurogenesis in the dentate gyrus of the hippocampus is regulated by specific groups of microglia and is functionally implicated in behavioral responses to stress. However, the role of microglia in modulating hippocampal neurogenesis in stress responses remains poorly understood. Here we investigated the effects of IL4-driven Arg1+ microglia in the restoration of hippocampal neurogenesis and conferment of stress resilience. We found that low IL4 levels in the hippocampus of mice was associated with greater stress vulnerability and, conversely, overexpression of IL4 in the hippocampus induced a large number of Arg1+ microglia and ameliorated stress-induced depressive-like behaviors. Knockdown of microglial IL4 receptors in the hippocampus of mice exacerbated the stress-induced inflammatory response and abolished the antidepressant effects of IL4 overexpression. Enhancement or inhibition of IL4 signaling in hippocampal microglia modulated neurogenesis, and blockade of neurogenesis abolished the resilience to stress-induced depression. We further show that IL4-activated microglia is associated with upregulation of BDNF levels and neurogenesis. Taken together, our findings suggest that IL4-driven microglia in the hippocampus trigger BDNF-dependent neurogenesis in response to chronic stress, helping protect against depressive-like symptoms. These findings identify the modulation of a specific microglial phenotype as a treatment strategy for mood disorders. In BriefZhang et al. show that IL4-induced Arg1+ microglia restore hippocampal neurogenesis and promote resilience against stress in mice by increasing BDNF levels. Targeting microglia with immunomodulatory factors may be a strategy for treating mood disorders. HighlightsO_LIVulnerability to stress in mice is associated with reduced IL4 signaling in the hippocampus C_LIO_LIBrain-derived IL4 promotes adult hippocampal neurogenesis and stress resistance by driving Arg1+ microglia C_LIO_LIIL4-driven Arg1+ microglia enhance hippocampal neurogenesis via a BDNF-dependent pathway C_LI

neuroscience↗

bioRxiv2018

Cities of the future, visualizing climate change to inspire actions

Combating against climate change requires unified action across all sectors of society. However, this collective action is precluded by the consensus gap between scientific knowledge and public opinion. A growing body of evidence suggests that facts do not persuade people to act. Instead, it is visualization - the ability to simulate relatable scenarios - is the most effective approach for motivating behavior change. Here, we exemplify this approach, using current climate projections to enable people to visualize cities of the future, rather than describing intangible climate variables. Analyzing city pairs for 520 major cities of the world, we characterize which cities will most closely resemble the climate conditions of which other major cities by 2050. On average, most cities will resemble cities that are over 1000km south, and 22% of cities will experience climate conditions that are not currently experienced by any existing major cities. We predict that Londons climate in 2050 will resemble Barcelonas climate today, Madrid will resemble to Marrakesh, Moscow to Sofia, Seattle to San Francisco, Stockholm to Budapest, Tokyo to Changsha, etc. Our approach illustrates how complex climate data can be packaged to provide tangible information. By allowing people to visualize their own climate futures, we hope to empower citizens, policy makers and scientists to visualize expected climate impacts and adapt decision making accordingly.

scientific communication and education↗

bioRxiv2018

Changes in pregnancy-related serum biomarkers early in gestation are associated with later development of preeclampsia

BackgroundPlacental protein expression plays a crucial biological role during normal and complicated pregnancies. We hypothesized that: (1) circulating pregnancy-associated, placenta-related protein levels throughout gestation reflect the uncomplicated, full-term temporal progression of human gestation, and effectively estimates gestational ages (GAs); (2) pregnancies with underlying placental pathology, such as preeclampsia (PE), are associated with disruptions in this GA estimation in early gestation; (3) malfunctions of this GA estimation can be employed to identify impending PE. In addition, to explore the underlying biology and PE etiology, we set to compare protein gestational patterns of human and mouse, using pregnant heme oxygenase-1 (HO-1) heterozygote (Het) mice, a mouse model reflecting PE-like symptoms.\n\nMethodsSerum levels of circulating placenta-related proteins - leptin (LEP), chorionic somatomammotropin hormone like 1 (CSHL1), elabela (ELA), activin A, soluble fms-like tyrosine kinase 1 (sFlt-1), and placental growth factor (PlGF)- were quantified by ELISA in blood serially collected throughout human pregnancies (20 normal subjects with 66 samples, and 20 PE subjects with 61 samples). Linear multivariate analysis of the targeted serological protein levels was performed to estimate the normal GA. Logarithmic transformed mean-squared errors of GA estimations were used to identify impending PE. Then the human gestational protein patterns were compared to those in the pregnant HO-1 mice.\n\nResultsAn elastic net (EN)-based gestational dating model was developed (R2 = 0.76) and validated (R2 = 0.61) using the serum levels of the 6 proteins at various GAs from women with normal uncomplicated pregnancies (n = 10 for training and n = 6 for validation). In pregnancies complicated by PE (n = 14), the EN model was not (R2 = -0.17) associated with GA at sampling in PE. Statistically significant deviations from the normal GA EN model estimations were observed in PE-associated pregnancies between GAs of 16-30 weeks (P = 0.01). The EN model developed with 5 proteins (ELA excluded due to the lack of robustness of the mouse ELA essay) performed similarly on normal human (R2 = 0.68) and WT mouse (R2 = 0.85) pregnancies. Disruptions of this model were observed in both human PE-associated (human: R2 = 0.27) and mouse HO-1 Het (mouse: R2 = 0.30) pregnancies. LEP out performed sFlt-1 and PlGF in differentiating impending PE at early human and late mouse gestations.\n\nConclusionsAs revealed in both human and mouse GA EN analyses, temporal serological placenta-related protein patterns are tightly regulated throughout normal human pregnancies and can be significantly disrupted in pathologic PE states. LEP changes earlier during gestation than the well-established late GA PE biomarkers (sFlt-1 and PlGF). Our HO-1 Het mouse analysis provides direct evidence of the causative action of HO-1 deficiency in LEP upregulation in a PE-like murine model. Therefore, longitudinal analyses of pregnancy-related protein patterns in sera, may not only help in the exploration of underlying PE pathophysiology but also provide better clinical utility in PE assessment.

molecular biology↗

bioRxiv2018

Loss of leaf-out and flowering synchrony under global warming

The temporal overlap of phenological stages, phenological synchrony, crucially influences ecosystem functioning. For flowering, among-individual synchrony influences gene flow. For leaf-out, it affects interactions with herbivores and competing plants. If individuals differ in their reaction to the ongoing change in global climate, this should affect population-level synchrony. Here, we use climate-manipulation experiments, Pan-European long-term (>15 years) observations, and common garden monitoring data on up to 72 woody and herbaceous species to study the effects of increasing temperatures on the extent of within-population leaf-out and flowering synchrony. Warmer temperatures reduce in situ leaf-out and flowering synchrony by up to 55%, and experiments on European beech provide a mechanism for how individual genetic differences may explain this finding. The rapid loss of reproductive and vegetative synchrony in European plants predicts changes in their gene flow and trophic interactions, but community-wide consequences remain largely unknown.

ecology↗