Biology subjects

Nolan, R.

Publications and source records attributed to Nolan, R..

6 recordsLinked to original sources

bioRxiv2026

Climate change drives declines in seed germination potential, particularly in woody species and warmer, drier landscapes of a temperate bioregion

Climate change is accelerating species losses in ecosystems across the world. Seed germination is a critical, climate-dependent phase of the plant life cycle; however, the ecological determinants of germination climate niches within diverse landscapes and across functional types (FTs) are still not well understood. In this study, we characterized seed germination temperature and water availability niches for 28 species that represent different FTs (tree, shrub, grass, forb) and vegetation types (grassy woodland, dry and wet forests) within a temperate bioregion (Sydney, Australia). We tested whether ecological determinants, specifically species climate of origin, seed traits, FT and vegetation type explain germination niches and predicted spatial and temporal patterns of germination potential across the landscape under high and low emission scenarios. We found wide variation in thermal and hydric germination niches among species. Optimal germination temperature (thermal niche) was predicted by FT, climate of origin and seed traits, such that shrubs, cool-origin species, and species with large seeds had significantly cooler optimal temperatures for germination. We also quantified spatial and temporal changes in germination potential to identify vulnerable areas and FTs. We found strong species-specific seasonal patterns in germination potential with future climate shifts affecting FTs differently; germination of woody species declined more than forbs. Future germination potential was predicted by historical climatic conditions, with warmer and drier localities being more vulnerable. Overall, our findings demonstrate that species germination responses to climate change depend on FT, seed traits, and species climate of origin, with woody species and warmer, drier parts of the landscape emerging as being particularly vulnerable to declines in recruitment. Our study provides a mechanistic understanding of germination responses to temperature and water availability, enabling predictions of vulnerable species and areas for conservation under climate change, and inform large-scale ecosystem restoration approaches through improved species selection and sowing times.

plant biology↗

bioRxiv2025

Ability to predict irregular periods of food deprivation improves body-weight regulation and reduces weight gain in food-insecure starlings

1.Food insecurity is associated with higher body weight in humans and other species, but the causal effect of unpredictable food availability on weight gain is unknown. We measured food intake and weight in starlings (Sturnus vulgaris) exposed to repeated irregular periods of food deprivation. We manipulated the predictability of deprivation between subjects with a 1-hour visual cue that either reliably preceded deprivation (Predictable), or was uncorrelated with deprivation (Unpredictable). During the cue, Predictable birds reduced their food intake and spent less time inactive, indicating that they had learnt the contingency. Despite these responses, they lost less weight during subsequent deprivation. They also ate less and gained less weight when food was returned. Birds with the largest behavioural response to the cue had the lowest overall variance in body weight. Consistent with the insurance hypothesis, food intake and body weight increased over time in both groups and body weight was higher in the Unpredictable group. Our results suggest that when food deprivation was predictable, birds were less reliant on stored fat and instead used conditioned hypometabolism to mitigate the effects of food deprivation. We discuss the implications of our findings for the differential health impacts of food insecurity and intermittent fasting.

animal behavior and cognition↗

bioRxiv2024

Dopamine-driven Increase in IL-1β in Myeloid Cells is Mediated by Differential Dopamine Receptor Expression and Exacerbated by HIV

The catecholamine neurotransmitter dopamine is classically known for regulation of central nervous system (CNS) functions such as reward, movement, and cognition. Increasing evidence also indicates that dopamine regulates critical functions in peripheral organs and is an important immunoregulatory factor. We have previously shown that dopamine increases NF-{kappa}B activity, inflammasome activation, and the production of inflammatory cytokines such as IL-1{beta} in human macrophages. As myeloid lineage cells are central to the initiation and resolution of acute inflammatory responses, dopamine-mediated dysregulation of these functions could both impair the innate immune response and exacerbate chronic inflammation. However, the exact pathways by which dopamine drives myeloid inflammation are not well defined, and studies in both rodent and human systems indicate that dopamine can impact the production of inflammatory mediators through both D1-like dopamine receptors (DRD1, DRD5) and D2-like dopamine receptors (DRD2, DRD3, and DRD4). Therefore, we hypothesized that dopamine-mediated production of IL-1{beta} in myeloid cells is regulated by the ratio of different dopamine receptors that are activated. Our data in primary human monocyte-derived macrophages (hMDM) indicate that DRD1 expression is necessary for dopamine-mediated increases in IL-1{beta}, and that changes in the expression of DRD2 and other dopamine receptors can alter the magnitude of the dopamine-mediated increase in IL-1{beta}. Mature hMDM have a high D1-like to D2-like receptor ratio, which is different relative to monocytes and peripheral blood mononuclear cells (PBMCs). We further confirm in human microglia cell lines that a high ratio of D1-like to D2-like receptors promotes dopamine-induced increases in IL-1{beta} gene and protein expression using pharmacological inhibition or overexpression of dopamine receptors. RNA-sequencing of dopamine-treated microglia shows that genes encoding functions in IL-1{beta} signaling pathways, microglia activation, and neurotransmission increased with dopamine treatment. Finally, using HIV as an example of a chronic inflammatory disease that is substantively worsened by comorbid substance use disorders (SUDs) that impact dopaminergic signaling, we show increased effects of dopamine on inflammasome activation and IL-1{beta} in the presence of HIV in both human macrophages and microglia. These data suggest that use of addictive substances and dopamine-modulating therapeutics could dysregulate the innate inflammatory response and exacerbate chronic neuroimmunological conditions like HIV. Thus, a detailed understanding of dopamine-mediated changes in inflammation, in particular pathways regulating IL-1{beta}, will be critical to effectively tailor medication regimens.

neuroscience↗

bioRxiv2023

The AusTraits Plant Dictionary

Traits with intuitive names, a clear scope and explicit description are essential for all trait databases. Reanalysis of data from a single database, or analyses that integrate data across multiple databases, can only occur if researchers are confident the trait concepts are consistent within and across sources. The lack of a unified, comprehensive resource for plant trait definitions has previously limited the utility of trait databases. Here we describe the AusTraits Plant Dictionary (APD), which extends the trait definitions included in the new trait database AusTraits. The development process of the APD included three steps: review and formalisation of the scope of each trait and the accompanying trait description; addition of trait meta-data; and publication in both human and machine-readable forms. Trait definitions include keywords, references and links to related trait concepts in other databases, and the traits are grouped into a hierarchy for easy searching. As well as improving the usability of AusTraits, the Dictionary will foster the integration of trait data across global and regional plant trait databases.

ecology↗

bioRxiv2021

Functional characterization of the biogenic amine transporter system on human macrophages

Monocyte-derived macrophages are key players in tissue homeostasis and disease regulated by a variety of signaling molecules. Recent literature has highlighted the ability for biogenic amines to regulate macrophage functions, but the mechanisms governing biogenic amine signaling on and around immune cells remains nebulous. In the central nervous system, biogenic amine transporters are regarded as the master regulators of neurotransmitter signaling. While we and others have shown macrophages express these transporters, relatively little is known of their function on these cells. To address these knowledge gaps, we interrogated the function of norepinephrine (NET) and dopamine (DAT) transporters on human monocyte-derived macrophages. We found that both NET and DAT are present and can uptake substrate from the extracellular space at baseline. Not only was DAT expressed in cultured macrophages, but it was also detected in a subset of intestinal macrophages in situ. Surprisingly, we discovered a NET-independent, DAT-mediated immuno-modulatory mechanism in response to lipopolysaccharide (LPS). LPS induced reverse transport of dopamine through DAT, engaging autocrine/paracrine signaling loop that regulated the macrophage response. Removing this signaling loop enhanced the pro-inflammatory response to LPS. Finally, we found that this DAT-immune axis was disrupted in disease. Collectively, our data introduce a novel role for DAT in the regulation of innate immunity during health and disease.

neuroscience↗

bioRxiv2019

Robin Hood: non-fitting, non-smoothing image detrending for bleaching correction

Recent advances in protein labelling--gene tagging with CRIPSR-Cas9--have made it possible to label proteins of interest endogenously. This represents a major breakthrough in the field of quantitative microscopy, especially when quantifying protein-protein interactions. This is because over-expression of labelled proteins may cause a distortion in localization, function and perhaps artificially force protein-protein interactions due to crowding effects. A microscopy technique that is particularly well suited to detect protein interactions with low photon budgets is number and brightness (N&B). Detrending (removal of global trends in data) is a necessary pre-processing step to N&B calculations, but all current detrending methods perform poorly at low intensities. Here, we present the Robin Hood automatic detrending algorithm which performs well at low intensities, evaluating it with simulated and low photon budget live cell images. RH is available as an ImageJ plugin and as an R package.\n\nSTATEMENT OF SIGNIFICANCEFluorescence microscopy in general and Fluorescence fluctuation methods in particular are very much dependent on detrend algorithms and so far, the user needs to decide an arbitrary number to correct for bleaching when using the box plot or the running average approach. Here, we have developed a tool available to everybody as an ImageJ plugin that is automatic, user-free and able to correct bleached images with very low photon counts.

biophysics↗