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Mooney, S.

Publications and source records attributed to Mooney, S..

2 recordsLinked to original sources

A spatially targeted metric of potential koala populations based on Bayesian Networks for conservation management

Koalas (Phascolarctos cinereus) face significant threats from habitat loss and fragmentation, with South-East Queensland (SEQ) experiencing some of the most severe population declines. Current metrics used to assess conservation impacts often lack spatial resolution, transparency, or integration of diverse data sources. We propose a novel, spatially targeted metric, Koala Population Potential (KPP), to estimate the potential number of koalas that could inhabit a given area under ideal conditions. This metric is derived from a Bayesian Network model that integrates ecological, environmental, and threat data, including satellite imagery, expert knowledge, and stakeholder input. We developed and validated the KPP within an interactive online platform, the Koala Bayesian Network Platform (KBNP), enabling stakeholders to visualise and assess the conservation impact of various management scenarios at the land-parcel scale. Application of the KPP across SEQ revealed substantial spatial variation in potential koala populations. Regional areas like Somerset and the Scenic Rim exhibited high KPP scores, while urban LGAs such as Redland City and Logan had lower scores due to elevated threat levels. Model predictions of habitat support were strongly correlated with independent habitat quality assessments (R{superscript 2} = 0.803, p < .001), supporting the validity of the approach. The KBNP provides an accessible, evidence-based decision-support tool that empowers landholders, planners, and conservation managers to evaluate and communicate the likely outcomes of their actions. While developed for koalas, this framework is adaptable to other vulnerable species requiring localised, data-driven conservation planning under uncertainty.

ecology↗

Proteomic Analysis of Huntington's Disease Medium Spiny Neurons Identifies Alterations in Lipid Droplets

Huntingtons disease (HD) is a neurodegenerative disease caused by a CAG repeat expansion in the Huntingtin (HTT) gene. The resulting polyglutamine (polyQ) tract alters the function of the HTT protein. Although HTT is expressed in different tissues, the medium spiny projection neurons (MSNs) in the striatum are particularly vulnerable in HD. Thus, we sought to define the proteome of human HD patient-derived MSNs. We differentiated HD72 induced pluripotent stem cells and isogenic controls into MSNs and carried out quantitative proteomic analysis by two approaches. First, using data-dependent acquisitions with FAIMS (FAIMS-DDA) for label-free quantification on the Orbitrap Lumos mass spectrometer, we identified 6,323 proteins with at least two unique peptides (FDR [&le;] 0.01). Of these, 901 proteins were significantly altered in the HD72-MSNs, compared to isogenic controls. Second, we quantitatively validated protein candidates by comprehensive data-independent acquisitions on a TripleTOF 6600 mass spectrometer quantifying 3,106 proteins with at least two unique peptides. Functional enrichment analysis identified pathways related to the extracellular matrix, including TGF-y regulation of extracellular matrix, epithelial-mesenchymal transition, DNA replication, senescence, cardiovascular system, organism development, regulation of cell migration and locomotion, aminoglycan glycosaminoglycan proteoglycan, growth factor stimulus and fatty acid processes. Conversely, processes associated with the downregulated proteins included neurogenesis-axogenesis, the brain-derived neurotrophic factor-signaling pathway, Ephrin-A: EphA pathway, regulation of synaptic plasticity, triglyceride homeostasis cholesterol, plasmid lipoprotein particle immune response, interferon-{gamma} signaling, immune system major histocompatibility complex, lipid metabolism and cellular response to stimulus. Moreover, proteins involved in the formation and maintenance of axons, dendrites, and synapses (e.g., Septin protein members) are dysregulated in HD72-MSNs. Importantly, lipid metabolism pathways were altered, and we found that lipid droplets accumulated in the HD72-MSNs, suggesting a deficit in lipophagy. Our proteomics analysis of HD72-MSNs identified relevant pathways that are altered in MSNs and confirm current and new therapeutic targets for HD.

neuroscience↗