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Biology subjects

Selimovic, A.

Publications and source records attributed to Selimovic, A..

3 recordsLinked to original sources

Segmentation and profile-based classification of movement strategies from animal tracking data

O_LIClassifying animal movement strategies from GPS tracking data is essential for understanding space use, population dynamics and conservation planning. However, existing approaches either require strong parametric assumptions about trajectory shape, large labelled datasets (i.e. expert-annotated) for machine learning, or lack formal uncertainty quantification. These limitations create barriers for researchers working with novel species or limited sample sizes. C_LIO_LIWe present a profile-based classification framework consisting of three steps. First, trajectories are segmented using breakpoint detection applied to Net Squared Displacement (NSD) time series. Movement metrics are then extracted from each segment and classified by comparing them to empirically derived behavioural profiles via Z-score distances transformed to softmax probabilities. Bootstrap resampling quantifies uncertainty in the resulting classifications from both training and test data. We validated the framework through simulation experiments and applied it to GPS tracking data from two ecologically contrasting species: gray wolf (Canis lupus;43 individuals) and northern lapwing (Vanellus vanellus;15 individuals). C_LIO_LISimulations showed that 5-10 training segments per movement strategy suffice for reliable classification, with overall accuracy of 91.1%across residential, floating and dispersal strategies. Segment duration of 30-60 days was required for confident discrimination of residential and floating behaviour. For wolves, the framework clearly distinguished residency, floating or dispersal (91.2%of segments classified with >50%probability). For lapwings, migration was identified with high confidence, while residential-floating discrimination reflected genuine ecological ambiguity confirmed by domain experts, with bootstrap confidence intervals transparently flagging uncertain cases. C_LIO_LIThe profile-based framework provides an accessible, interpretable alternative to parametric NSD fitting and machine learning approach, requiring modest training data while delivering probabilistic classifications with honest uncertainty estimates. An R package (moveprofile) implementing the complete workflow is freely available. The framework is applicable to any tracked species where distinct movement strategies can be identified by experts knowledge. C_LI

ecology↗

Mutant ATXN1 impacts human and mouse microglia and contributes to cognitive, mood, and motor deficits in SCA1 mice

Microglia, resident immune cells of the brain, are important players in neurodegeneration. While microglial activation is a hallmark of many neurodegenerative diseases, the specific role of microglia intrinsic factors in microglial activation and disease pathogenesis remains unknown. Spinocerebellar ataxia type-1 (SCA1) is an inherited autosomal dominant neurodegenerative disease characterized by severe neuronal loss and early microglial activation in the cerebellum. SCA1 is caused by CAG repeat expansion in the ubiquitously expressed ATAXIN1 (ATXN1) gene. Using human microglia differentiated from SCA1 patient derived iPSCs, we found that mutant ATXN1 is sufficient to alter morphology, gene and protein expression in human microglia in a cell-autonomous manner. Moreover, compared to controls, human SCA1 microglia exhibited increased phagocytosis and pro-inflammatory cytokine production, indicating an immune priming. To determine the extent to which mutant ATXN1 in microglia contributes to SCA1 pathogenesis and behavioral symptoms, we removed mutant ATXN1 from microglia and macrophages in a novel conditional SCA1 mouse model, f-ATXN1146Q/2Q mice. Microglial mutant ATXN1 reduction led to a marked correction in microglia phenotype, in particular in the transcriptomic signature of interferon type 1 mediated immune response, reduced microglial density and resulted in smaller microglia with reduced branching in the cerebellum. Pathology of Purkinje neurons and cerebellar astrogliosis were also ameliorated. Utilizing a battery of behavioral tests, we found that microglia and macrophage mutant ATXN1 reduction ameliorated cognitive, mood, and motor deficits in SCA1 mice. Together, these results indicate that mutant ATXN1 directly impacts microglial phenotype in SCA1, contributing to SCA1 pathology and behavioral deficits.

neuroscience↗

Lamp1 mediates lipid transport, but is dispensable for autophagy in Drosophila

The endolysosomal system not only is an integral part of the cellular catabolic machinery that processes and recycles nutrients for synthesis of biomaterials, but also acts as signaling hub to sense and coordinate the energy state of cells with growth and differentiation. Lysosomal dysfunction adversely influences vesicular transport-dependent macromolecular degradation and thus causes serious problems for human health. In mammalian cells, loss of the lysosome associated membrane proteins LAMP1/2 strongly impacts autophagy and cholesterol trafficking. Here we show that the previously uncharacterized Drosophila Lamp1 is a bona fide homolog of vertebrate LAMP1/2. Surprisingly and in contrast to Lamp1/2 double mutant mice, Drosophila Lamp1 is not required for viability or autophagy, suggesting that autophagy defects in Lamp1/2 mutants may have indirect causes. However, Lamp1 deficiency results in an expansion of the acidic compartment in flies. Furthermore, we find that Lamp1 mutant larvae have defects in lipid metabolism as they show elevated levels of sterols and diacylglycerols (DAGs). Since DAGs are the main lipid species used for transport though the hemolymph (blood) in insects, our results indicate broader functions of Lamp1 in lipid transport. Our findings make Drosophila an ideal model to study the role of LAMP proteins in lipid assimilation without the confounding effects of their storage and without interfering with autophagic processes.

cell biology↗