Biology subjects

Minnig, S.

Publications and source records attributed to Minnig, S..

4 recordsLinked to original sources

bioRxiv2025

Rewilding beyond the wilderness: Beavers can restore stream biodiversity from urban to agricultural to natural landscapes

1 Beavers have been promoted as a cost-effective nature-based solution to restore degraded stream ecosystems and enhance overall biodiversity. However, the extent to which beaver-engineering boosts biodiversity in human-impacted landscapes remains poorly understood. 2 We assessed the responses of aquatic and terrestrial taxa (amphibians, dragonflies, fish, macrophytes, plankton, terrestrial vegetation, bats, aquatic, flying and terrestrial invertebrates) to beaver-engineering along a gradient of human land-use intensity in Switzerland. In 16 streams, we measured species richness, abundance, unique species richness, evenness, beta and gamma diversity in a beaver-engineered site with beaver dams and a control site without beaver activity. 3 Especially aquatic and semi-aquatic species profited from beaver-engineering. In response to beaver-engineering, amphibians, dragonflies, macrophytes, and plankton increased in species richness, abundance and unique species richness, while fish and terrestrial plants increased in species richness and unique species richness. Bats only increased in unique species richness, while for the other terrestrial taxa, we found no difference between beaver-engineered and control sites. Community evenness remained largely unaffected across all groups. 4 Overall, beaver-engineering increased biodiversity across a land-use gradient. For macrophytes and amphibians (species richness, unique species richness and abundance), as well for dragonflies (species richness and unique species richness), increases were smaller under higher land-use intensity. For the remaining taxa and metrics, we found no relationship between land-use intensity and responses to beaver engineering. 5 However, for beta-diversity, we found that sites with a high land-use intensity had a lower component of nestedness and stronger community turnover in comparison to more natural sites, with a significant effect for macrophytes. Gamma species richness was generally unaffected by land- use intensity, except for amphibians, which were often only found in beaver-engineered sites in high- land-use intensity areas. 6 Synthesis and applications. Our findings demonstrate that beaver-engineering significantly enhances local biodiversity across aquatic and terrestrial ecosystems, even at sites with high land-use intensity. Hence, beavers can effectively restore stream biodiversity from urban to agricultural to natural landscapes. Integrating beaver-engineering into river restoration strategies can substantially advance biodiversity goals under frameworks such as the EU Water Framework Directive and national conservation policies.

ecology↗

bioRxiv2017

Early Detection of Apathetic Phenotypes in Huntington’s Disease Knock-in Mice Using Open Source Tools

Apathy is one of the most prevalent and progressive psychiatric symptom in Huntingtons disease (HD) patients. However, preclinical work in HD mouse models tend to focus on molecular and motor, rather than affective, phenotypes. Measuring behavior in mice often produces noisy data and requires large cohorts to detect phenotypic rescue with appropriate power. The operant equipment necessary for measuring affective phenotypes is typically expensive, proprietary to commercial entities, and bulky which can render adequately sized mouse cohorts as cost-prohibitive. Thus, we describe here a home-built open-source alternative to commercial hardware that is reliable, scalable, and reproducible. Using off-the-shelf hardware, we adapted and built several of the rodent operant buckets (ROBucket) designed to test HttQ111/+ mice for attention deficits in fixed ratio (FR) and progressive ratio (PR) tasks. We find that, despite normal performance in reward attainment in the FR task, HttQ111/+ mice exhibit reduced PR performance at 9-11 months of age, suggesting motivational deficits. We replicated this in two independent cohorts, which demonstrates the reliability and utility of both the apathetic phenotype, and these ROBuckets, for preclinical HD studies.

animal behavior and cognition↗

bioRxiv2016

Peripheral Htt silencing does not ameliorate central signs of disease in the B6.HttQ111/+ mouse model of Huntington’s Disease

Huntingtons disease (HD) is an autosomal dominant neurodegenerative disease whose neuropathological signature is a selective loss of medium spiny neurons in the striatum. Despite this selective neuropathology, the mutant protein (huntingtin) is found in virtually every cell so far studied, and, consequently, phenotypes are observed in a wide range of organ systems both inside and outside the central nervous system. We, and others, have suggested that peripheral dysfunction could contribute to the rate of progression of striatal phenotypes of HD. To test this hypothesis, we lowered levels of huntingtin by treating mice with antisense oligonucleotides (ASOs) targeting the murine Huntingtin gene. To study the relationship between peripheral huntingtin levels and striatal HD phenotypes, we utilized a knock-in model of the human HD mutation (the B6.HttQ111/+ mouse). We treated mice with ASOs from 2-10 months of age, a time period over which significant HD-relevant signs progressively develop in the brains of HttQ111+ mice. Peripheral treatment with ASOs led to persistent reduction of huntingtin protein in peripheral organs, including liver, brown and white adipose tissues. This reduction was not associated with alterations in the severity of HD-relevant signs in the striatum of HttQ111/+ mice at the end of the study, including transcriptional dysregulation, the accumulation of neuronal intranuclear inclusions, and behavioral changes such as subtle hypoactivity and reduced exploratory drive. These results suggest that the amount of peripheral reduction achieved in the current study does not significantly impact the progression of HD-relevant signs in the central nervous system.

neuroscience↗

bioRxiv2016

Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.HttQ111/+ model of Huntington’s disease

We investigated the appearance and progression of disease-relevant signs in the B6.HttQ111/+ mouse, a genetically precise model of the mutation that causes Huntingtons disease (HD). We find that B6.HttQ111/+ mice are healthy, show no overt signs of central or peripheral inflammation, and no gross motor impairment as late as 12 months of age. Behaviorally, we find that 4-9 month old B6.HttQ111/+ mice have normal activity levels and show no clear signs of anxiety or depression, but do show clear signs of reduced motivation. The neuronal density, neuronal size, synaptic density and number of glia is normal in B6.HttQ111/+ striatum, the most vulnerable brain region in HD, up to 12 months of age. Despite this preservation of the synaptic and cellular composition of the striatum, we observe clear progressive, striatal-specific, transcriptional dysregulation and accumulation of neuronal intranuclear inclusions (NIIs). Simulation studies suggest these molecular endpoints are sufficiently robust for future preclinical studies, and that B6.HttQ111/+ mice are a useful tool for modeling disease-modifying or neuroprotective strategies for disease processes before the onset of overt phenotypes.

neuroscience↗