Leipzig University

Earth is experiencing substantial biodiversity losses at the global scale, while both species gains and losses are occurring locally and regionally. Nonrandom changes in species distributions could profoundly influence ecosystem functions and services. However, few experimental tests have examined the influences of invasive ecosystem engineers, which can have disproportionally strong impacts on native ecosystems. Invasive earthworms are a prime example of ecosystem engineers that influence many ecosystems around the world. In particular, European earthworms invading northern North American forests may cause simultaneous species gains and losses with significant consequences for essential ecosystem processes like nutrient cycling and crucial services like carbon sequestration. Using a synthetic combination of field observations, field experiments, lab experiments, and meta-analyses, the proposed work will be the first systematic examination of earthworm effects on relationships between plant communities, soil food webs, and ecosystem processes. Further, effects of a changing climate on the spread and consequences of earthworm invasion will be investigated. Meta-analyses will be used to test if earthworms cause invasion waves, invasion meltdowns, habitat homogenization, and ecosystem state shifts. Global data will be synthesized to test if the relative magnitude of effects differ from place to place depending on the functional dissimilarity between native soil fauna and exotic earthworms. Moving from local to global scale, the present proposal examines the influence of earthworm invasions on biodiversity–ecosystem functioning relationships from an aboveground–belowground perspective. This approach is highly innovative as it utilizes exotic earthworms as an exciting model system that links invasion biology with trait-based community ecology, global change research, and ecosystem ecology, pioneering a new generation of biodiversity–ecosystem function research.

This project will document and explain a substantial number of grammatical universals by demonstrating a link between cross-linguistic patterns of language form and general trends of language use. The claim is that frequently expressed meanings tend to be expressed by short forms, not only at the level of words, but also throughout the grammars of languages around the world (form-frequency correspondences). A simple example is the asymmetry in the coding of present-tense forms and future-tense forms in the world’s languages, as one out of a multitude of analogous cases: Present-tense forms tend to be short or zero-coded, while future-tense forms tend to be longer or to have an overt marker. This corresponds to a usage asymmetry: Present-tense forms are generally more frequent than future-tense forms, in all languages. The proposed explanation is that higher-frequency items are more predictable than lower-frequency items, and predictable content need not be expressed overtly or can be expressed by shorter forms. Form-frequency correspondences thus make language structure more efficient, but it still needs to be shown that there exists a mechanism that creates and maintains these efficient structures: recurrent instances of language change driven by the speakers’ preference for user- friendly utterances. The project thus combines cross-linguistic research on grammar, cross-linguistic corpus research and historical linguistics in a ground- breaking way. For reasons that have to do with the history of the discipline, form-frequency correspondences are still largely overlooked and ignored by linguists, so the current project will have a significant impact on our general understanding of human language.

Neuromuscular disorders belong to the most common but least treatable neurological conditions and are caused by defects in cell types that together build the neuromuscular unit – motoneurons and their axons, glial cells and myocytes. Clinically, neuromuscular diseases share an impairment of motor function and the intimate functional relationship of involved cell types suggests overlapping pathological mechanisms. As our current understanding is largely confined to locally isolated processes, the present AxoMyoGlia proposal will undertake the ambitious approach to elucidate the spatial dimensions of the molecular interplay among the key cellular players of the neuromuscular unit. By taking demyelinating peripheral neuropathies as a powerful model system, I aim at unravelling basic principles of how local glial impairment propagates malfunction within the neuromuscular unit, including potential remote axon and muscle feedback mechanisms. To this end, I will employ neuropathic mouse models and generate a holistic transcriptional cellular interactome of the diseased neuromuscular unit at single cell resolution level. With milli- to nanometer imaging precision, this interactome will be extended to the first visualization of the spatial relation between glial and axonal dysfunction along the entire longitudinal dimension of the nerve. In order to untangle local and distant causes from consequences, I will develop an innovative mouse model that will offer the unprecedented option to specifically induce and examine the global consequences of locally restricted glial neuropathy at any position in the neuromuscular system. With its pioneering multimodal approach to converge different areas of neuromuscular research, AxoMyoGlia aims at uncovering general pathological mechanisms at the interface of basic neuroscience and applied neurology - that will be highly relevant for therapeutic advance in neuromuscular diseases and related disorders of the central nervous system.