Biology subjects

Schott, T.

Publications and source records attributed to Schott, T..

2 recordsLinked to original sources

bioRxiv2025

Quantifying the net effect of biodiversity on stability

Understanding the relationship between biodiversity and both the functioning and stability of ecosystems has been a central focus of ecologists for decades. A step-change in our understanding of the biodiversity-ecosystem functioning relationship was enabled by explicit measurement of the additional functioning provided by biodiversity through comparing expected and observed yields in multi-species communities. However, we lack an equivalent measure for stability. Here, we quantify the net biodiversity effect on stability using model simulations and a microcosm experiment that exposed different phytoplankton species and their combinations to temperature increases and fluctuations. As an emergent property of communities, stability frequently exceeded the expected stability of the combined component species, leading to a net biodiversity effect on stability analogous to the effect on functioning. In our simulations, these effects depended on the strength of competitive interactions as well as species composition and their thermal niche. Experimentally, the stabilising effect of diversity was, however, non-linear, greatest for two-species combinations, and varied with both community composition and disturbance regime. Quantifying the net biodiversity effect on stability advances our mechanistic understanding of the biodiversity-stability relationship, and provides crucial information to support ecosystem management and conservation.

ecology↗

bioRxiv2025

Kremen1 dependence receptor induces SEC24C- and ATG9A-dependent autophagic cell death

Dependence receptors (DRs) induce cell death by apoptosis when unbound by their cognate ligands. Among them, Kremen1 was first described to induce cancer cell death in the absence of its ligand, DKK1. However, the precise mechanism of Kremen1-induced cell death remains unclear. In this study, we demonstrate that Kremen1 induces cell death with autophagic features, contrasting with the apoptotic process typically associated with dependence receptors. Specifically, the pharmacological inhibition of autophagy, or genetic silencing of key autophagy effectors, efficiently suppresses this cell death process. A biotin proximity labeling for protein-protein interactions identified SEC24C, a component of the COP-II complex, as a critical effector in Kremen1-induced autophagy and cell death. Our findings further reveal that Kremen1 is in proximity with SEC24C and ATG9A after vesicular trafficking and fosters the interaction of SEC24C with ATG8, ERGIC and ATG9A. This potentially underlies the increased number of autophagosomes leading to cell death. The induction of aberrant autophagy by Kremen1 deserves particular attention, especially as the Kremen1/DKK1 pair is frequently altered in cancers. Thus, targeting this pathway may offer a potential strategy for treating cancers resistant to current therapies.

cancer biology↗