Biology subjects

Dollinger, C.

Publications and source records attributed to Dollinger, C..

3 recordsLinked to original sources

bioRxiv2026

Loss of competitive strength in European conifer species under climate change

Climate change is expected to alter species assemblages by affecting the outcome of competition between species. Investigating processes of competition remains challenging particularly in tree communities, as they unfold over extensive spatio-temporal scales. Here, we developed a deep-learning approach to leverage a novel database of 135 million simulated local-scale tree responses to climate across continental Europe to investigate changes in the competitiveness of nine major tree species under different scenarios of climate change. Specifically, we trained a Deep Neural Network on local process model projections to investigate climate change effects on indicators of competitive strength and species dominance. We found decreasing competitive strength for all investigated evergreen coniferous species across their distribution, while major deciduous broadleaved species such as Quercus robur and Fagus sylvatica increased in competitiveness. Changes in tree species competition with climate differed locally, but most investigated species lost competitive strength at their warm range edges. As a consequence of these changes, up to 19% of Europes forests could experience a change in the dominant tree species until the end of the 21st century. Our results suggest a profound climate-induced reassembly of Europes forests and identify areas that may require specific attention in forest policy and management.

ecology↗

bioRxiv2025

Nuclear Phase Separation Drives NPM1-mutant Acute Myeloid Leukemia

During cancer development, mutations promote gene expression changes that cause transformation. Leukemia is frequently associated with aberrant HOXA expression driven by translocations in nucleoporin genes or KMT2A, and mutations in NPM1. How disparate mutations converge on this regulatory pathway is not understood. Here we demonstrate that mutant NPM1 (NPM1c) forms nuclear condensates in multiple human cell lines, mouse models, and primary patient samples. We show NPM1c phase separation is necessary and sufficient to coordinate the recruitment of NUP98 and KMT2A to condensates. Through extensive mutagenesis and pharmacological destabilization of phase separation, we find that NPM1c condensates are necessary for regulating gene expression, promoting in vivo expansion, and maintaining the undifferentiated leukemic state. Finally, we show that nucleoporin and KMT2A fusion proteins form condensates that are biophysically indistinguishable from NPM1c condensates. Together, these data define a new condensate underlying leukemias that we term coordinating bodies (C-bodies), and propose C-bodies as a therapeutic vulnerability.

biophysics↗

bioRxiv2025

Nanometer condensate organization in live cells derived from partitioning measurements

Biomolecules self-organize into membrane-less organelles known as condensates that compartmentalize essential biochemical processes, such as ribosome biogenesis in the nucleolus1-3. Molecular dynamics within condensates are governed by chemical preferences and interaction networks that can imbue nanoscale structure4-7. Such organization is typically inferred from ensemble-averaged measurements, such as scattering and electron microscopy, which reveal molecular arrangements8-14. However, the complexity of cells obscures the interpretability of these techniques, limiting insight into condensate internal structure and roles in macromolecular assembly and transport. Here, we develop an approach to quantify the average microenvironment surrounding specific proteins within condensates in live cells, using thermodynamic principles to interpret the partitioning of designed protein probes. Using this approach, we find that condensates in cells, including the nucleolus, stress granule, and nuclear pore, exhibit spatial inhomogeneity, aligning with emerging views of condensates as networked fluids5,6,15-18. Within the nucleolus, we link spatial inhomogeneity to ribosome biogenesis, which progressively loosens the average local meshwork, facilitating transport of assembled ribosomal subunits. Within the nuclear pore, we find that transporters experience a weaker local meshwork than nucleoporins, consistent with the selective phase model19,20. Together, our approach uncovers a distinct mode of biomolecular control arising from nanoscale structure, which we term microenvironment coupling, whereby internal interaction landscapes shape transport to enable regulation and proofreading.

biophysics↗