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Bouwman, M.

Publications and source records attributed to Bouwman, M..

2 recordsLinked to original sources

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↗

Prrx1b directs pro-regenerative fibroblasts during zebrafish heart regeneration

RationaleThe human heart loses millions of cardiomyocytes after an ischemic injury, but is unable to regenerate the lost tissue. Instead, the injured human heart is repaired by pro-fibrotic fibroblasts that form a large permanent scar. In contrast, the injured zebrafish heart regenerates efficiently without the formation of a permanent scar. While fibroblasts have been shown to be indispensable for zebrafish heart regeneration, very little is known about the mechanisms balancing the fibrotic and regenerative response. A better understanding of these mechanisms could lead to the discovery of novel therapeutic strategies to reduce fibrosis and promote heart regeneration. ObjectiveTo identify novel mechanisms that regulate the balance between cardiac fibrosis and scar-free regeneration. Methods and ResultsUsing a genetic approach, we first show that zebrafish prrx1b loss-of-function mutants display reduced cardiomyocyte proliferation and impaired heart regeneration. Using a lineage tracing approach, we show that Prrx1b is expressed in tcf21+ epicardial-derived cells localizing around and inside the injured area. Next, we used a single cell RNA-sequencing approach on sorted tcf21+ cells isolated from injured prrx1b-/- and wild-type hearts and identified two distinct fibroblast populations. With combined bioinformatic and histological analysis we found that prrx1b-/- hearts contain an excess of pro-fibrotic fibroblasts that produce TGF-{beta} ligands and collagens, while fewer pro-regenerative Nrg1-expressing fibroblasts are formed. Furthermore, by injecting recombinant NRG1 in prrx1b-/- fish we were able to rescue their cardiomyocyte proliferation defect. Finally, using cultured human fetal epicardial cells and siRNA mediated knock-down of PRRX1 we found that PRRX1 is required for NRG1 induction in human epicardial-derived cells. ConclusionsPrrx1b in the injured heart restricts fibrosis and stimulates regeneration by directing epicardial-derived cells towards a pro-regenerative Nrg1-producing fibroblast state.

developmental biology↗