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Biology subjects

Ulrich, J.

Publications and source records attributed to Ulrich, J..

4 recordsLinked to original sources

Large parks and city-wide tree cover boost butterfly diversity across 22 major U.S. cities

Accelerating global urbanization necessitates a better understanding of how to manage cities that promote biodiversity. However, we currently lack multi-year, multi-city studies, which limits a generalizable understanding of how both within and between city differences impact the spatial and temporal dynamics of urban biodiversity. Here, we tested hypotheses about the drivers of butterfly diversity within and across urban parks by applying Bayesian oc-cupancy models to five years of iNaturalist community science data from 2,550 parks in 22 major U.S. cities. We found that cities with bigger parks supported more species per park, including more disturbance- and edge-avoidant species. This was driven by a positive effect of park size on butterfly species colonization rates. We also found that attributes of habitat quality (plant diversity within parks and tree cover surrounding parks) contributed to butter-fly species occupancy. Park connectivity increased species persistence, but the overall effects on butterfly species occupancy varied across cities. Finally, we found that the total area of tree cover throughout a city, rather than the size or connectivity of individual parks, was the primary determinant of city-wide diversity: Increasing total tree canopy cover from below-average ([~] 6%) to above-average ([~] 22%) increased city-wide species richness by[~] 10%. These findings highlight the need for cities to maintain large parks while also increasing city-wide tree cover to support biodiversity across local to regional scales. By integrat-ing high-resolution community science data across the continental U.S., this study provides mechanistic insight into how cross-scale processes shape urban biodiversity dynamics and identifies generalizable recommendations for improving urban conservation management. Significance statementAdvancing urban sustainability hinges on better understanding how to promote biodiver-sity in urban landscapes. Yet, it is largely unclear how urban biodiversity is affected by both within- and between-city differences. Applying Bayesian occupancy models to 5 years of iNaturalist community science butterfly data from 22 U.S. cities, we found that cities with larger parks supported more species per park, including species of higher conservation concern. Simultaneously, increasing city-wide tree canopy cover area, including area both within and outside of parks, increased total city-wide butterfly diversity. Integrating biodi-versity conservation recommendations from this study into urban management planning will reinforce the benefits of participating in community science programs, thereby strengthening positive feedbacks between the health of people and nature.

ecology↗

Maternal smoking in early pregnancy disrupts placental function through syncytiotrophoblast and macrophage dysregulation.

Smoking in pregnancy is the leading avoidable cause of gestational morbidity and mortality, causally linked to fetal growth restriction (FGR). The placenta, functional interface between mother and fetus is essential for healthy fetal development. For the first time, we studied cell type-resolved smoking effects on placental development at high molecular resolution using single-nucleus RNA sequencing and deep visual proteomics of matched tissues. We validated our findings through an independent cohort and in-vitro cigarette smoke exposure to primary human trophoblast cells. Our results show placental macrophages (Hofbauer cells; HBC) and the syncytiotrophoblast (STB) barrier are most affected by smoking, with dysregulation of cell-cell adhesion, extracellular matrix organization, and stress phenotype. STBs show moderate compositional increases in smokers and in-silico trophoblast differentiation modelling indicates a preferential shift towards the STB lineage in this group. The trophoblast displays a large upregulation of pro-angiogenic effectors, increases in xenobiotic detoxification, reduced mitochondrial function, and vastly altered transmembrane transport. These molecular changes affect placental development with important consequences for fetal growth. We provide insight into placental dysfunction contributing to FGR early in pregnancy, before clinical symptoms appear. We anticipate this data to advance diagnostics and therapies to improve FGR outcomes.

systems biology↗

Redirecting full-length FLT1 expression towards its soluble isoform promotes postischemic angiogenesis

Vascular endothelial growth factors and their tyrosine kinase receptors are key mediators of vasculogenesis and angiogenesis with FLT1 (VEGFR1) serving as a decoy receptor. A truncated mRNA transcript encoding soluble (s) FLT1 can be generated by premature cleavage and polyadenylation (APA). Although a shortening of transcripts is described in pathological settings, including heart diseases, the functional in vivo impact of FLT1 gene isoform generation and relevance for angiogenesis remain unknown. Here, we show that specific splice site mutations within Flt1 inhibit telescripting and activate APA in vivo to efficiently modulate gene isoform expression, inducing a complete loss of full-length (fl) Flt1 and a switch towards sFlt1 in mice. FLT1 is a high-affinity decoy receptor of VEGF limiting vessel overgrowth. We show that sFLT1 was sufficient for developmental vasculogenesis, whereas flFLT1 controlled ischemia-driven angiogenesis. Our results demonstrate that telescripting is essential in vivo for controlling Flt1 isoform expression and angiogenesis and can be harnessed to improve reparative revascularization. Furthermore, given the widespread abundance of APA signals, our approach may serve as a blueprint for studying telescripting and generating other truncated gene isoforms in vivo.

cell biology↗

Molecular characterization of a DyP-type peroxidase from the human parasitic cestode Echinococcus multilocularis

The lethal zoonosis alveolar echinococcosis is caused by the metacestode larval stage of the tapeworm Echinococcus multilocularis. During the chronic phase of the disease, metacestode tissue is growing infiltratively into liver tissue and provokes an immunes response of the host. Mechanisms of parasite defence against reactive oxygen species (ROS), which are produced during parasite growth and host immune responses, are incompletely understood so far. We herein describe the characterization of an Echinococcus Dyp (dye decolorizing) - type peroxidase, EmDyp, family members of which are typically expressed by bacteria and fungi. EmDyp showed significant homologies to bacterial and fungal Dyp peroxidases and recombinantly expressed EmDyp displayed profound enzymatic activity towards different substrates such as 3,3-diaminobenzidine or luminol. Furthermore, although structurally not being related to classical catalases, EmDyp showed catalase activity in respective activity gels. In situ hybridization experiments showed expression of the EmDyp expressing gene, emdyp, in the germinal layer of the metacestode as well as in the posterior region of the protoscolex, both in differentiated and in germinative (stem) cells of the parasite. Interestingly, RT-qPCR experiments demonstrated that emdyp expression is induced in the metacestode upon growth under aerobic conditions. Particularly high expression of emdyp was observed under in vivo growth conditions in jirds within the liver. These data indicate a role of EmDyp in the defence of the metacestode against host- and/or parasite-derived ROS during chronic alveolar echinococcosis. Since Dyp-type peroxidases are not encoded on the genomes of mammalian hosts for E. multilocularis, EmDyp might be used as a target molecule for developing novel therapeutics against the parasite.

molecular biology↗