Press releases

Like carbon dioxide, many gaseous substances containing halogens such as chlorine or fluorine contribute to the greenhouse effect. Researchers from Goethe University Frankfurt have now put a measuring device into operation at the Taunus Observatory on Kleiner Feldberg, a mountain near Frankfurt, which continuously monitors the concentrations of such gases with very high accuracy for the first time in Germany and within an international network. Initial results indicate that sources of special fluorinated gases (F-gases) are present in Germany as well. The scientists in Frankfurt emphasize that recording F-gases ought to be included in the official air monitoring program in the long term. 

In the past, they were found in every refrigerator and aerosol until it was discovered that they had ripped a hole in the ozone layer protecting Earth's atmosphere: chlorofluorocarbons, in short CFCs. Since 2000, the Montreal Protocol has practically abolished CFC production worldwide. Halogenated hydrocarbons without chlorine, known as F-gases, were increasingly used as a substitute – until it emerged that these gases, although they do not constitute a threat to the ozone layer, are nonetheless potent greenhouse gases, just like CFCs. Accordingly, F-gases were added to the Montreal Protocol in 2016 within the “Kigali Amendment". In Europe, the F-Gas Regulation (517/2014) aims to ensure the reduction of emissions. 

Despite their low concentrations, halogenated greenhouse gases play a significant role in climate change: They are responsible for up to nine percent of the anthropogenic greenhouse effect – one kilogram of these gases can have the same impact on the climate as ten tons of carbon dioxide. To date, however, their occurrence in the atmosphere has not been systematically monitored in Germany. 

Within the ACTRIS research infrastructure, scientists from Goethe University Frankfurt have now put a measuring device called “Medusa" into operation at the Taunus Observatory on Kleiner Feldberg, a mountain near Frankfurt, which continuously measures the concentration of many trace gases relevant for the atmosphere. Their measurements of halogenated greenhouse gases are also incorporated in the international AGAGE network, which has been monitoring the occurrence of climate-relevant trace gases at stations all over the world since 1978. These are the first high-quality measurements of this kind in Germany that can also be compared with data worldwide.

Professor Andreas Engel from the Institute for Atmospheric and Environmental Sciences at Goethe University Frankfurt, who is in charge of “Medusa", says: “Our measurements have already clearly shown that there are significant sources of F-gases in Germany. We have therefore joined forces within an EU-funded project with other researchers, primarily from Germany, Switzerland and the UK, to quantify F-gas emissions on the basis of these measurements with the help of computer models and to further narrow down their regions of origin." 

The very low concentrations, the large number of components to be measured and the high accuracies required make the measurements very complex, he says. He is convinced, however, that – because of their significance – measuring F-gases should shift from research to official air monitoring in the long term: “We need to set up a program that also integrates the systematic recording of halogenated greenhouse gases, including F-gases, into the official atmospheric measurement system. This could deliver sufficient data to identify sources and take appropriate countermeasures." 

Background:
Greenhouse gases thought dead (Forschung Frankfurt 2-2020)
https://www.forschung-frankfurt.uni-frankfurt.de/108794305.pdf 

AGAGE: Advanced Global Atmospheric Gases Experiment
https://agage.mit.edu/ 

Picture download: https://www.uni-frankfurt.de/140750923 

Caption: The Taunus Observatory on the mountain Kleiner Feldberg near Frankfurt am Main houses the new "Medusa" device, which detects climate-relevant F-gases. Photo: Markus Bernards, Goethe University 

Further information
Professor Andreas Engel
Institute for Atmospheric and Environmental Sciences
Goethe University Frankfurt
Tel.: + 49 (0)69 798-40259
an.engel@iau.uni-frankfurt.de
Website: http://www.geo.uni-frankfurt.de/iau
Twitter: @goetheuni

Editor: Dr. Markus Bernards, Science Editor, PR & Communication Office, Theodor-W.-Adorno-Platz 1, 60323 Frankfurt am Main, Tel: +49 (0) 69 798-12498, Fax: +49 (0) 69 798-763 12531, bernards@em.uni-frankfurt.de.

In all living organisms, the biomolecule transfer RNA (tRNA) plays a fundamental role in protein production. tRNAs are generated from precursor molecules in several steps. The enzyme tRNA splicing endonuclease (TSEN), among other things, catalyzes one step in this process. Mutations in TSEN lead to a neurodegenerative disorder called pontocerebellar hypoplasia, which is associated with severe disabilities and early death. Researchers at Goethe University Frankfurt and at Johannes Gutenberg University Mainz have now deduced the function of TSEN from its structure and in so doing paved the way in the search for active substances against pontocerebellar hypoplasia. 

Transfer RNAs (tRNAs) are among the most common types of RNA in a cell and are indispensable for protein production in all known organisms. They have an important “translation" function: They determine how the sequence of nucleic acids, in which the genetic information is encoded, is transcribed into a sequence of amino acids from which proteins are built. 

Transfer RNAs are generated from precursor tRNAs (pre-tRNAs), which are converted in several steps into the mature tRNA with a complex three-dimensional structure. In some tRNAs, this includes a step in which a certain section, known as an intron, is excised. In humans, the tRNA splicing endonuclease (TSEN) performs this task. 

The enzyme RNA kinase CLP1, which binds directly to TSEN, also plays a role in ensuring the correct conversion of tRNAs. If TSEN and CLP1 are unable to interact with each other due to a genetic mutation, it seems that tRNAs can no longer form correctly either. The consequences of this are often seen in the development of neurodegenerative disorders. One of these is pontocerebellar hypoplasia, which leads to severe disabilities and premature death in earliest childhood. This very rare progressive disorder manifests itself in an abnormal development of the cerebellum and the pons, a part of the brain stem. 

Although TSEN activity is essential for life, it was to date mostly unclear how the enzyme binds pre-tRNAs and how introns are excised. The lack of a three-dimensional structure of the enzyme also made it difficult to assess the changes triggered by specific pathogenic mutations. By means of cryo-electron microscopy (cryo-EM) conducted at facilities of the Julius-Maximilians University of Würzburg and of the Institute of Biochemistry at Goethe University Frankfurt, researchers led by Dr. Simon Trowitzsch from the Institute of Biochemistry at Goethe University have now succeeded in shedding light on the three-dimensional structure of a TSEN/pre-tRNA complex. 

With the aid of their cryo-EM reconstructions, the research team was able to show for the first time how TSEN interacts with the L-shaped pre-tRNA. TSEN then excises the intron from the long arm of the L. “First, TSEN settles in the corner of the L. It can then recognize both the short and the long arm as well as the angle between them," explains Trowitzsch. 

The TSEN subunit 54 (TSEN54) plays a key role in pre-tRNA recognition, as the researchers have now been able to corroborate. The subunit serves as a “molecular ruler" and measures the distance between the long and the short arm of the L. In this way, TSEN recognizes at which point the pre-tRNA needs to be cleaved in order to remove the intron. 

New findings on the interaction of the RNA kinase CLP1 and the TSEN subunit TSEN54 were a surprise: CLP1 evidently binds to an unstructured and thus very flexible region of TSEN54. It is precisely this region that contains an amino acid most frequently mutated in patients with pontocerebellar hypoplasia. “For us, this is an important indication that drug development in the future should concentrate on maintaining the interaction of TSEN and CLP1," Samoil Sekulovski, first author of the study, is convinced. 

The scientists now hope that the structural data will make it possible to simulate models that can be used to search for potential active substances. Trowitzsch sums up: “Although a promising therapy is still a long way ahead of us, our structure indeed forms a solid foundation for a better understanding of how TSEN works and what the disease patterns of its mutants are." 

Publication: Samoil Sekulovski, Lukas Sušac, Lukas S. Stelzl, Robert Tampé, Simon Trowitzsch: Structural basis of substrate recognition by human tRNA splicing endonuclease TSEN. Nature Structural & Molecular Biology (2023) https://doi.org/10.1038/s41594-023-00992-y 

News&Views: Anita K. Hopper & Jinwei Zhang: Captured: the elusive eukaryotic tRNA splicing enzyme. Nature Structural & Molecular Biology (2023) https://doi.org/10.1038/s41594-023-00995-9 

Picture download: https://www.uni-frankfurt.de/140143743 

Caption: Trimmed: Like scissors, the enzyme TSEN shapes tRNA (colored) by removing parts of the precursor molecule pre-tRNA. Image: Trowitzsch Lab, Goethe University 

Further information
Dr. Simon Trowitzsch
Institute of Biochemistry, Biocenter
Goethe University Frankfurt
Tel.: +49 (0) 69 798 29 273
trowitzsch@biochem.uni-frankfurt.de
Website: https://www.biochem.uni-frankfurt.de/index.php?id=256

Editor: Markus Bernards, PhD, Science Editor, PR & Communication Office, Theodor-W.-Adorno-Platz 1, 60323 Frankfurt am Main, Tel: +49 (0) 69 798-12498, Fax: +49 (0) 69 798-763 12531, bernards@em.uni-frankfurt.de

As part of the immune system, dendritic cells are essential for fighting body cells that have degenerated or are infected with a virus. They trigger an immune response by presenting protein fragments, for example of viruses, to T cells. In so doing, they activate the latter so that these recognize the fragments as foreign. Certain membrane proteins, MHC-I molecules, enable this process within dendritic cells. Researchers at Goethe University Frankfurt and its partner institutes have now identified further interaction partners of the protein complex responsible for loading MHC-I molecules in dendritic cells. 

The specific or acquired immune system of vertebrates is a powerful weapon against pathogens and pathologically altered body cells. Here, T cells play a special role. After activation, they can systematically kill off target cells that have degenerated or are infected with a virus. They carry a receptor on their surface that recognizes small protein fragments – antigens – presented to them by specialized immune cells, including the highly efficient dendritic cells. These are phagocytes (scavenger cells) that patrol through the body in search of infected or degenerated cells, ingest them and degrade them inside a membrane vesicle. During this process, antigens are produced that enable the dendritic cells to bind to MHC-I receptors and then present them on the cell surface. 

The antigenic MHC-I molecules remain stable for several days. During this time, their purpose is to activate immature (naïve) T cells and transform them into potent killer cells (cytotoxic T cells). Thanks to this “armoring function", dendritic cells constitute a ray of hope for personalized immunotherapy. With the participation of Dr. Christian Schölz from the Max von Pettenkofer Institute in Munich as well as Professor Reinhold Förster and Professor Ulrich Kalinke from Hannover Medical School, a team led by Professor Robert Tampé from Goethe University Frankfurt has now been able to show that the protein complex responsible for loading MHC-I molecules in dendritic cells is organized in supramolecular assemblies for particularly efficient antigen presentation. 

Like all surface proteins, MHC-I molecules are incorporated into the membrane of the intracellular endoplasmic reticulum (ER) during synthesis. The ER is a system of tubules and sacs inside the cell, in which the MHC-I molecules are loaded with antigens carried there via a transporter called TAP. 

Small vesicles with the loaded MHC-I molecules bud off from the endoplasmic reticulum, migrate to the cell membrane and fuse with it so that they appear on the cell surface and can interact with T cells. “All body cells with a nucleus present their own antigens to the immune system," Tampé explains, “but dendritic cells are the ones that present the antigens of other cells on MHC-I best of all and in this way are able to arm T cells." This is because dendritic cells have an ER with a particularly extensive network of tubules and sacs. 

For their experiments, the researchers examined dendritic cells in an early stage of cell development, known as progenitor cells, allowing them to develop first into immature and then mature dendritic cells. In all three groups of cells, they found an antigenic peptide loading complex composed of TAP, MHC-I and three other proteins: tapasin, ERp57 and calreticulin, folding enzymes (chaperones) that help the three-dimensional structure of MHC-I to form correctly. 

In the mature dendritic cells, three other proteins further enriched the loading complex: The researchers discovered VAPA and ESYT1 in close proximity, which normally appear at contact sites between the ER and other cell membranes, as well as BAP31. BAP31 occurs at ER exit sites, that is, where the vesicles with the folded proteins bud off from the ER. “This result indicates that antigen processing in dendritic cells is more efficient when the loading complex does not operate on its own but works in organized alliances," says Martina Barends, one of the first authors of the research paper. 

This cooperation with the newly described partners suggests that loading of MHC-I molecules occurs at ER exit sites, which could enable the complexes to reach the cell surface particularly quickly. Moreover, loading complexes at contact sites between the ER and plasma membrane could facilitate direct transport to the cell surface. Tampé is convinced: “This would make antigen presentation far more efficient." The hope now is that these findings will help in the development of new immunization strategies and immunotherapies. “We now have a better idea of how antigens are produced in dendritic cells that can be used therapeutically," summarizes Tampé. 

Publication: Martina Barends, Nicole Koller, Christian Schölz, Verónica Durán, Berislav Bosnjak, Jennifer Becker, Marius Döring, Hanna Blees, Reinhold Förster, Ulrich Kalinke, Robert Tampé: Dynamic interactome of the MHC I peptide loading complex in human dendritic cells. PNAS (2023) https://doi.org/10.1073/pnas.2219790120 

Further information:
Professor Robert Tampé
CRC 1507 – Protein Assemblies and Machineries in Cell Membranes (https:/sfb1507.de)
Institute for Biochemistry, Biocenter
Goethe University Frankfurt, Germany
Tel.: +49 69 798-29475
tampe@em.uni-frankfurt.de
Website: https://www.biochem.uni-frankfurt.de/index.php?id=10
CRC 1507: https://sfb1507.de

Editor: Dr. Markus Bernards, Science Editor, PR & Communication Office, Theodor-W.-Adorno-Platz 1, 60323 Frankfurt am Main, Tel: +49 (0) 69 798-12498, Fax: +49 (0) 69 798-763 12531, bernards@em.uni-frankfurt.de.

For solid tumors to grow efficiently, they generally need the help of non-transformed, endogenous cells around them. Through the communication of these cells between each other, networks form in the tumor's environment which stimulate growth. With the support of the Wilhelm Sander Foundation, researchers at Goethe University Frankfurt have now examined such networks. In the process, they discovered that these networks are very resistant to intervention, but the team also succeeded in identifying possible weak points. 

Tumors consist of both the actual, malignant cancer cells and healthy, non-transformed cells in the immediate environment. These include, among other things, the endogenous scavenger cells of the immune system, called macrophages, as well as types of cells that form connective tissue, such as fibroblasts. Both macrophages and fibroblasts normally contribute to keeping tissue in its original healthy state and to restoring its structure after minor or major damage. These capabilities also play an important role in defending the body against the proliferation and spread of cancer cells. 

However, cancer cells have developed strategies to reprogram both macrophages and fibroblasts into tumor-promoting cells. In this process, the fibroblasts are altered in such a way that they change the tissue structure so that it helps the tumor cells to survive and spread. For example, if metastases form in the lung, the fibroblasts in the lung are activated first. Macrophages secrete growth and survival factors, which the tumors use, for example, to give themselves a better supply of nutrients and oxygen. 

It has long been assumed in cancer research that the deactivation of specific, non-transformed types of cells might be enough for therapy to be successful. However, despite the promising results achieved in research such strategies have so far hardly been successful in the treatment of patients. 

A research team led by Professor Andreas Weigert and Professor Bernhard Brüne from Goethe University Frankfurt has now identified possible reasons for this. For their analyses, the researchers used genetically modified mice that spontaneously develop tumors in their breast tissue. Through further genetic modifications, a fat-like molecule produced by the macrophages and released into the tumor environment, the hormone prostaglandin E2, was deactivated in the mammary carcinoma of these mice. Prostaglandin E2 was previously believed – on the basis of cell culture experiments – to have above all tumor-promoting properties. As expected, deactivating prostaglandin E2 also inhibited the growth of mammary carcinoma in the mice. To the surprise of the research team, however, tissue analyses showed that the fibroblasts divided extensively and were activated, and at the same time more metastases developed in the lungs of the mice. 

In further trials, the transcriptome of the fibroblasts was analyzed, that is, all the genes read from the genome at that point in time. The researchers were able to show that prostaglandin E2 keeps the fibroblasts in mammary carcinoma in an inactive state by means of a previously unknown signaling pathway, which explains why removing the molecule in the mice led to increased metastasis. The process is evidently similar in humans: Fibroblasts activated in a similar way were also found in the breast tumors of some patients, and these patients were far less likely to survive. 

In the course of their histological study of mammary carcinoma, the researchers also encountered a subgroup of macrophages which, similar to fibroblasts, produce parts of the extracellular matrix (the connective tissue between the cells) – above all collagens. Such macrophages, called fibrocytes, were already known from fibrotic disorders (pathological proliferation of connective tissue) of the lung, but their role in tumors was unclear. 

That is why the researchers in Frankfurt, together with Professor Rajkumar Savai from the Max Planck Institute for Heart and Lung Research in Bad Nauheim, examined the role of fibrocytes in lung tumors by systematically deactivating them during tumor growth. By means of single-cell sequencing, they were able to corroborate, among other things, that these cells are a key population which coordinates both the growth of the tumor cells and their supply with blood vessels as well as the tumor-promoting activation of other macrophage subtypes. 

“The results of our studies illustrate that there are many types of cells in the tumor microenvironment that promote tumor survival, growth and spread in a similar way. The tumor uses central molecular hubs through which it simultaneously reprograms various endogenous cells into tumor promoters. If we want to fight cancer effectively, we need to advance the detection and therapeutic use of such hubs," says Weigert, summarizing the study results, which were published in the renowned journals Cancer Research and Nature Communications. Identifying such hubs will be a research priority for the participating laboratories in the future. 

Publications:
1) E. Strack, P.A. Rolfe, A.F. Fink, K. Bankov, T. Schmid, C. Solbach, R. Savai, W. Sha, L. Pradel, S. Hartmann, B. Brüne, A. Weigert. Identification of tumor-associated macrophage subsets that are associated with breast cancer prognosis. Clin Transl Med (2020), 10:e239. https://doi.org/10.1002/ctm2.239
2) E. Elwakeel, M. Brüggemann, J. Wagih, O. Lityagina, M.A.F. Elewa, Y. Han, T. Froemel, R. Popp, A.M. Nicolas, Y. Schreiber, E. Gradhand, D. Thomas, R. Nüsing, J. Steinmetz-Späh, R. Savai, E. Fokas, I. Fleming, F.R. Greten, K. Zarnack, B. Brüne, A. Weigert. Disruption of prostaglandin E2 signaling in cancer-associated fibroblasts limits mammary carcinoma growth but promotes metastasis. Cancer Res. (2022), 82(7):1380-1395. https://doi.org/10.1158/0008-5472.can-21-2116
3) A. Weigert, X. Zheng, A. Nenzel, K. Turkowski, S. Günther, E. Strack, E. SiraitFischer, E. Elwakeel, I.M. Kur, V.S. Nikam, C. Valasarajan, H. Winter, A. Wissgott, R. Voswinkel, F. Grimminger, B. Brüne, W. Seeger, S. Savai Pullamsetti, R. Savai. Fibrocytes boost tumor-supportive phenotypic switches in the lung cancer niche via the endothelin system. Nat Commun. (2022), 13:6078 https://doi.org/10.1038/s41467-022-33458-8 

Picture download: https://www.uni-frankfurt.de/139734297 

Caption: Tissue section of a lung tumor showing different cells in the tumor microenvironment: macrophages (red), collagen-producing macrophages or fibrocytes (yellow), fibroblasts (green). Photo: Institute of Biochemistry I, Faculty of Medicine, Goethe University Frankfurt 

Further information:
Professor Andreas Weigert
Professor for Biochemistry of Innate Immunity
Institute of Biochemistry I
Faculty of Medicine
Goethe University Frankfurt
Theodor-Stern-Kai 7
60590 Frankfurt am Main
Tel.: +49 (0) 69 6301 4593
weigert@biochem.uni-frankfurt.de

Editor: Markus Bernards, PhD, Science Editor, PR & Communication Office, Theodor-W.-Adorno-Platz 1, 60323 Frankfurt am Main, Tel: +49 (0) 69 798-12498, Fax: +49 (0) 69 798-763 12531, bernards@em.uni-frankfurt.de.

Science does not take a deep enough look at chemicals in the environment as one of the causes of the decline in biodiversity. Forty scientists in the RobustNature research network of Goethe University Frankfurt and collaborating institutes have corroborated this in a study that has now been published in the journal “Nature Ecology and Evolution". The researchers regard an interdisciplinary approach as a new opportunity to better understand biodiversity loss in order to be able to take more efficient countermeasures. To this end, they are studying the interactions between chemical pollution and biodiversity loss. 

Declining biodiversity threatens the very basis of human life. Science contends that there are many reasons for this decline. However, while much research is being conducted into the connection between species decline on the one hand and loss of habitats, invasion by non-native species or climate change on the other, science is giving less attention to the impact of chemicals on biodiversity. A recent study by a team of researchers led by Professor Henner Hollert, Dr. Francisco Sylvester and Fabian Weichert from Goethe University Frankfurt corroborates this. 

The team has analyzed in depth the scientific literature on this topic from 1990 to 2021. According to their analysis, the very many research papers on environmental pollution through chemicals were published in only a small number of highly specialized ecotoxicological journals, in which papers on biodiversity loss are only occasionally found. “This suggests that the field is highly encapsulated, which is in stark contrast to publication behavior in relation to other causes of global biodiversity loss," says Henner Hollert. “Research on the environmental impact of chemicals is still mostly dissociated from the assessment of biodiversity loss." 

The authors call for a stronger interdisciplinary focus in research so that the impacts of chemical substances on biodiversity can be better understood and mitigated. What makes the researchers optimistic here is the fact that there have been many methodological advances in ecotoxicology and ecology in recent years. For example, with the help of state-of-the-art chemical and effect-based analytics as well as big data science it is possible to detect thousands of known and unknown substances in environmental samples at the same time. In addition, there are technologies for remote environmental monitoring, for example with satellites, as well as computer models for predicting the ecological risks of chemicals and methods for determining biodiversity with the help of environmental DNA. 

However, the scientists also see quite considerable challenges despite the interdisciplinary approach. For example, basic data are often lacking; each area under study has specific characteristics; the processes at ecosystem scale are complex. To meet these challenges, the researchers have made 16 recommendations. They suggest, for example, obligating industry to make relevant data public. Or they propose developing ecological test models that cover not only individual organisms but also populations, communities or even entire ecosystems. 

The RobustNature research network is examining the robustness and resilience of nature-society systems in the developing Anthropocene and specifically the interaction of chemical pollution and biodiversity loss. To address important questions related to human-ecosystem dynamics, RobustNature has established interdisciplinary collaboration with partners from Germany and abroad. https://www.robustnature.de/en/ 

• Goethe University Frankfurt (Coordination; Faculty of Biological Sciences (15) with the faculties of Law (1), Economics & Business (2), Social Sciences (3), Educational Sciences (4), Geosciences & Geography (11), Computer Science & Mathematics (12), Medicine (16) and the profile area Sustainability & Biodiversity)
• Institute for Social-Ecological Research (ISOE) 
• Senckenberg – Leibniz Institution for Biodiversity and Earth System Research (SGN) 
• LOEWE Center for Translational Biodiversity Genomics (LOEWE TBG) 
• Helmholtz Center for Environmental Research (UFZ), Leipzig 
• Leibniz Institute for Financial Research SAFE, Frankfurt 
• Fraunhofer Institute for Molecular Biology and Applied Ecology (IME), Schmallenberg 
• RWTH Aachen University 
• University of Saskatchewan, Canada 
• ETH Zurich, Switzerland 
• Stockholm University, Sweden 

Publication:
Francisco Sylvester, Fabian G. Weichert, Verónica L. Lozano, Ksenia J. Groh, Miklós Bálint, Lisa Baumann, Claus Bässler, Werner Brack, Barbara Brandl, Joachim Curtius, Paul Dierkes, Petra Döll, Ingo Ebersberger, Sotirios Fragkostefanakis, Eric J. N. Helfrich, Thomas Hickler, Sarah Johann, Jonas Jourdan, Sven Klimpel, Helge Kminek, Florencia Liquin, Darrel Möllendorf, Thomas Müller, Jörg Oehlmann, Richard Ottermanns, Steffen U. Pauls, Meike Piepenbring, Jakob Pfefferle, Gerrit Jasper Schenk, J.F. Scheepens, Martin Scheringer, Sabrina Schiwy, Antje Schlottmann, Flurina Schneider, Lisa M. Schulte, Maria Schulze-Sylvester, Ernst Stelzer, Frederic Strobl, Andrea Sundermann, Klement Tockner, Tobias Tröger, Andreas Vilcinskas, Carolin Völker, Ricarda Winkelmann, Henner Hollert: Better integration of chemical pollution research will further our understanding of biodiversity loss. Nature Ecology and Evolution (2023) http://dx.doi.org/10.1038/s41559-023-02117-6 

Picture download: https://www.uni-frankfurt.de/138808301 

Caption: Pesticides used in agriculture contribute to biodiversity loss. Photo: Markus Bernards 

Further information
Professor Henner Hollert
Institute of Ecology, Diversity and Evolution
Goethe University Frankfurt
and Fraunhofer Institute for Molecular Biology and Applied Ecology (IME), Schmallenberg
and LOEWE Center for Translational Biodiversity Genomics (LOEWE‐TBG), Frankfurt
Tel.: +49 (0)69 798-42171
hollert@bio.uni-frankfurt.de
https://www.bio.uni-frankfurt.de/43970666/Abt__Hollert
Twitter: @hhollert @goetheuni @LOEWE_TBG @fraunhofer_IME @isoewikom @senckenberg @UFZ_de @SAFE_Frankfurt @RWTH @USask_INTL @ETH @ETH_en @Stockholm_Uni

Editor: Markus Bernards, PhD, Science Editor, PR & Communication Office, Theodor-W.-Adorno-Platz 1, 60323 Frankfurt am Main, Tel: +49 (0) 69 798-12498, Fax: +49 (0) 69 798-763 12531, bernards@em.uni-frankfurt.de