Institut für Biologie

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The emergence of ecotypes in a parasitoid wasp: a case of incipient sympatric speciation in Hymenoptera?
(2021) Malec, Pawel; Weber, Justus; Böhmer, Robin; Fiebig, Marc; Meinert, Denise; Rein, Carolin; Reinisch, Ronja; Henrich, Maik; Polyvas, Viktoria; Pollmann, Marie; von Berg, Lea; König, Christian; Steidle, Johannes L. M.
Background: To understand which reproductive barriers initiate speciation is a major question in evolutionary research. Despite their high species numbers and specific biology, there are only few studies on speciation in Hymenoptera. This study aims to identify very early reproductive barriers in a local, sympatric population of Nasonia vitripennis (Walker 1836), a hymenopterous parasitoid of fly pupae. We studied ecological barriers, sexual barriers, and the reduction in F1-female offspring as a postmating barrier, as well as the population structure using microsatellites. Results: We found considerable inbreeding within female strains and a population structure with either three or five subpopulation clusters defined by microsatellites. In addition, there are two ecotypes, one parasitizing fly pupae in bird nests and the other on carrion. The nest ecotype is mainly formed from one of the microsatellite clusters, the two or four remaining microsatellite clusters form the carrion ecotype. There was slight sexual isolation and a reduction in F1-female offspring between inbreeding strains from the same microsatellite clusters and the same ecotypes. Strains from different microsatellite clusters are separated by a reduction in F1-female offspring. Ecotypes are separated only by ecological barriers. Conclusions: This is the first demonstration of very early reproductive barriers within a sympatric population of Hymenoptera. It demonstrates that sexual and premating barriers can precede ecological separation. This indicates the complexity of ecotype formation and highlights the general need for more studies within homogenous populations for the identification of the earliest barriers in the speciation process.
Exploring ND-011992, a quinazoline-type inhibitor targeting quinone reductases and quinol oxidases
(2023) Kägi, Jan; Sloan, Willough; Schimpf, Johannes; Nasiri, Hamid R.; Lashley, Dana; Friedrich, Thorsten; Kägi, Jan; Institut für Biochemie, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany; Sloan, Willough; Department of Chemistry, William & Mary, Williamsburg, USA; Schimpf, Johannes; Institut für Biochemie, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany; Nasiri, Hamid R.; Department of Cellular Microbiology, University Hohenheim, Stuttgart, Germany; Lashley, Dana; Department of Chemistry, William & Mary, Williamsburg, USA; Friedrich, Thorsten; Institut für Biochemie, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany
Bacterial energy metabolism has become a promising target for next-generation tuberculosis chemotherapy. One strategy to hamper ATP production is to inhibit the respiratory oxidases. The respiratory chain of Mycobacterium tuberculosis comprises a cytochrome bcc:aa3 and a cytochrome bd ubiquinol oxidase that require a combined approach to block their activity. A quinazoline-type compound called ND-011992 has previously been reported to ineffectively inhibit bd oxidases, but to act bactericidal in combination with inhibitors of cytochrome bcc:aa3 oxidase. Due to the structural similarity of ND-011992 to quinazoline-type inhibitors of respiratory complex I, we suspected that this compound is also capable of blocking other respiratory chain complexes. Here, we synthesized ND-011992 and a bromine derivative to study their effect on the respiratory chain complexes of Escherichia coli. And indeed, ND-011992 was found to inhibit respiratory complex I and bo3 oxidase in addition to bd-I and bd-II oxidases. The IC50 values are all in the low micromolar range, with inhibition of complex I providing the lowest value with an IC50 of 0.12 µM. Thus, ND-011992 acts on both, quinone reductases and quinol oxidases and could be very well suited to regulate the activity of the entire respiratory chain.
Hitze als Schlüssel zur Aufklärung der Lysogenie beim SPß-Phagen
(2025) Kohm, Katharina; Kohm, Katharina; Institut Biologie, Universität Hohenheim, Garbenstraße 30, D-70599, Stuttgart, Deutschland
Identification of novel genes including NAV2 associated with isolated tall stature
(2023) Weiss, Birgit; Ott, Tim; Vick, Philipp; Lui, Julian C.; Roeth, Ralph; Vogel, Sebastian; Waldmüller, Stephan; Hoffmann, Sandra; Baron, Jeffrey; Wit, Jan M.; Rappold, Gudrun A.
Very tall people attract much attention and represent a clinically and genetically heterogenous group of individuals. Identifying the genetic etiology can provide important insights into the molecular mechanisms regulating linear growth. We studied a three-generation pedigree with five isolated (non-syndromic) tall members and one individual with normal stature by whole exome sequencing; the tallest man had a height of 211 cm. Six heterozygous gene variants predicted as damaging were shared among the four genetically related tall individuals and not present in a family member with normal height. To gain insight into the putative role of these candidate genes in bone growth, we assessed the transcriptome of murine growth plate by microarray and RNA Seq. Two (Ift140, Nav2) of the six genes were well-expressed in the growth plate. Nav2 (p-value 1.91E-62) as well as Ift140 (p-value of 2.98E-06) showed significant downregulation of gene expression between the proliferative and hypertrophic zone, suggesting that these genes may be involved in the regulation of chondrocyte proliferation and/or hypertrophic differentiation. IFT140, NAV2 and SCAF11 have also significantly associated with height in GWAS studies. Pathway and network analysis indicated functional connections between IFT140, NAV2 and SCAF11 and previously associated (tall) stature genes. Knockout of the all-trans retinoic acid responsive gene, neuron navigator 2 NAV2, in Xenopus supports its functional role as a growth promotor. Collectively, our data expand the spectrum of genes with a putative role in tall stature phenotypes and, among other genes, highlight NAV2 as an interesting gene to this phenotype.
Metabolic rewiring compensates for the loss of amino acid biosynthesis in Bacillus subtilis
(2024) Yousef Mardoukhi, Mohammad Saba; Commichau, Fabian M.
Amino acids are considered as some of the earliest organic molecules to form on Earth. Serving as the building blocks of proteins, they are intricately connected to nearly every life process. Therefore, amino acid metabolism needs to be precisely regulated in any living organism. Amino acid metabolism includes the biochemical pathways responsible for the synthesis, degradation, and utilization of amino acids. Most of the bacteria, particularly the Gram-positive model bacterium Bacillus subtilis, have the capability to synthesize all proteinogenic amino acids or, if available, import them from the environment. Throughout evolution, different metabolic pathways have emerged to maintain metabolites level inside the cells. Some biosynthetic pathways are unknown as they are not primary routes or are typically inactive under normal conditions. However, they may become active under specific circumstances. Two very important pathways, previously not known to be substituted by alternative routes, involve de novo biosynthesis of glutamate, which is an essential amino group donor in every cell. Many bacteria can synthesize glutamate using a NADPH + H+-dependent glutamate dehydrogenase (GDH). Alternatively, glutamate can be produced by the combined action of the ATP-dependent glutamine synthetase (GS) and the NADPH + H+-dependent glutamate synthase (GOGAT). B. subtilis only employs the GS-GOGAT pathway for de novo synthesis of glutamate. In the context of this work, it was shown that a B. subtilis deficient for the GS-GOGAT pathway may employ the aspartase AnsB and aspartate transaminase AspB for the synthesis of glutamate in biologically significant amounts. Genetic analyses revealed that the aspartase AnsB converts ammonium and the tricarboxylic acid cycle intermediate fumarate to aspartate. Subsequently, the aspartate transaminase AspB transfers the amino group from aspartate to α-ketoglutarate, resulting in the production of L-glutamate and oxaloacetate. This observation challenges the well-established point of view of whether the GS-GOGAT-dependent pathway is indeed the only route for de novo synthesis of glutamate in nature. It was also set out to explore which amino acids could serve as the sole sources of carbon and nitrogen in the background of a B. subtilis strain that is a genetically stable glutamate auxotroph. The aim was to understand the conversion of the amino acids into glutamate and further to α-ketoglutarate, a reaction that is facilitated by the enzymatic activity of the GDHs RocG/GudB. It turned out that some of the amino acids are toxic for B. subtilis. However, B. subtilis can quickly develop resistance by the acquisition of mutations that result in reduced and enhanced amino acid uptake and export, respectively. Moreover, the toxicity of some amino acids may be reduced by increased degradation of glutamate. Furthermore, with focus on the toxicity of asparagine, it could be demonstrated that AimA, which has been characterized as a general amino acid importer, serves as a low affinity asparagine transporter in B. subtilis. Finally, AzlCD, which was previously described as an exporter for histidine and branched-chain amino acids, also exports asparagine. Thus, B. subtilis can adapt to amino acid toxicity in various ways.
Nucleo-cytoplasmic shuttling of murine RBPJ by Hairless protein matches that of Su(H) protein in the model system Drosophila melanogaster
(2021) Wolf, Dorina B.; Maier, Dieter; Nagel, Anja C.
CSL transcription factors are central to signal transduction in the highly conserved Notch signaling pathway. CSL acts as a molecular switch: depending on the cofactors recruited, CSL induces either activation or repression of Notch target genes. Unexpectedly, CSL depends on its cofactors for nuclear entry, despite its role as gene regulator. In Drosophila, the CSL homologue Suppressor of Hairless (Su(H)), recruits Hairless (H) for repressor complex assembly, and eventually for nuclear import. We recently found that Su(H) is subjected to a dynamic nucleo-cytoplasmic shuttling, thereby strictly following H subcellular distribution. Hence, regulation of nuclear availability of Su(H) by H may represent a new layer of control of Notch signaling activity. Here we extended this work on the murine CSL homologue RBPJ. Using a ‘murinized’ fly model bearing RBPJwt in place of Su(H) at the endogenous locus we demonstrate that RBPJ protein likewise follows H subcellular distribution. For example, overexpression of a H*NLS3 protein variant defective of nuclear import resulted in a cytosolic localization of RBPJ protein, whereas the overexpression of a H*NES protein variant defective in the nuclear export signal caused the accumulation of RBPJ protein in the nucleus. Evidently, RBPJ is exported from the nucleus as well. Overall these data demonstrate that in our fly model, RBPJ is subjected to H-mediated nucleo-cytoplasmic shuttling as is Su(H). These data raise the possibility that nuclear availability of mammalian CSL proteins is likewise restricted by cofactors, and may hence present a more general mode of regulating Notch signaling activity.

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