Welcome to theDepartment of Genetics ("Struktureinheit Genetik")
The overall goal of the Department is to investigate the genetic mechanisms that generate evolutionary novelties and biodiversity. In a framework of evolutionary developmental biology ("evo-devo"), we study the phylogeny of developmental control genes and their impact on morphological evolution in animals and plants. To achieve our goal we use a wide range of tools from genetics, molecular biology and bioinformatics.
The Department consists of three research groups:
The Theißen lab investigates the structure, function and evolution of transcription factors, concentrating on proteins encoded by MADS-box genes. Our interests range from the relationship between structure and function on the molecular level via the mechanisms underlying gene regulation (including the importance of microRNAs) to the role of transcription factors in the evolution of gene regulatory networks and developmental processes. A major focus of our work is on elucidating the role of MADS-box genes in the evolution of flowers and fruits and in the origin of biodiversity. Our model systems comprise diverse land plants ranging from mosses to flowering plants, and includes important crop plants such as cabbage, rice, maize, tulips and spruce as well as wild plants (e.g. field pepperweed) and typical model organisms (thale cress, Arabidopsis thaliana). To achieve our goals we use tools from genetics, molecular biology, biophysics and bioinformatics.
The Haenold Lab at the Leibniz Institute on Aging, Fritz Lipmann Institute e.V. in Jena sets its research focus on molecular processes in the young and aging brain. We are particularly interested in the role of the transcription factor Nuclear Factor kappa B (NF-κB), which acts as transcriptional regulator of gene expression in neuronal plasticity. NF-κB consists of five subunits that form dimers and can be activated via a classical (RelA/p50 dimers) or an alternative (p52/RelB dimers) signaling pathway. Depending on the involved subunits, NF-κB can either activate or repress target gene expression. Studies on various species and tissues have demonstrated an age-associated increase in NF-κB activity. The increased expression of NF-κB regulated target genes particularly involves pro-inflammatory and anti-regenerative factors, thus NF-κB directly contributes to organismic aging. Using genetically modified mice, we have demonstrated that loss of the transcriptional activator subunit RelA reduces NF-κB activity, whereas loss of the transcriptional repressor subunit p50 can increase NF-κB activity. As demonstrated for the murine visual system, we have shown that subunit-specific modulations of NF-κB can either accelerate or delay aging-associated impairments of neuronal networks. Moreover, our results show that both subunits, p50 and RelA, are required for the induction of synaptic plasticity, which is a key process in learning and memory formation. Currently, we aim to identify NF-κB-dependent gene expression programs involved in neuronal plasticity and neurosenescence, respectively, and how these expression patterns change with aging and under cognitive training paradigms.
The Brantl lab focuses mainly on gene regulation in Gram-positive bacteria by small regulatory RNAs (sRNAs) and transcription factors. We use Bacillus subtilis as model organism. On the one hand, we investigate a small trans-encoded sRNA – SR1 – discovered in our group. SR1 is a dual-function sRNA: it acts as base-pairing sRNA in arginine catabolism, but also encodes a peptide that does not only play a role in sugar metabolism, but has a global function in RNA degradation. On the other hand, we explore three type I toxin-antitoxin systems whose antitoxins are cis-encoded sRNAs. In both cases, we are interested in the biological functions of these sRNAs, their molecular mechanisms of action as well as their regulation by transcription factors. We employ a combination of in vitro and in vivo techniques to characterize RNA and DNA-binding proteins.