graduationCongratulations on your PhD!

Joanna Liwocha


Mechanisms of polyubiquitin chain formation

RG: Brenda Schulman



graduationCongratulations on your PhD!

Verónica Solís González


Understanding the role of epithelial MyD88 signals in the early development of Experimental Autoimmune Encephalomyelitis (EAE)

RG: Hartmut Wekerle



Many neurological disorders are associated with dysfunctions in cellular power plants, the mitochondria. Angelika Harbauer and her team at the MPI for Biological Intelligence (in foundation) study mitochondria in nerve cells to better understand the development of disease and the mode of action of pharmaceuticals. Among other things, the scientists want to know how cellular communication pathways influence the production and function of mitochondria. This research will now be supported by a Starting Grant from the European Research Council (ERC) of € 1.5 million for the next five years.

Mitochondria are part of the "critical infrastructure" of our cells – they provide most of the energy our cells need to function. In neurons, mitochondria are particularly busy, since the transmission of information along the cells' long projections requires a lot of energy. Consequently, mitochondrial dysfunction can lead to a number of neurological disorders. These include neurodegenerative diseases such as Alzheimer's, and neuropsychiatric diseases such as bipolar disorders.

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Hees, J.T., and Harbauer, A.B.
Biomolecules, 2022, 12, 1595.
doi: 10.3390/biom12111595

Metabolic Regulation of Mitochondrial Protein Biogenesis from a Neuronal Perspective

Neurons critically depend on mitochondria for ATP production and Ca2+ buffering. They are highly compartmentalized cells and therefore a finely tuned mitochondrial network constantly adapting to the local requirements is necessary. For neuronal maintenance, old or damaged mitochondria need to be degraded, while the functional mitochondrial pool needs to be replenished with freshly synthesized components. Mitochondrial biogenesis is known to be primarily regulated via the PGC-1α-NRF1/2-TFAM pathway at the transcriptional level. However, while transcriptional regulation of mitochondrial genes can change the global mitochondrial content in neurons, it does not explain how a morphologically complex cell such as a neuron adapts to local differences in mitochondrial demand. In this review, we discuss regulatory mechanisms controlling mitochondrial biogenesis thereby making a case for differential regulation at the transcriptional and translational level. In neurons, additional regulation can occur due to the axonal localization of mRNAs encoding mitochondrial proteins. Hitchhiking of mRNAs on organelles including mitochondria as well as contact site formation between mitochondria and endolysosomes are required for local mitochondrial biogenesis in axons linking defects in any of these organelles to the mitochondrial dysfunction seen in various neurological disorders.



graduationCongratulations on your PhD!

Anna Kolz


T:B cell communication in ectopic lymphoid follicles in CNS autoimmunity

RG: Anneli Peters



graduationCongratulations on your PhD!

Thomas van Emden


Regulation of Transcription and Stability of Repetitive DNA in S. pombe

RG: Sigurd Braun



graduationCongratulations on your PhD!

Martina Peritore


Strand-specific ChIP-sequencing reveals nucleosome dynamics at DNA double-strand breaks

RG: Boris Pfander



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Brüggenthies, J.B., Fiore, A., Russier, M., Bitsina, C., Brötzmann, J., Kordes, S., Menninger, S., Wolf, A., Conti, E., Eickhoff, J.E., and Murray, P.J.
(IMPRS-LS students are in bold)
J Biol Chem, 2022, 102629
doi: 10.1016/j.jbc.2022.102629

A cell-based chemical-genetic screen for amino acid stress response inhibitors reveals torins reverse stress kinase GCN2 signaling

mTORC1 and GCN2 are serine/threonine kinases that control how cells adapt to amino acid availability. mTORC1 responds to amino acids to promote translation and cell growth while GCN2 senses limiting amino acids to hinder translation via eIF2α phosphorylation. GCN2 is an appealing target for cancer therapies because malignant cells can harness the GCN2 pathway to temper the rate of translation during rapid amino acid consumption. To isolate new GCN2 inhibitors, we created cell-based, amino acid limitation reporters via genetic manipulation of Ddit3 (encoding the transcription factor CHOP). CHOP is strongly induced by limiting amino acids and in this context, GCN2-dependent. Using leucine starvation as a model for essential amino acid sensing, we unexpectedly discovered ATP-competitive PI3 kinase-related kinase inhibitors, including ATR and mTOR inhibitors like torins, completely reversed GCN2 activation in a time-dependent way. Mechanistically, via inhibiting mTORC1-dependent translation, torins increased intracellular leucine, which was sufficient to reverse GCN2 activation and the downstream integrated stress response including stress-induced transcriptional factor ATF4 expression. Strikingly, we found that general translation inhibitors mirrored the effects of torins. Therefore, we propose that mTOR kinase inhibitors concurrently inhibit different branches of amino acid sensing by a dual mechanism involving direct inhibition of mTOR and indirect suppression of GCN2 that are connected by effects on the translation machinery. Collectively, our results highlight distinct ways of regulating GCN2 activity.



Fruit flies can move the retinas of their otherwise rigid compound eyes to visually follow objects and successfully cross obstacles. This is what researchers at the Max Planck Institute for Biological Intelligence (in formation) and colleagues in the USA have discovered. The retinal movements are made by two small muscles in the fly's eye and closely resemble those of the human eye. They help the insects to see crisp images of moving objects and could also provide them with information on the distance of nearby objects.

Pick an object in front of you – a teacup, for example – and fix your gaze on it. You may think that you’re keeping your eyes still, but you’re not: Your eyes are frequently moving unbeknownst to you, making tiny involuntary jitters called microsaccades.

In fact, these jitters are the reason you continue to see the teacup at all – they introduce just enough variety in the light patterns on your eyes to prevent your visual neurons from completely adapting to what they’re looking at. Without microsaccades, the image of the teacup would soon start to fade, in the same way your nose may go blind to a constant odor.

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Kohyama, S.#, Merino-Salomón, A.#, and Schwille, P.
# equal contribution
Nat Commun, 2022, 13, 6098.
doi: 10.1038/s41467-022-33679-x

In vitro assembly, positioning and contraction of a division ring in minimal cells

Constructing a minimal machinery for autonomous self-division of synthetic cells is a major goal of bottom-up synthetic biology. One paradigm has been the E. coli divisome, with the MinCDE protein system guiding assembly and positioning of a presumably contractile ring based on FtsZ and its membrane adaptor FtsA. Here, we demonstrate the full in vitro reconstitution of this machinery consisting of five proteins within lipid vesicles, allowing to observe the following sequence of events in real time: 1) Assembly of an isotropic filamentous FtsZ network, 2) its condensation into a ring-like structure, along with pole-to-pole mode selection of Min oscillations resulting in equatorial positioning, and 3) onset of ring constriction, deforming the vesicles from spherical shape. Besides demonstrating these essential features, we highlight the importance of decisive experimental factors, such as macromolecular crowding. Our results provide an exceptional showcase of the emergence of cell division in a minimal system, and may represent a step towards developing a synthetic cell.