Dr. Christoph Schmal

Profil

Zusammenfassung

Dr. Christoph Schmal erforscht die mathematischen und biologischen Grundlagen circadianer Rhythmen — also der inneren 24-Stunden-Uhren von Organismen. Er kombiniert theoretische Modellierung mit experimentellen Daten, um zu verstehen, wie sich biologische Oszillatoren synchronisieren, wie sie sich an äußere Zeitgeber (wie Licht) anpassen, und welche Folgen Störungen dieser Rhythmen für Immunsystem, Gehirn und Krebstherapie haben. Seine Expertise ist praktisch relevant für die Entwicklung von Therapien, die Tageszeiten berücksichtigen, und für die Optimierung von Behandlungsprotokollen.

Skills

Name

Dr. Christoph Schmal

Titel

Dr.

Fakultät

Lebenswissenschaftliche Fakultät

Institut

Institut für Biologie

Arbeitsgruppe

Theorie neuronaler Systeme

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HU-FIS-Profil

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28.6.2026, 01:12:25

• Synchronisation und Entrainment circadianer Systeme: Oszillatortheorie trifft Chronobiologie

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  Förderer: DFG Eigene Stelle (Sachbeihilfe) Zeitraum: 09/2019 - 12/2022 Projektleitung: Dr. Christoph Schmal

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• Lymphocyte Circadian Clocks Control Lymph Node Trafficking and Adaptive Immune Responses

  2017

  Immunity · 451 Zitationen · DOI

  Lymphocytes circulate through lymph nodes (LN) in search for antigen in what is believed to be a continuous process. Here, we show that lymphocyte migration through lymph nodes and lymph occurred in a non-continuous, circadian manner. Lymphocyte homing to lymph nodes peaked at night onset, with cells leaving the tissue during the day. This resulted in strong oscillations in lymphocyte cellularity in lymph nodes and efferent lymphatic fluid. Using lineage-specific genetic ablation of circadian clock function, we demonstrated this to be dependent on rhythmic expression of promigratory factors on lymphocytes. Dendritic cell numbers peaked in phase with lymphocytes, with diurnal oscillations being present in disease severity after immunization to induce experimental autoimmune encephalomyelitis (EAE). These rhythms were abolished by genetic disruption of T cell clocks, demonstrating a circadian regulation of lymphocyte migration through lymph nodes with time-of-day of immunization being critical for adaptive immune responses weeks later.

• The choroid plexus is an important circadian clock component

  2018

  Nature Communications · 195 Zitationen · DOI

  Mammalian circadian clocks have a hierarchical organization, governed by the suprachiasmatic nucleus (SCN) in the hypothalamus. The brain itself contains multiple loci that maintain autonomous circadian rhythmicity, but the contribution of the non-SCN clocks to this hierarchy remains unclear. We examine circadian oscillations of clock gene expression in various brain loci and discovered that in mouse, robust, higher amplitude, relatively faster oscillations occur in the choroid plexus (CP) compared to the SCN. Our computational analysis and modeling show that the CP achieves these properties by synchronization of "twist" circadian oscillators via gap-junctional connections. Using an in vitro tissue coculture model and in vivo targeted deletion of the Bmal1 gene to silence the CP circadian clock, we demonstrate that the CP clock adjusts the SCN clock likely via circulation of cerebrospinal fluid, thus finely tuning behavioral circadian rhythms.

• A Circadian Clock-Regulated Toggle Switch Explains AtGRP7 and AtGRP8 Oscillations in Arabidopsis thaliana

  2013

  PLoS Computational Biology · 94 Zitationen · DOI

  The circadian clock controls many physiological processes in higher plants and causes a large fraction of the genome to be expressed with a 24h rhythm. The transcripts encoding the RNA-binding proteins AtGRP7 (Arabidopsis thaliana Glycine Rich Protein 7) and AtGRP8 oscillate with evening peaks. The circadian clock components CCA1 and LHY negatively affect AtGRP7 expression at the level of transcription. AtGRP7 and AtGRP8, in turn, negatively auto-regulate and reciprocally cross-regulate post-transcriptionally: high protein levels promote the generation of an alternative splice form that is rapidly degraded. This clock-regulated feedback loop has been proposed to act as a molecular slave oscillator in clock output. While mathematical models describing the circadian core oscillator in Arabidopsis thaliana were introduced recently, we propose here the first model of a circadian slave oscillator. We define the slave oscillator in terms of ordinary differential equations and identify the model's parameters by an optimization procedure based on experimental results. The model successfully reproduces the pertinent experimental findings such as waveforms, phases, and half-lives of the time-dependent concentrations. Furthermore, we obtain insights into possible mechanisms underlying the observed experimental dynamics: the negative auto-regulation and reciprocal cross-regulation via alternative splicing could be responsible for the sharply peaking waveforms of the AtGRP7 and AtGRP8 mRNA. Moreover, our results suggest that the AtGRP8 transcript oscillations are subordinated to those of AtGRP7 due to a higher impact of AtGRP7 protein on alternative splicing of its own and of the AtGRP8 pre-mRNA compared to the impact of AtGRP8 protein. Importantly, a bifurcation analysis provides theoretical evidence that the slave oscillator could be a toggle switch, arising from the reciprocal cross-regulation at the post-transcriptional level. In view of this, transcriptional repression of AtGRP7 and AtGRP8 by LHY and CCA1 induces oscillations of the toggle switch, leading to the observed high-amplitude oscillations of AtGRP7 mRNA.

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