Principal Investigators

Prof. Dr. Anne-Kathrin Classen

Prof. Dr. Anne-Kathrin Classen

Contact

Prof. Dr. Anne-Kathrin Classen
(she/her)

Hilde Mangold Haus
University of Freiburg

T +49 761 203 97190
anne.classen(at)biologie.uni-freiburg.de

Further Information

WWW

The epithelial linings of skin, colon or lungs act as barriers between the internal and external organ environment. The exposed position of epithelial tissues makes them susceptible to injury and even tumorigenic transformation. My lab investigates how epithelia sense, assess and respond to these challenges. In CIBSS, we specifically investigate how stress signals drive gene expression programs during wound healing, and how these in turn facilitate crucial cell behaviors, such as resistance to ROS stress, metabolic reprogramming, and ultimately, regenerative proliferation. We integrate spatial information of wound field patterning with a temporal analysis of tissue damage on transient and chronic time scales. We combine different genomic approaches with the excellent experimental tractability of the Drosophila system to explore these questions in vivo. Our work aims to uncover fundamental principles to address medical conditions with tremendous societal impact, such as chronic wound healing pathologies and inflammation-associated disorders of ageing, diabetes and cancer. 

 

Keywords

Regeneration, Drosophila, Chronic Wounds, DamID, JNK 



Isaac Asimov

The most exciting phrase to hear in science, the one that heralds new discoveries, is not 'Eureka!' but 'That's funny…’

10 selected publications:

  • Mutual repression between JNK/AP-1 and JAK/STAT stratifies senescent and proliferative cell behaviors during tissue regeneration.
    Jaiswal J, Egert J, Engesser R, Peyrotón AA, Nogay L, Weichselberger V, Crucianelli C, Grass I, Kreutz C, Timmer J, Classen AK (2023).
    PLoS Biol. 21(5):e3001665.
  • Shared enhancer gene regulatory networks between wound and oncogenic programs.
    Floc'hlay S, Balaji R, Stanković D, Christiaens VM, Bravo González-Blas C, De Winter S, Hulselmans GJ, De Waegeneer M, Quan X, Koldere D, Atkins M, Halder G, Uhlirova M, Classen AK, Aerts S (2023).
    Elife. 12:e81173.
  • Bilateral JNK activation is a hallmark of interface surveillance and promotes elimination of aberrant cells.
    Prasad D, Illek K, Fischer F, Holstein K, Classen AK (2023).
    Elife. 12:e80809.
  • Distinct signaling signatures drive compensatory proliferation via S-phase acceleration.
    Crucianelli C, Jaiswal J, Vijayakumar Maya A, Nogay L, Cosolo A, Grass I, Classen AK (2022).
    PLoS Genet. 18(12):e1010516.
  • Eya-controlled affinity between cell lineages drives tissue self-organization during Drosophila oogenesis.
    Weichselberger V, Dondl P, Classen AK (2022).
    Nat Commun. 13(1):6377
  • JNK-dependent cell cycle stalling in G2 promotes survival and senescence-like phenotypes in tissue stress
    Cosolo A, Jaiswal J, Csordás G, Grass I, Uhlirova M, Classen AK (2019).
    Elife. 8. pii: e41036.
  • Response of Drosophila epithelial cell and tissue shape to external forces in vivo.
    Balaji R, Weichselberger V, Classen AK (2019).
    Development. 146(17):dev171256.
  • Interface contractility between differently fated cells drives cell elimination and cyst formation.
    Bielmeier C, Alt S, Weichselberger V, La Fortezza M, Harz H, Jülicher F, Salbreux G, Classen AK (2016).
    Curr Biol. 26, 563-74.
  • JAK/STAT signalling mediates cell survival in response to tissue stress.
    La Fortezza M, Schenk M, Cosolo A, Kolybaba A, Grass I, Classen AK (2016).
    Development. 143(16):2907-19.
  • A tumor suppressor activity of Drosophila Polycomb genes mediated by JAK-STAT signaling.
    Classen AK, Bunker BD, Harvey KF, Vaccari T, Bilder D (2009).
    Nat Genet. 41(10):1150-5