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Home>Research>Subarea 4: Cell Dynamics and Molecular Damages in Aging
Research focus of Subarea 4.

Subarea 4: Cell Dynamics and Molecular Damages in Aging

The research focus of Subarea 4 is on studying damages of macromolecules (proteins, nucleic acids) and determining the structure-function relationship of biomolecules relevant to damage and damage repair processes and responses to molecular damage that might lead to aging and aging-associated pathologies.

The studies are focused on the following research areas: DNA replication, DNA damage responses (DDR), stress responses, metabolic stresses, protein trafficking and protein damages.

The research is defined by four focus areas:

  • DNA damage response in tissue homeostasis and neuropathies,
  • Quality control in the endoplasmic reticulum for secretory pathway in aging processes,
  • Intrinsic and extrinsic factors implicated in cellular decline during aging, and
  • DNA replication and genomic integrity preventing premature aging and diseases.

Research focus of Subarea 4.

The accumulation of damaged macromolecules or subcellular organelles is associated with dysfunction of a cell, which contributes to tissue & organ failure. DNA damage, genomic instability, protein misfolding or defects in toxic protein degradation can compromise cell functionality. Alterations of mitochondrial DNA and protein complexes affect cellular metabolism, which will have a general impact on cell integrity.

Publications

(since 2016)

2024

  • Aging-associated decline of phosphatidylcholine synthesis is a malleable trigger of natural mitochondrial aging
    Poliezhaieva T, Alonso Pernas P, Espada L, Bayar M, Li Y, Melike Dönertaş H, A.Ermolaeva M
    bioRxiv 2024, https://doi.org/10.1101/2024.04.
  • DNA repair deficiencies and neurodegeneration.
    Ropert B, Gallrein C, Schumacher B
    DNA Repair (Amst) 2024, 138, 103679
  • Nodal Modulator (NOMO) is a force-bearing transmembrane protein required for muscle differentiation
    S Naughton B, C Devarkar S, Mallik S, Oxendine S, Junnarkar S, Ren Y, Todorow V, Berro J, Kirstein J, Xiong Y, Schlieker C
    bioRxiv 2024, 10.1101/2024.09.06.611727
  • Circadian clock disruption engages the DREAM complex in suppressing cellular health
    Santos Valentim I, Javier Romero-Expósito F, Schwab K, Bayar M, Riege K, Fischer M, Olmedo M, Hoffmann S, A.Ermolaeva M
    bioRxiv 2024, https://doi.org/10.1101/2024.06.
  • Reducing the metabolic burden of rRNA synthesis promotes healthy longevity in Caenorhabditis elegans.
    Sharifi* S, Chaudhari* P, Martirosyan A, Eberhardt AO, Witt F, Gollowitzer A, Lange L, Woitzat Y, Okoli EM, Li H, Rahnis N, Kirkpatrick J, Werz O, Ori A, Koeberle A, Bierhoff** H, Ermolaeva** M
    Nat Commun 2024, 15(1), 1702 * equal contribution, ** co-corresponding authors
  • Fe-S cluster biosynthesis in chromatin protects genome stability and promotes DNA replication
    Shi R
    Dissertation 2024, Jena, Germany
  • Repopulated microglia after pharmacological depletion decrease dendritic spine density in adult mouse brain.
    Wickel J, Chung HY, Ceanga M, von Stackelberg N, Hahn N, Candemir Ö, Baade-Büttner C, Mein N, Tomasini P, Woldeyesus DM, Andreas N, Baumgarten P, Koch P, Groth M, Wang ZQ, Geis C
    Glia 2024, 72(8), 1484-500
  • Role of UFMylation and Ubiquitylation of MCM7 during DNA replication
    Yuan S
    Dissertation 2024, Jena, Germany

2023

  • Targeting cellular pathways in hyper- and ultramutated cancer cells with exonuclease-defective DNA polymerase epsilon
    Borges G
    Dissertation 2023, Jena, Germany
  • UPF3A is dispensable for nonsense-mediated mRNA decay in mouse pluripotent and somatic cells.
    Chen C, Shen Y, Li L, Ren Y, Wang ZQ, Li T
    Life Sci Alliance 2023, 6(6), e202201589. doi: 10.26508/lsa.20