We are a team of geneticists, biochemists, and biotechnologists and study the genetics of ageing and age-related disorders (neurodegeneration, cancer, stress responses). We are interested in identifying how environmental influences (chemicals, temperature, toxins, the microbiome) are integrated by an organism, and how its reactions are modulated by stress signaling mechanisms. We combine in our research one of the best model organisms for ageing research, the nematode C. elegans, and human cell culture to translate our findings into a better understanding of human health. One of our project aims at understanding how tumors can be induced by external (stress) signals, and identified an intriguing new signal mechanism, by which the mother may sacrifice her own well-being to protect her progeny. In a related project, we study how protein complexes dynamically combine insulin (diabetes) and mTORC (stress and metabolism) pathways to protect from nutritional and oxygen deprivation. Crucial goals are identifying genes involved in these processes, and the mechanisms of (inter-)actions of their endoded proteins. Our findings can be translated into a better understanding of tumor biology and may also contribute to improving survival, e.g. after organ transplantation, by allowing the organism to slow/stop biological reactions while preserving physiological capabilities (suspended animation).   

Keywords:

ageing, insulin signaling, mTORC signaling, C. elegans, suspended animation, hypoxia, non-cellautonomous signaling, CRISPR/Cas9, RNA interference

10 selected publications:

• Mitochondrial perturbations couple mTORC2 to autophagy in C. elegans.
  Aspernig H, Heimbucher T, Qi W, Gangurde D, Curic S, Yan Y, Donner von Gromoff E, Baumeister R(*), Thien A. (2019) *corresponding author.
  Cell Rep. 5; 29(6): 1399-1409.
• Retromer and TBC1D5 maintain late endosomal RAB7 domains to enable amino acid-induced mTORC1 signalling.
  Kvainickas A, Nägele H, Qi W, Dokladal L, Jimenez-Orgaz A, Hu Z, Stehl L, Gangurde, D, Zhao Q, Hu Z, Dengjel J, de Virgilio C, Baumeister R, Steinberg F (2019).
  J Cell Biol 218(9): 3019-3038.
• C. elegans DAF-16/FOXO interacts with TGF-ß/BMP signaling to induce germline tumor formation via mTORC1 activation.
  Qi W, Yan Y, Pfeifer D, Donner V Gromoff E, Wang Y, Maier W, Baumeister R (2017).
  PLoS Genet. 13(5):e1006801
• TSC1 activates TGF-β-Smad2/3 signaling in growth arrest and epithelial-to-mesenchymal transition.
  Thien A, Prentzell MT, Holzwarth B, Kläsener K, Kuper I, Boehlke C, Sonntag AG, Ruf S, Maerz L, Nitschke R, Grellscheid SN, Reth M, Walz G, Baumeister R, Neumann-Haefelin E, Thedieck K (2015).
  Dev Cell. 32(5):617-30.
• Inhibition of mTORC1 by astrin and stress granules prevents apoptosis in cancer cells.
  Thedieck K, Holzwarth B, Prentzell MT, Boehlke C, Kläsener K, Ruf S, Sonntag AG, Maerz L, Grellscheid SN, Kremmer E, Nitschke R, Kuehn EW, Jonker JW, Groen AK, Reth M, Hall MN, Baumeister R (2013). Cell. 154(4):859-74
• Surveillance-activated defenses block the ROS-induced mitochondrial unfolded protein response.
  Runkel ED, Liu S, Baumeister R, Schulze E (2013).
  PLoS Genet. 9(3):e1003346
• Cell-nonautonomous signaling of FOXO/DAF-16 to the stem cells of Caenorhabditis elegans.
  Qi W, Huang X, Neumann-Haefelin E, Schulze E, Baumeister R (2012).
  PLoS Genet. 8(8):e1002836.
• SHC-1/p52Shc targets the insulin/IGF-1 and JNK signaling pathways to modulate life span and stress response in C. elegans.
  Neumann-Haefelin E, Qi W, Finkbeiner E, Walz G, Baumeister R, Hertweck M (2008).
  Genes Dev. 22(19):2721-35.
• Direct inhibition of the longevity-promoting factor SKN-1 by insulin-like signaling in C. elegans.
  Tullet JM, Hertweck M, An JH, Baker J, Hwang JY, Liu S, Oliveira RP, Baumeister R, Blackwell TK (2008).
  Cell. 132(6):1025-38
• Regulation of the myosin-directed chaperone UNC-45 by a novel E3/E4-multiubiquitylation complex in C. elegans.
  Hoppe T, Cassata G, Barral JM, Springer W, Hutagalung AH, Epstein HF, Baumeister R (2004).
  Cell. ;118(3):337-49.