C. elegans genetics as a model to study basic biological problems

Research

Despite of its simplicity, C. elegans is a multicellular organism that shares many fundamental genetic programs with humans. Thus many results obtained in the C. elegans system are likely to be applicable to mammalian systems. Our studies on C. elegans are facilitated by the simplicity of the organism at the developmental and anatomical level, by the ease of its maintenance, as well as by the power of forward and reverse genetic procedures. Furthermore, we take advantage of the complete genome information and by shared resources of the "worm community".

In response to DNA damage organisms activate checkpoint pathways. In multicellular organisms these pathways lead the activation of DNA repair processes, to a transient cell cycle arrest, or to programmed cell death to eliminate cells that might potentially become harmful for the entire organism.The analysis of the pathways needed for DNA damage sensing, DAN repair and the elucidation of checkpoint responses are currently under intense investigation. We were among the first to use C. elegans to contribute to the understanding of DNA damage dependent apoptosis. Given that genome instability is a major course of human cancers we hope, that in the long run, we might contribute to better tumour-diagnostics and treatment.

Furthermore, we also started to explore C. elegans to uncover molecular mechanisms leading to Parkinson's Disease. Finally we engage in multiple collaborations within the college. Projects include the visualization of key aspects of DNA replication in early C. elegans embryos, and taking full advantage of advanced quantitative mass spectroscopy based approaches.

Teaching

Publications

R. Sonneville, M. Querenet. A. Craig, A. Gartner*and J. Blow (2012). The dynamics of replication licensing in live C. elegans embryos, in press Journal of Cell Biology *Co-corresponding author

M. Larance, AP. Bailly, E. Pourkarimi, RT. Hay,G. Buchanan, S. Coulthurst, DP. Xirodimas, A. Gartner and AI. Lamond(2011) SILAN: Stable Isotope Labeling with Amino acids in Nematodes, Nature Methods, under revision. Co-corresponding author Aug. 28, 7(8), e1002238

R. Rutkowski, R Dickinson, G. Stewart, A. Craig, M. Schimpl, S. Keyse, and A. Gartner(2011) ERK signalling is activated by irradiation and positively regulates CEP-1/p53 dependent apoptosis in C.  elegans, Plos Genetics,7(8): e1002238

E. Pourkarimi, S. Greiss and A. Gartner (2011) Evidence that CED-9/Bcl2 and CED-4/Apaf-1 localization is not consistent with the current model for C. elegans apoptosis induction, Cell Death and Differentiation, Sept. 2, (Epub) cdd.2011.104

A. Bailly, A. Freeman, J. Hall, A. Déclais, A. Alpi, D. Lilley, S. Ahmed and A. Gartner (2010). The C. elegans homolog of Gen1/Yen1 resolvases links DNA damage signaling to DNA double-strand break repair, Plos Genetics,6(7): e1001025.

R. Rutkowski, K. Hofmann, A. Gartner. (2010). Phylogeny and Function of the Invertebrate p53 Superfamily,Cold Spring Harbor Persepect. Biol. 2010 Jul; 1; 2(7) Epub May5.

B. Meier, L. Barber, Y. Liu Y, I, Clejan, S. Boulton, A. Gartner*, S. Ahmed.* (2009), The MRT-1 nuclease is required for DNA cross link repair and telomerease activity in vivo in C. elegans,  EMBO J. 28(22):3549-63. *equal senior author contribution with S. Ahmed

S. Moser, S. von Elsner, I. Buessing, A. Alpi, R. Schnabel, A. Gartner. (2009).  Functional Dissection of C. elegans CLK2/TEL2 cell cycle defects during embryogenesis and germ line development, PLOS Genetics,April 5(4)

S. Greiss, J. Hall, S. Ahmed, A. Gartner. C. elegans SIR-2.1 translocation is linked to a pro-apoptotic pathway parallel to cep-1/p53-like during DNA damage induced apoptosis (2008) Genes & Development, Oct, 22(20): 2831-41.

A. Gartner, PR. Boag and TK. Blackwell (2008). Germline Survival and Apoptosis, WormBook, ed. The C. elegans Research Community, WormBook, Sept; 1-20

B. Schumacher, M. Hanazawa, MH. Lee, S. Nayak, K. Volkmann; R. Hofmann, M. Hengartner, T. Schedl and A. Gartner (2005). Translational Repression of C. elegans p53 by GLD-1 regulates DNA damage induced apoptosis. Cell 120:  357-368