Bergmann Lab

Normally, cells which have lost a classical tumor suppressor gene become highly proliferative and resistant to apoptosis, thus permitting autonomous tumor growth. However, the Bergmann Lab has discovered a novel class of tumor suppressor genes: non-autonomous tumor suppressors. If these genes are mutant, it is not the mutant cells which are overgrowing. Instead, the mutant cells influence the behavior of neighboring wild-type (non-mutant) cells and promote their proliferation and increased apoptotic resistance, causing non-autonomous overgrowth.

  • Herzet al. (2006). vps25 mosaics display non-autonomous cell survival and overgrowth, and autonomous apoptosis. Development 133, 1871-1880.
  • Lee et al. (2008). The E1-ubiquitin-acitivating-enzyme uba1 in Drosophila controls apoptosis autonomously and tissue growth non-autonomously. Development 135, 43-52.
  • Christiansen et al. (2012). Ligand-independent activation of the Hedgehog pathway displays non-autonomous proliferation and differentiation during eye development in Drosophila. Mechanisms of Development 129, 98-108.
  • Christiansen et al. (2013). Non-autonomous and context-dependent control of apoptosis by deregulated Hedgehog signaling in Drosophila. Cell Death & Differentiation 20:302-11.