Helen Morrison
Helen Morrison


Solveigh Koeberle

Lars-Björn Riecken

Susann Schirmer

Alexander Schulz

Yan Cui

Ansgar Zoch

PhD Students

Robert Büttner

Annemarie Carlstedt

Carsten Dornblut

Frederike Kramer

Stephan Schacke

Kassandra Walluks

Technicians / Engineers

Uta Petz (apprentice trainer)


Juliane Rübsam


Morrison Research Group

Tumor biology

Molecular mechanisms involved in cancer development

Our lab is generally interested in the regulation and function of Ras and Ras like small GTPases. With a special emphasis on Ras in proliferation control and in the development and function of synapses. We use a multidisciplininary approach which includes structural, cellular and mouse models.



Contact inhibition of growth

In tissues, cells proliferate to occupy the space allotted to them and then stop proliferating when they contact other cells or dense extracellular matrix. This process, referred to as contact inhibition of growth must be tightly regulated, since alterations can cause profound cellular changes such as cellular transformation. In our working group we are trying to elucidate how a cell senses contact and influences cellular proliferation though regulation of Ras. Our special interest is a candidate sensor complex, containing cell adhesion molecules, the Nf2 tumor suppressor merlin and the ERM family members (ezrin, radixin and moesin) (Figure 1).


growth inhibitory mode



» Figure 1: Contact sensor complex involved in a molecular switch that signals either celluar growth or growth inhibition. Cell adhesion molecules (co-receptor), merlin and ERM proteins appear to play a critical role in mitogenic signalling through interactions with receptor tyrosine kinases. Ezrin a protein that links cortical F-actin to these cell adhesion molecules is necessary for growth factor induced Ras activation. This ezrin/F-actin mediated link is subject to physiological regulation since the tumor suppressor protein merlin which binds to the same cell adhesion molecule inhibits signal transfer to Ras when cells become confluent.



Synaptic plasticity, learning and memory

It is well known that Ras and Ras like proteins play a role in synaptic and structural plasticity, the cellular and molecular basis for processes such as learning and memory. A new focus of our lab is to study the role of ERM and adhesion dependent Ras regulation in the development and function of synapses.


Recent selected publications

  • Morrison H (2014). Understanding cell communication. International Innovation, 146, 58-60. [PDF]
  • Schulz A, Kyselyova A, Baader SL, Jung MJ, Zoch A, Mautner VF, Hagel C, Morrison H (2014). Neuronal merlin influences ErbB2 receptor expression on Schwann cells via neuregulin 1 type III signalling. Brain, 137, 420-432. [PubMed]
  • Schulz A, Baader SL, Niwa-Kawakita M, Jung MJ, Bauer R, Garcia C, Zoch A, Schacke S, Hagel C, Mautner VF, Hanemann CO, Dun XP, Parkinson DB, Weis J, Schröder JM, Gutmann DH, Giovannini M, Morrison H (2013). Merlin isoform 2 in neurofibromatosis type 2-associated polyneuropathy. Nat Neurosci, 16, 426-433. [PubMed]
  • Lam EK, Wang X, Shin VY, Zhang S, Morrison H, Sun J, Ng EK, Yu J, Jin H (2011). A microRNA contribution to aberrant Ras activation in gastric cancer. Am J Transl Res, 3, 209-218. [PubMed]
  • Sperka T, Geissler KJ, Merkel U, Scholl I, Rubio I, Herrlich P, Morrison HL (2011). Activation of Ras requires the ERM-dependent link of actin to the plasma membrane. PLoS One, 6, e27511. [PubMed]
  • Schulz A, Geissler KJ, Kumar S, Leichsenring G, Morrison H*, Baader SL* (2010). Merlin inhibits neurite outgrowth in the CNS. J Neurosci, 30, 10177-10186. [PubMed] *equal contribution
  • Saleh HS, Merkel U, Geissler KJ, Sperka T, Sechi A, Breithaupt C, Morrison H (2009) Properties of an ezrin mutant defective in F-actin binding. J Mol Biol, 385, 1015-1031. [PubMed]
  • Morrison H, Sperka T, Manent J, Giovannini M, Ponta H, Herrlich P (2007) Merlin/neurofibromatosis type 2 suppresses growth by inhibiting the activation of Ras and Rac. Cancer Res, 67, 520-527. [PubMed]
  • Orian-Rousseau V*, Morrison H*, Matzke A, Kastilan T, Pace G, Herrlich P, Ponta H (2007) Hepatocyte growth factor-induced Ras activation requires ERM proteins linked to both CD44v6 and F-actin. Mol Biol Cell, 18, 76-83. [PubMed] *equal contribution
  • Jin H, Sperka T, Herrlich P, Morrison H (2006) Tumorigenic transformation by CPI-17 through inhibition of a merlin phosphatase. Nature, 442, 576-579. [PubMed]
  • Pust S*, Morrison H*, Wehland J, Sechi AS, Herrlich P (2005) Listeria monocytogenes exploits ERM protein functions to efficiently spread from cell to cell. EMBO J, 24, 1287-1300. [PubMed] *equal contribution
  • Scoles DR, Nguyen VD, Qin Y, Sun CX, Morrison H, Gutmann DH, Pulst SM (2002) Neurofibromatosis 2 (NF2) tumor suppressor schwannomin and its interacting protein HRS regulate STAT signaling. Hum Mol Gen, 11, 3179-3189. [PubMed]
  • Morrison H, Sherman LS, Legg J, Banine F, Isacke C, Haipek CA, Gutmann DH, Ponta H, Herrlich P (2001) The NF2 tumor suppressor gene product, merlin, mediates contact inhibition of growth through interactions with CD44. Genes Dev, 15, 968-980. [PubMed]
  • Sherman LS, Wobus M, Kuns R, Banine F, Rangwala R, Morrison H, Tuohy T (2001) Interactions between CD44 and type I receptors mediate tumor growth and metastasis. Rec Res Dev Cancer, 3, 19-34.


Last update: March 25, 2015

top of the page