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Gene Review

Mer  -  Merlin

Drosophila melanogaster

Synonyms: BG01543, CG14228, D-Mer, Dmel\CG14228, Dmerlin, ...
 
 
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Disease relevance of Mer

  • The neurofibromatosis-2 homologue, Merlin, and the tumor suppressor expanded function together in Drosophila to regulate cell proliferation and differentiation [1].
  • Loss of Merlin function in Drosophila results in hyperplasia of the affected tissue without significant disruptions in differentiation [1].
 

High impact information on Mer

  • The tumor suppressors Merlin, expanded, hippo, salvador and mob as tumor suppressor also share multiple Fat pathway phenotypes but regulate Warts activity independently [2].
  • Here, we show that Drosophila Merlin and Expanded are components of the Hippo signalling pathway, an emerging tumour-suppressor pathway [3].
  • The tumour-suppressor genes NF2/Merlin and Expanded act through Hippo signalling to regulate cell proliferation and apoptosis [3].
  • Merlin, and its function as a negative regulator of growth, is conserved in Drosophila, where it functions with Expanded, a related FERM domain protein [3].
  • In addition, we provide evidence that the COOH-terminal region of Merlin has a negative regulatory role, as has been shown for ERM proteins [4].
 

Biological context of Mer

  • Removal of a seven-amino acid conserved sequence within this domain results in a dominant-negative form of Merlin that is stably associated with the plasma membrane and causes overproliferation when expressed ectopically in the wing [4].
  • Using in vitro mutagenesis, we define functional domains within Merlin required for proper subcellular localization and for genetic rescue of lethal Merlin alleles [4].
  • Conversely, loss of mer substantially compromises normal developmental apoptosis in the pupal retina, while loss of ex has only mild effects [5].
  • By individually analyzing ex and mer mutant phenotypes, we have found important qualitative and quantitative differences in the ways Mer and Ex function to regulate cell proliferation and cell survival [5].
  • Though both mer and ex restrict cell and tissue growth, ex clones exhibit delayed cell cycle exit in the developing eye, while mer clones do not [5].
 

Anatomical context of Mer

  • Investigation of Dmerlin cultured cells demonstrates that it is associated with endocytic compartments [6].
  • Although many proteins in this family are thought to act by linking the actin-based cytoskeleton to transmembrane proteins, the cellular functions of merlin have not been defined [6].
  • Merlin mutants show defects in nuclear migration and mRNA localisation in the oocyte [7].
 

Associations of Mer with chemical compounds

  • Remarkably, the results of these experiments demonstrate that all essential genetic functions reside in the plasma membrane- associated NH2-terminal 350 amino acids of Merlin [4].
  • Mutations that inactivate either merlin (mer) or expanded (ex) result in increased cell growth and proliferation in Drosophila [5].
 

Other interactions of Mer

  • As a result of these studies, we propose that the merlin protein has unique functions in the cell which differ from those of other ERM family members [6].
  • The Drosophila tumor suppressors Expanded and Merlin differentially regulate cell cycle exit, apoptosis, and Wingless signaling [5].
  • Both Mer and Ex are members of the Band 4.1 protein superfamily, and, based on analyses of mer ex double mutants, they are proposed to function together in at least a partially redundant manner upstream of the Hippo (Hpo) and Warts (Wts) proteins to regulate cell growth and division [5].
  • Finally, ex has a role in regulating Wingless protein levels in the eye that is not obviously shared by either mer or hpo [5].
  • We propose that Merlin acts in response to the Gurken signal by apically targeting the signal that initiates axis specification in the oocyte [7].

References

  1. The neurofibromatosis-2 homologue, Merlin, and the tumor suppressor expanded function together in Drosophila to regulate cell proliferation and differentiation. McCartney, B.M., Kulikauskas, R.M., LaJeunesse, D.R., Fehon, R.G. Development (2000) [Pubmed]
  2. Delineation of a Fat tumor suppressor pathway. Cho, E., Feng, Y., Rauskolb, C., Maitra, S., Fehon, R., Irvine, K.D. Nat. Genet. (2006) [Pubmed]
  3. The tumour-suppressor genes NF2/Merlin and Expanded act through Hippo signalling to regulate cell proliferation and apoptosis. Hamaratoglu, F., Willecke, M., Kango-Singh, M., Nolo, R., Hyun, E., Tao, C., Jafar-Nejad, H., Halder, G. Nat. Cell Biol. (2006) [Pubmed]
  4. Structural analysis of Drosophila merlin reveals functional domains important for growth control and subcellular localization. LaJeunesse, D.R., McCartney, B.M., Fehon, R.G. J. Cell Biol. (1998) [Pubmed]
  5. The Drosophila tumor suppressors Expanded and Merlin differentially regulate cell cycle exit, apoptosis, and Wingless signaling. Pellock, B.J., Buff, E., White, K., Hariharan, I.K. Dev. Biol. (2007) [Pubmed]
  6. Distinct cellular and subcellular patterns of expression imply distinct functions for the Drosophila homologues of moesin and the neurofibromatosis 2 tumor suppressor, merlin. McCartney, B.M., Fehon, R.G. J. Cell Biol. (1996) [Pubmed]
  7. Merlin, the Drosophila homologue of neurofibromatosis-2, is specifically required in posterior follicle cells for axis formation in the oocyte. MacDougall, N., Lad, Y., Wilkie, G.S., Francis-Lang, H., Sullivan, W., Davis, I. Development (2001) [Pubmed]
 
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