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Perlecan participates in proliferation activation of quiescent Drosophila neuroblasts

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Voigt,  A.
Department of Molecular Developmental Biology, MPI for biophysical chemistry, Max Planck Society;

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Pflanz,  R.
Department of Molecular Developmental Biology, MPI for biophysical chemistry, Max Planck Society;

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Schaefer,  U.
Department of Molecular Developmental Biology, MPI for biophysical chemistry, Max Planck Society;

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Jaeckle,  H.
Department of Molecular Developmental Biology, MPI for biophysical chemistry, Max Planck Society;

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Citation

Voigt, A., Pflanz, R., Schaefer, U., & Jaeckle, H. (2002). Perlecan participates in proliferation activation of quiescent Drosophila neuroblasts. Developmental Dynamics, 224(4), 403-412. Retrieved from http://onlinelibrary.wiley.com/doi/10.1002/dvdy.10120/pdf.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0012-F34E-2
Abstract
Drosophila neuroblasts act as stem cells. Their proliferation is controlled through cell cycle arrest and activation in a spatiotemporal pattern. Several genes have been identified that control the pattern of neuroblast quiescence and proliferation in the central nervous system (CNS), including anachronism (ana), even skipped (eve) and terribly reduced optic lobes (trot). eve acts in a non-cell-autonomous manner to produce a transacting factor in the larval body that stimulates cell division in the population of quiescent optic lobe neuroblasts. ana encodes a secreted glial glycoprotein proposed to repress premature proliferation of optic lobe and thoracic neuroblasts. trot was shown to act downstream of ana to activate proliferation of quiescent neuroblasts either by inactivating or bypassing ana-dependent repression. Here, we show that trot codes for Drosophila Perlecan, a large multidomain heparan sulfate proteoglycan originally identified in extracellular matrix structures of mammals. The results suggest that trot acts in the extracellular matrix and binds, stores, and sequesters external signals and, thereby, participates in the stage- and region-specific control of neuroblast proliferation. (C) 2002 Wiley-Liss, Inc.