Premium
Perlecan participates in proliferation activation of quiescent Drosophila neuroblasts
Author(s) -
Voigt Aaron,
Pflanz Ralf,
Schäfer Ulrich,
Jäckle Herbert
Publication year - 2002
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.10120
Subject(s) - neuroblast , biology , perlecan , microbiology and biotechnology , extracellular matrix , cell division , cell , proteoglycan , genetics , neurogenesis
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 ( trol ). 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. trol 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 trol codes for Drosophila Perlecan, a large multidomain heparan sulfate proteoglycan originally identified in extracellular matrix structures of mammals. The results suggest that trol 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. © 2002 Wiley‐Liss, Inc.