a transient expression of prospero promotes cell cycle exit of drosophila postembryonic neurons through the regulation of dacapo普洛斯彼罗的瞬时表达促进果蝇胚胎神经元的细胞周期退出通过dacapo的规定.pdfVIP
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a transient expression of prospero promotes cell cycle exit of drosophila postembryonic neurons through the regulation of dacapo普洛斯彼罗的瞬时表达促进果蝇胚胎神经元的细胞周期退出通过dacapo的规定
A Transient Expression of Prospero Promotes Cell Cycle
Exit of Drosophila Postembryonic Neurons through the
Regulation of Dacapo
1 1¤ 2 1
Jordi Colonques , Julian Ceron , Heinrich Reichert , Francisco J. Tejedor *
1 Instituto de Neurociencias, CSIC-UMH, Alicante, Spain, 2 Biozentrum, University of Basel, Basel, Switzerland
Abstract
Cell proliferation, specification and terminal differentiation must be precisely coordinated during brain development to
ensure the correct production of different neuronal populations. Most Drosophila neuroblasts (NBs) divide asymmetrically to
generate a new NB and an intermediate progenitor called ganglion mother cell (GMC) which divides only once to generate
two postmitotic cells called ganglion cells (GCs) that subsequently differentiate into neurons. During the asymmetric
division of NBs, the homeodomain transcription factor PROSPERO is segregated into the GMC where it plays a key role as
cell fate determinant. Previous work on embryonic neurogenesis has shown that PROSPERO is not expressed in postmitotic
neuronal progeny. Thus, PROSPERO is thought to function in the GMC by repressing genes required for cell-cycle
progression and activating genes involved in terminal differentiation. Here we focus on postembryonic neurogenesis and
show that the expression of PROSPERO is transiently upregulated in the newly born neuronal progeny generated by most of
the larval NBs of the OL and CB. Moreover, we provide evidence that this expression of PROSPERO in GCs inhibits their cell
cycle progression by activating the expression of the cyclin-dependent kinase inhibitor (CKI) DACAPO. These findings imply
that PROSPERO, in addition to its known role as cell fate de
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