ON THE FUNCTIONAL OVERLAP BETWEEN 2 DROSOPHILA POU HOMEO DOMAIN GENESAND THE CELL FATE SPECIFICATION OF A CNS NEURAL PRECURSOR

Citation
Sl. Yee et al., ON THE FUNCTIONAL OVERLAP BETWEEN 2 DROSOPHILA POU HOMEO DOMAIN GENESAND THE CELL FATE SPECIFICATION OF A CNS NEURAL PRECURSOR, Genes & development, 9(10), 1995, pp. 1223-1236
Citations number
53
Categorie Soggetti
Developmental Biology","Genetics & Heredity
Journal title
ISSN journal
08909369
Volume
9
Issue
10
Year of publication
1995
Pages
1223 - 1236
Database
ISI
SICI code
0890-9369(1995)9:10<1223:OTFOB2>2.0.ZU;2-T
Abstract
The similar to 200 distinct neurons comprising each hemisegment of the Drosophila embryonic CNS are derived from a stereotypic array of simi lar to 30 progenitor stem cells, called neuroblasts (NBs). Each NE und ergoes repeated asymmetric divisions to produce several smaller gangli on mother cells (GMCs), each of which, in turn, divides to produce two neurons and/or glia cells. To understand the process by which cell ty pe diversity is generated in the CNS, we are focusing on identifying g enes that affect cell identity in the NB4-2 lineage from which the RP2 motoneuron is derived. We show here that within the early part of the NB4-2 lineage, two closely linked and structurally related POU homeo domain genes, pdm-2 (dPOU28) and pdm-1 (dPOU19), both encode proteins that accumulate to high levels only in the first GMC (GMC4-2a) and not in its progeny, the RP2 motoneuron. Our results from the genetic and developmental analysis of pdm-1 and pdm-2 demonstrate that these genes are not required for the birth of GMC4-2a; however, they are both inv olved in specifying the identity of GMC4-2a and, ultimately, in the ge nesis of RP2 neurons, with pdm-2 being the more dominant player in thi s process. In mutant animals where both pdm-1 and pdm-2 functions are removed, GMC4-2a fails to express markers consistent with a GMC4-2a id entity and no mature (Eve protein expressing) RP2 neurons are produced . We demonstrate that in some mutant combinations in which no mature R P2 neurons are produced, some GMC4-2a cells can nevertheless divide. H ence, the failure of the POU mutants to produce mature RP2 neurons is not attributable to a block in GMC4-2a cell division per se but, rathe r, because the GMC4-2a cells fail to acquire their correct cellular id entity.