Abstract:
:Gliogenesis in animal development is spatiotemporally regulated so that correct numbers of glia are present to support various neuronal functions. During Drosophila embryonic development, the glial regulatory gene, glial cell missing/glial cell deficient (gcm/glide), promotes glial cell fate and differentiation. Here we describe the ubiquitin-proteasome regulation of the Gcm protein and the consequence in gliogenesis without timely degradation of Gcm. Gcm binds to 2 F-box proteins, Supernumerary limbs (Slimb) and Archipelago (Ago), adaptors of SCF E3 ubiquitin ligases. Ubiquitination and proteasomal degradation of Gcm depend on slimb and ago. In slimb and ago double mutants, Gcm protein levels are enhanced. Concomitantly, glial cell numbers increase owing to proliferation, which can be phenocopied by Gcm overexpression only at the onset of glial differentiation. The glial lineage 5-6A in slimb ago mutants displays excess glial progenies and enhanced Gcm protein levels. We propose that downregulation of Gcm protein levels by Slimb and Ago is required for glial progenitors to exit the cell cycle for differentiation.
journal_name
Proc Natl Acad Sci U S Aauthors
Ho MS,Chen H,Chen M,Jacques C,Giangrande A,Chien CTdoi
10.1073/pnas.0808899106subject
Has Abstractpub_date
2009-04-21 00:00:00pages
6778-83issue
16eissn
0027-8424issn
1091-6490pii
0808899106journal_volume
106pub_type
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