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Characterization of missense alleles of the glial cells missing gene of Drosophila.
- Source :
-
Genesis (New York, N.Y. : 2000) [Genesis] 2014 Oct; Vol. 52 (10), pp. 864-9. Date of Electronic Publication: 2014 Jul 21. - Publication Year :
- 2014
-
Abstract
- Glial cells missing (Gcm) is the primary regulator of glial cell fate in Drosophila. Gcm belongs to a small family of transcriptional regulators involved in fundamental developmental processes found in diverse animal phyla including vertebrates. Gcm proteins contain the highly conserved DNA-binding GCM domain, which recognizes an octamer DNA sequence. To date, studies in Drosophila have primarily relied on gcm alleles caused by P-element induced DNA deletions at the gcm locus, as well as a null allele caused by a single base pair substitution in the GCM domain that completely abolishes DNA binding. Here I characterize two hypomorphic missense alleles of gcm with intermediate glial cells missing phenotypes. In embryos homozygous for either of these gcm alleles the number of glial cells in the central nervous cystem (CNS) is reduced approximately in half. Both alleles have single amino acid changes in the GCM domain. These results suggest that Gcm protein activities in these mutant alleles have been attenuated such that they are operating at threshold levels, and trigger glial cell differentiation in neural precursors in the CNS in a stochastic fashion. These hypomorphic alleles provide additional genetic resources for understanding Gcm functions and structure in Drosophila and other species.<br /> (© 2014 Wiley Periodicals, Inc.)
- Subjects :
- Alleles
Animals
Cell Differentiation
DNA-Binding Proteins metabolism
Drosophila Proteins metabolism
Drosophila melanogaster genetics
Drosophila melanogaster metabolism
Embryo, Nonmammalian metabolism
Neuroglia cytology
Transcription Factors metabolism
DNA-Binding Proteins genetics
Drosophila Proteins genetics
Drosophila melanogaster embryology
Mutation, Missense
Neuroglia metabolism
Transcription Factors genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1526-968X
- Volume :
- 52
- Issue :
- 10
- Database :
- MEDLINE
- Journal :
- Genesis (New York, N.Y. : 2000)
- Publication Type :
- Editorial & Opinion
- Accession number :
- 25044731
- Full Text :
- https://doi.org/10.1002/dvg.22801