Alfonso and Jones, 2002, Dev. Biol. 248(2): 369--383

From FlyBase Wiki
Jump to: navigation, search
Alfonso and Jones, 2002, Dev. Biol. 248(2): 369--383
FlyBase Identifier FBrf0151252
FlyBase URL http://flybase.org/reports/FBrf0151252.html
Publication Type paper
Publication Year 2002
PubMed ID 12167411
PubMed URL http://www.ncbi.nlm.nih.gov/pubmed/12167411

Title

gcm2 promotes glial cell differentiation and is required with glial cells missing for macrophage development in Drosophila.

Abstract

glial cells missing (gcm) is the primary regulator of glial cell fate in Drosophila. In addition, gcm has a role in the differentiation of the plasmatocyte/macrophage lineage of hemocytes. Since mutation of gcm causes only a decrease in plasmatocyte numbers without changing their ability to convert into macrophages, gcm cannot be the sole determinant of plasmatocyte/macrophage differentiation. We have characterized a gcm homolog, gcm2. gcm2 is expressed at low levels in glial cells and hemocyte precursors. We show that gcm2 has redundant functions with gcm and has a minor role promoting glial cell differentiation. More significant, like gcm, mutation of gcm2 leads to reduced plasmatocyte numbers. A deletion removing both genes has allowed us to clarify the role of these redundant genes in plasmatocyte development. Animals deficient for both gcm and gcm2 fail to express the macrophage receptor Croquemort. Plasmatocytes are reduced in number, but still express the early marker Peroxidasin. These Peroxidasin-expressing hemocytes fail to migrate to their normal locations and do not complete their conversion into macrophages. Our results suggest that both gcm and gcm2 are required together for the proliferation of plasmatocyte precursors, the expression of Croquemort protein, and the ability of plasmatocytes to convert into macrophages.

Genes from Reference

Gene(s) Dmel\w
Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox