glide/gcm, glide, glial cell missing, glial cell deficient
transcription factor - novel - required for glial cell fate - controlling hemocyte and tendon cell differentiation - controls initiation of collective cell migration by regulating Frazzled
Please see the JBrowse view of Dmel\gcm for information on other features
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.47
2.2 (northern blot)
504 (aa)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\gcm using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: anlage in statu nascendi
Comment: reported as head epidermis primordium
Comment: reported as head epidermis primordium
Comment: reported as head epidermis primordium
Comment: reported as glioblasts of ventral nervous system
Comment: reported as plasmatocytes anlage
gcm transcripts are detected in medulla neuropil glial cells as well as in streams of glial cells migrating within the outer proliferation center to reach the medulla neuropil.
In the larval visual system, gcm transcript is expressed not only in specific glial subtypes, but also in the lineage that gives rise to lamina neurons.
gcm expression is observed in the larval optic lobe in some glial subtypes and in a lineage that gives rise to lamina neurons. Expression begins in glial precursor cells at the lamina margins that will give rise to epithelial and marginal glial cells. Expression is also observed in neruonal precursors in the lamina.
expressed first in presumptive glial cell of dbd lineage after decrease in nub expression.
gcm transcripts are first detected by in situ hybridization in the head region of the embryo at the end of the blastoderm stage. At stage 10, expression is still very prominent in the procephalic mesoderm. Additionally staining is seem in one cell per hemisegment in the lateral ectoderm which may correspond to PNS. A second, more medially located cell, may be the longitudinal glioblast. By stage 11, expression decreases in the hemocyte lineage and becomes more prominent in glial cells of the PNS and CNS. The staining pattern appears d fferent in the thoracic and abdominal segments reflecting the different organization of the glial cells. No signal is observed in cells migrating from the procephalic mesoderm after stage 11.
gcm transcripts are expressed in glial precursors and immature glial cells during a short period of gliogenesis. Expression is first detected in early stage 11 in the longitudinal glioblast. By mid stage 11, 2-3 other cells per hemisegment express gcm. Two of these have been identified as NB6-4 and the medial-most cell body glial cell (VUM support cell). By early stage 12, expression is detected in several other cells which are also developing glial cells. Expression fades during stage 12 and is hardly detectable in stage 13. Enhancer trap expression was used to trace the gcm-expressing cells to later developmental stages. It was found that gcm is expressed in all glial precursors and immature glial cells except those derived from the mesectoderm. Outside of the CNS, gcm is expressed in the most anterior region of the presumptive mesoderm beginning at the cellular blastoderm stage, in the brain neurogenic region, and in the PNS neurogenic region.
gcm transcripts are initially expressed in an anterior ventral patch in the cellular blastoderm embryo. During gastrulation, these cells invaginate at the end of the ventral furrow just anterior to the cephalic furrow in an area that gives rise to the cephalic mesoderm. Cephalic expression fades after stage 10. During stages 11-12, in each hemisegment, two patches of 3-5 ectodermal cells sequentially and transiently express gcm. From each patch, a single large blast cell delaminates and maintains gcm expression. These are tentatively identified as the peripheral glioblast and the longitudinal glioblast. By late stage 11, all of the progeny of these glioblasts as well as additional glial cells express gcm. Glial expression is gone by stage 15. In the brain lobes, gcm is expressed in a complex pattern through stage 17. In the PNS, gcm is transiently expressed in all repo-positive glia along peripheral axon pathways and associated with sensory organs.
gcm is first detected in stage 10 embryos in one lateral cell thought to be a longitudinal glial cell. In stage 11 and 13 embryos, it is expressed in a number of CNS precursor cells including glial cells. By stage 15 staining has tailed off and is observed in scattered puncta.
In the larval visual system, gcm protein is expressed not only in specific glial subtypes, but also in the lineage that gives rise to lamina neurons.
gcm protein is detected in nuclei in a subset of cells in the glial precursor cell areas at the margin of the lamina and in lamina precursor cells.
gcm protein is initially expressed in an anterior ventral patch in the cellular blastoderm embryo. During gastrulation, these cells invaginate at the end of the ventral furrow just anterior to the cephalic furrow in an area that gives rise to the cephalic mesoderm. Cephalic expression fades after stage 10. During stages 11-12, in each hemisegment, two patches of 3-5 ectodermal cells sequentially and transiently express gcm. From each patch, a single large blast cell delaminates and maintains gcm expression. These are tentatively identified as the peripheral glioblast and the longitudinal glioblast. By late stage 11, all of the progeny of these glioblasts as well as additional glial cells express gcm and expression is gone by stage 15. In the brain lobes, gcm is expressed in a complex pattern through stage 17. In the PNS, gcm is transiently expressed in all repo-positive glia along peripheral axon pathways and associated with sensory organs.
JBrowse - Visual display of RNA-Seq signals
View Dmel\gcm in JBrowse




2-35
2-30.9
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see JBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
polyclonal
gcm is required for the formation of subperineurial glial cells.
The decision to express gcm in the sensory organ lineage is dependent upon cell-cell communication.
Restricted expression of gcm is required for the developmental program of embryonic plasmatocytes.
gcm is necessary to induce glial differentiation in the peripheral nervous system.
Gliogenesis depends on gcm through asymmetric division of neuroglioblasts.
gcm can induce gliogenesis in mesodermal cells, indicating that gliogenesis does not require a ground neural state.
gcm is required in the hemocyte/macrophage cell lineage.
On the basis of structural as well as functional criteria gcm is a transcription factor with novel DNA binding domain that recognises the motif AT(G/A)CGGGT.
gcm is necessary for glial cell fate commitment. Mutations prevent glial cell determination in the embryonic central and peripheral nervous system. Absence of glial cells is the consequence of a cell fate switch from glia to neurones.
Mutations at gcm have severely disrupted longitudinal connectives. gcm was identified during an enhancer detector screen, imprecise excisions of the P-element generated severe alleles in which the longitudunal connectives have few axons in most segments. Expression patterns of mutant alleles indicate that the gcm mutation disrupts early steps of glial development. gcm may be an upstream element in the cascade that controls the repo expression.
Phenotypic analysis reveals that glial/neuron determination is governed by a single molecule, gcm. All CNS cells are originally bipotential so that they can differentiate into both neurons and glial cells with neuronal differentiation as a default. They differentiate into neurons when gcm is absent while they differentiate into glial cells when gcm is present.
Cloning, molecularly characterisation and genetic analysis of gcm.
gcm is involved in the migratory, not rotatory, aspect of lateral chordotonal (Lch) neuron development.