The developmental distribution of vimentin in the chick retina

Glutamine synthetase (GS) activity and spatial and temporal patterns of GS expression in the developing chick retina: Relationship with synaptogenesis in the outer plexiform layer

“…In addition, they are not apparently labeled in sections stained with antibodies against glial fibrillary acidic protein. This marker, typical of astrocytes, does not label the chick retina until 3 weeks after hatching (Lemmon and Rieser, 1983), and it hardly labels Mü ller cells. As regards their origin, our results of GS expression in precociously induced retinas suggest that they are generated close to the ventricle and migrate to their final position, but they do not prove the identity of the positive GS cells (non-Mü ller cells) scattered through the retinal layers, the possibility being that they are neurons (instead of migrating glial cells), which could be anomalously induced by the hydrocortisone to increase GS.…”

Late proliferation of retinal Müller cell progenitors facilitates preferential targeting with retroviral vectors in vitro

“…Later in development, neuronal cells turn off such markers as a function of their specialization and maturation. Included in this category are such marker gene products as vimentin [Lemmon and Reiser, 1983], a-crystallin [Moscona et al, 1985], the 5A11/HT7 antigen [Fadool and Linser, 1993a,b] and CA-II [Linser and Moscona, 1981;Linser, 1991]. The second category is composed of marker gene products that are only expressed in Mü ller cells late in development as a maturation-specific function of Mü ller cell differentiation.…”

“…Among the most significant technical advances has been the characterization of a wide range of biochemical, molecular and immunochemical markers for cell-type or stage-specific gene products. The types of markers that have been reported cover a very broad range of functions, including metabolic enzymes, such as carbonic anhydrase-II (CA-II) [Linser and Moscona, 1981] and glutamine synthetase (GS) [Riepe and Norenberg, 1977;Linser and Moscona, 1979]; cell surface molecules, such as the 5A11 antigen [Fadool and Linser, 1993b], NCAM [Edelman, 1983], and N-cadherin [Lagunowich and Grunwald, 1989]; transcription factors, including Pax genes [Martin et al, 1992]; and Islet-1 [Thor et al, 1991] and structural protein genes, such as various intermediate filament proteins [Lemmon and Reiser, 1983], tubulins [Vinores et al, 1995], and associated proteins [McCloon and Barnes, 1989;Prada et al, 1995]. Some useful markers of developmental events remain undefined in terms of their own function.…”

rek, a Gene Expressed in Retina and Brain, Encodes a Receptor Tyrosine Kinase of the Axl/Tyro3 Family

“…By 7-10 days, a mixed culture developed consisting of a monolayer of flat cells underlying a network of neuronal fascicles and cell clumps, which were removed by gentle mechanical agitation. As described previously, the identification of the flat cells as Mü ller glia is supported by abundant intermediate filaments (47), staining with vimentin antibodies (48), lack of binding to tetanus toxin, [ 3 H]thymidine incorporation, GABA and glutamate uptake (49, 50), expression of a filamin-related protein (51), and the presence of carbonic anhydrase and glutamine synthetase (52). The glial-like cells do not show induction of glutamine synthetase by hydrocortisone, a response characteristic of Mü ller cells in vivo (52), and are negative for expression of glial fibrillary acidic protein, perhaps due to the absence of necessary intercellular interactions in the monolayers.…”