The Drosophila anachronism locus: A glycoprotein secreted by glia inhibits neuroblast proliferation

Ebens, Allen; Garren, Hideki; Cheyette, Benjamin N.R.; Zipursky, S. Lawrence

doi:10.1016/0092-8674(93)90291-w

Cited by 193 publications

(132 citation statements)

References 26 publications

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“…The subset of trol-dependent neuroblasts is normally kept quiescent in response to the gene product of ana (Datta, 1995), a secreted glial glycoprotein that represses premature proliferation of optic lobe and thoracic neuroblasts (Ebens et al, 1993). Several studies on trol and ana have led to the proposal that trol may regulate the reactivation of neuroblast proliferation by suppressing or bypassing the repression by ana, thereby stimulating the G1/S transition through up-regulation of Cyclin E expression (Caldwell and Datta, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…Several genes have been identified that affect neuroblast proliferation in Drosophila (Lipshitz and Kankel, 1985;Datta and Kankel, 1992;Ebens et al, 1993;Prokop and Technau, 1994;Park et al, 1998;. These genes include anachroism (ana), terribly reduced optic lobes (trol), and even-skipped (eve).…”

Section: Introductionmentioning

confidence: 99%

“…ana encodes a secreted glial glycoprotein proposed to repress premature proliferation of quiescent optic lobe and thoracic neuroblasts (Ebens et al, 1993). Interestingly, however, when proliferation is activated in quiescent neuroblasts, expression of ana and the levels of the protein appear to remain constant.…”

Section: Introductionmentioning

confidence: 99%

“…Interestingly, however, when proliferation is activated in quiescent neuroblasts, expression of ana and the levels of the protein appear to remain constant. Because the amount of ana repressor remained unchanged when neuroblasts undergo the transition from quiescence to activation of proliferation, a second factor has been proposed to be needed to override ana-dependent repression (Ebens et al, 1993). ana-mediated proliferation repression of neuroblasts is antagonized by the activity of trol (Datta, 1995).…”

Section: Introductionmentioning

confidence: 99%

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Perlecan participates in proliferation activation of quiescent Drosophila neuroblasts

Voigt¹,

Pflanz²,

Schäfer³

et al. 2002

Developmental Dynamics

117

114

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Drosophila neuroblasts act as stem cells. Their proliferation is controlled through cell cycle arrest and activation in a spatiotemporal pattern. Several genes have been identified that control the pattern of neuroblast quiescence and proliferation in the central nervous system (CNS), including anachronism (ana), even skipped (eve) and terribly reduced optic lobes (trol). eve acts in a non-cell-autonomous manner to produce a transacting factor in the larval body that stimulates cell division in the population of quiescent optic lobe neuroblasts. ana encodes a secreted glial glycoprotein proposed to repress premature proliferation of optic lobe and thoracic neuroblasts. trol was shown to act downstream of ana to activate proliferation of quiescent neuroblasts either by inactivating or bypassing ana-dependent repression. Here, we show that trol codes for Drosophila Perlecan, a large multidomain heparan sulfate proteoglycan originally identified in extracellular matrix structures of mammals. The results suggest that trol acts in the extracellular matrix and binds, stores, and sequesters external signals and, thereby, participates in the stage-and regionspecific control of neuroblast proliferation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Perlecan participates in proliferation activation of quiescent Drosophila neuroblasts

Voigt¹,

Pflanz²,

Schäfer³

et al. 2002

Developmental Dynamics

117

114

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“…Several factors have been found that govern the initial G10S transition of reactivating neuroblasts. The anachronism (ana) gene is expressed in a subset of glial cells that neighbour neuroblasts, and codes for a secreted glycoprotein of unknown biochemical function (Ebens et al 1993). Loss of Ana function results in precocious neuroblast reactivation, with neuroblasts entering their first S phase around 8 h early.…”

Section: (D) Neuroblast Reactivationmentioning

confidence: 99%

Insights into neural stem cell biology from flies

Egger

Chell

Brand

2007

Phil. Trans. R. Soc. B

134

126

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Drosophila neuroblasts are similar to mammalian neural stem cells in their ability to self-renew and to produce many different types of neurons and glial cells. In the past two decades, great advances have been made in understanding the molecular mechanisms underlying embryonic neuroblast formation, the establishment of cell polarity and the temporal regulation of cell fate. It is now a challenge to connect, at the molecular level, the different cell biological events underlying the transition from neural stem cell maintenance to differentiation. Progress has also been made in understanding the later stages of development, when neuroblasts become mitotically inactive, or quiescent, and are then reactivated postembryonically to generate the neurons that make up the adult nervous system. The ability to manipulate the steps leading from quiescence to proliferation and from proliferation to differentiation will have a major impact on the treatment of neurological injury and neurodegenerative disease.

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Neurogenesis in adult insect mushroom bodies

et al. 1996

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The occurrence of neurogenesis in mushroom bodies of adult insects belonging to several orthopteroid and coleopteran families is described. Using injections of 5-bromo, T2'-deoxyuridine, we showed that neuroblasts, which are progenitors of Kenyon cells during preimaginal instars, continue to divide in adult Acheta domesticus. Their progeny constitute a central column in mushroom body cortices of 3-week-old females. Other Gryllidae, Gryllus bimaculatus and Gryllomorpha dalmatina, show the same pattern of neuroblast activity and migration of their progeny. Immunocytochemical staining of glial cells failed to reveal any immunoreactivity, either in proliferating regions or in the resulting cells. In another orthopteran, Locusta migratoria, discrete clusters of cells, located dorsolateral to the Kenyon cells, incorporated 5-bromo, 2'-deoxyuridine, but we could not detect any neuronal progeny migrating to the mushroom body cortices. These cells were strongly labeled with an antiglial antibody, indicating that the replicating cells are glioblasts rather than neuroblasts. In Periplaneta americana (Dictyoptera), cells replicating their DNA were similarly shown to immunoreact with glial antibodies. In contrast, three coleopterans (Tenebrio molitor, Zophobas species, Harmonia axyridis) have two large neuroblasts located in the middle of the mushroom body cortices. These produce cells which migrate within the group of Kenyon cells, their nuclei having the same shape and size as those of surrounding Kenyon cells. In adult insects, neurogenesis in mushroom bodies occurs in Gryllidae and several coleopteran families, but could not be demonstrated in Dictyoptera and Acrididae. Its occurrence and distribution raise the issue of unexpected plasticity in the adult insect brain.

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The Drosophila anachronism locus: A glycoprotein secreted by glia inhibits neuroblast proliferation

Cited by 193 publications

References 26 publications

Perlecan participates in proliferation activation of quiescent Drosophila neuroblasts

Perlecan participates in proliferation activation of quiescent Drosophila neuroblasts

Insights into neural stem cell biology from flies

Neurogenesis in adult insect mushroom bodies

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