The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Chris Q. Doe - One of the best experts on this subject based on the ideXlab platform.
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Temporal and spatial expression of Drosophila miR-124.
2012Co-Authors: Kailiang Sun, Jakub Orzechowski Westholm, Kazuya Tsurudome, Joshua W. Hagen, Minoree Kohwi, Doron Betel, Fen-biao Gao, Pejmun A. Haghighi, Chris Q. DoeAbstract:(A) Northern analysis using staged preparations of total RNA. (B–D) Nascent transcription of pri-mir-124 detected with a 1 kb probe. (B and C) are ventral views and (D) is a lateral view. Inset of panel (B) highlights the detection of nuclear dots that reflect the chromosomal locations of mir-124 transcription. (E–I) Expression of a miR-124:DsRed transgene colabeled with various neural markers, Deadpan (neuroblast marker) and Prospero (Ganglion Mother Cell marker) and Elav (differentiated neuron marker); embryos in H–I are counterstained with DAPI. In all panels, miR-124:DsRed is at left, the neural markers in the middle, and merged images at right; the signal in the center of panels G is gut autofluorescence. Activity of mir-124 initiates in neuroblasts and is maintained in GMCs and CNS neurons. High magnification insets of panels E–F show gradual expression of miR-124:DsRed in all Deadpan+ and Prospero+ positive Cells in CNS.
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Polarity
2009Co-Authors: Chiswili Chabu, Chris Q. DoeAbstract:Asymmetric Cell division is a mechanism for generating Cell diversity as well as maintaining stem Cell homeostasis in both Drosophila and mammals. In Drosophila, larval neuroblasts are stem Cell-like progenitors that divide asymmetrically to generate neurons of the adult brain. Mitotic neuroblasts localize atypical protein kinase C (aPKC) to their apical cortex. Cortical aPKC excludes cortical localization of Miranda and its cargo proteins Prospero and Brain tumor, resulting in their partitioning into the differentiating, smaller Ganglion Mother Cell (GMC) where they are required for neuronal differentiation. In addition to aPKC, the kinases Aurora-A and Polo also regulate neuroblast self-renewal, but the phosphatases involved in neuroblast self-renewal have not been identified. Here we report that aPKC is in a protein complex in vivo with Twins, a Drosophila B-type protein phosphatase 2A (PP2A) subunit, and that Twins and the catalytic subunit of PP2A, called Microtubule star (Mts), are detected in larval neuroblasts. Both Twins and Mts are required to exclude aPKC from the basal neuroblast cortex: twins mutant brains, twins mutant single neuroblast mutant clones, or mts dominant negative single neuroblast clones all show ectopic basal cortical localization of aPKC. Consistent with ectopic basal aPKC is the appearance of supernumerary neuroblasts in twins mutant brains or twins mutant clones. We conclude that Twins/PP2A is required to maintain aPKC at the apical cortex of mitotic neuroblasts, keeping it out of the differentiating GMC, and thereby maintaining neuroblast homeostasis. © 2009 Elsevier Inc. All rights reserved
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drosophila neuroblast 7 3 Cell lineage a model system for studying programmed Cell death notch numb signaling and sequential specification of Ganglion Mother Cell identity
The Journal of Comparative Neurology, 2005Co-Authors: Rachel Karcavich, Chris Q. DoeAbstract:Cell lineage studies provide an important foundation for experimental analysis in many systems. Drosophila neural precursors (neuroblasts) sequentially generate Ganglion Mother Cells (GMCs), which generate neurons and/or glia, but the birth order, or Cell lineage, of each neuroblast is poorly understood. The best-characterized neuroblast is NB7-3, in which GMC-1 makes the EW1 serotonergic interneuron and GW motoneuron; GMC-2 makes the EW2 serotonergic interneuron and a programmed Cell death; and GMC-3 gives rise to the EW3 interneuron. However, the end of this lineage has not been determined. Here, we use positively marked genetic clones, bromodeoxyuridine (BrdU) labeling, mutations that affect Notch signaling, and antibody markers to further define the end of the Cell lineage of NB7-3. We provide evidence that GMC-3 directly differentiates into EW3 and that the sibling neuroblast undergoes programmed Cell death. Our results confirm and extend previous work on the early portion of the NB7-3 lineage (Novotny et al. [2002] Development 129:1027–1036; Lundell et al. [2003] Development 130:4109 – 4121). J. Comp. Neurol. 481:240 –251, 2005. © 2004 Wiley-Liss, Inc. Indexing terms: Cell lineage; neuroblast; programmed Cell death; Notch; sanpodo; numb; serotonin; corazonin; NB7-3
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miranda directs prospero to a daughter Cell during drosophila asymmetric divisions
Nature, 1997Co-Authors: Hiroko Ikeshimakataoka, Chris Q. Doe, James B Skeath, Yoichi Nabeshima, Fumio MatsuzakiAbstract:Asymmetric Cell division is a general process used in many developmental contexts to create two differently fated Cells from a single progenitor Cell. Intrinsic mechanisms like the asymmetric transmission of Cell-fate determinants during Cell division, and extrinsic Cell-interaction mechanisms, can mediate asymmetric divisions1,2,3. During embryonic development of the Drosophila central nervous system, neural stem Cells called neuroblasts divide asymmetrically to produce another multipotent neuroblast and a Ganglion Mother Cell (GMC) of more restricted developmental potential. Intrinsic mechanisms promote asymmetric division of neuroblasts: for example, the transcription factor Prospero localizes to the basal Cell cortex of mitotic neuroblasts and then segregates exclusively into the GMC, which buds off from the basal side of the neuroblast4,5,6. In the GMC, Prospero translocates to the nucleus, where it establishes differential gene expression between sibling Cells. Here we report the identification of a gene, miranda, which encodes a new protein that co-localizes with Prospero in mitotic neuroblasts, tethers Prospero to the basal cortex of mitotic neuroblasts, directing Prospero into the GMC, and releases Prospero from the Cell cortex within GMCs. miranda thus creates intrinsic differences between sibling Cells by mediating the asymmetric segregation of a transcription factor into only one daughter Cell during neural stem-Cell division.
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Extrinsic cues, intrinsic cues and microfilaments regulate asymmetric protein localization in Drosophila neuroblasts
Current biology : CB, 1997Co-Authors: Julie Broadus, Chris Q. DoeAbstract:Abstract Background: The Drosophila central nervous system develops from stem Cell like precursors called neuroblasts, which divide unequally to bud off a series of smaller daughter Cells called Ganglion Mother Cells. Neuroblasts show Cell-cycle-specific asymmetric localization of both RNA and proteins: at late interphase, prospero RNA and Inscuteable, Prospero and Staufen proteins are all apically localized; at mitosis, Inscuteable remains apical whereas prospero RNA, Prospero protein and Staufen protein form basal cortical crescents. Here we use in vitro culture of neuroblasts to investigate the role of intrinsic and extrinsic cues and the cytoskeleton in asymmetric localization of Inscuteable, Prospero and Staufen proteins. Results: Neuroblast cytokinesis is normal in vitro , producing a larger neuroblast and a smaller Ganglion Mother Cell. Apical localization of Inscuteable, Prospero and Staufen in interphase neuroblasts is reduced or eliminated in vitro , but all three proteins are localized normally during mitosis (apical Inscuteable, basal Prospero and Staufen). Microfilament inhibitors result in delocalization of all three proteins. Inscuteable becomes uniform at the cortex, whereas Prospero and Staufen become cytoplasmic; inhibitor washout leads to recovery of microfilaments and asymmetric localization of all three proteins. Microtubule disruption has no effect on protein localization, but disruption of both microtubules and microfilaments results in cytoplasmic localization of Inscuteable. Conclusions: Both extrinsic and intrinsic cues regulate protein localization in neuroblasts. Microfilaments, but not microtubules, are essential for asymmetric protein anchoring (and possibly localization) in mitotic neuroblasts. Our results highlight the similarity between Drosophila, Caenorhabditis elegans , vertebrates, plants and yeast: in all organisms, asymmetric protein or RNA localization and/or anchoring requires microfilaments.
Fumio Matsuzaki - One of the best experts on this subject based on the ideXlab platform.
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heterotrimeric g proteins regulate daughter Cell size asymmetry in drosophila neuroblast divisions
Current Biology, 2003Co-Authors: Naoyuki Fuse, Kanako Hisata, Alisa L Katzen, Fumio MatsuzakiAbstract:Cell division often generates unequally sized daughter Cells by off-center cleavages, which are due to either displacement of mitotic spindles or their asymmetry. Drosophila neuroblasts predominantly use the latter mechanism to divide into a large apical neuroblast and a small basal Ganglion Mother Cell (GMC), where the neural fate determinants segregate. Apically localized components regulate both the spindle asymmetry and the localization of the determinants. Here, we show that asymmetric spindle formation depends on signaling mediated by the Gβ subunit of heterotrimeric G proteins. Gβ13F distributes throughout the neuroblast cortex. Its lack induces a large symmetric spindle and causes division into nearly equal-sized Cells with normal segregation of the determinants. In contrast, elevated Gβ13F activity generates a small spindle, suggesting that this factor suppresses spindle development. Depletion of the apical components also results in the formation of a small symmetric spindle at metaphase. Therefore, the apical components and Gβ13F affect the mitotic spindle shape oppositely. We propose that differential activation of Gβ signaling biases spindle development within neuroblasts and thereby causes asymmetric spindles. Furthermore, the multiple equal cleavages of Gβ mutant neuroblasts accompany neural defects; this finding suggests indispensable roles of eccentric division in assuring the stem Cell properties of neuroblasts.
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miranda localizes staufen and prospero asymmetrically in mitotic neuroblasts and epithelial Cells in early drosophila embryogenesis
Development, 1998Co-Authors: Fumio Matsuzaki, Hiroko Ikeshimakataoka, Tomokazu Ohshiro, Hitomi IzumiAbstract:When neuroblasts divide, prospero protein and mRNA segregate asymmetrically into the daughter neuroblast and sibling Ganglion Mother Cell. miranda is known to localize prospero protein to the basal Cell cortex of neuroblasts while the staufen RNA-binding protein mediates prospero mRNA localization. Here we show that miranda is required for asymmetric staufen localization in neuroblasts. Analyses using miranda mutants reveal that prospero and staufen interact with miranda under the same Cell-cycle-dependent control. miranda thus acts to partition both prospero protein and mRNA. Furthermore, miranda localizes prospero and staufen to the basolateral cortex in dividing epithelial Cells, which express the three proteins prior to neurogenesis. Our observations suggest that the epithelial Cell and neuroblast (both of epithelial origin) share the same molecular machinery for creating Cellular asymmetry.
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miranda directs prospero to a daughter Cell during drosophila asymmetric divisions
Nature, 1997Co-Authors: Hiroko Ikeshimakataoka, Chris Q. Doe, James B Skeath, Yoichi Nabeshima, Fumio MatsuzakiAbstract:Asymmetric Cell division is a general process used in many developmental contexts to create two differently fated Cells from a single progenitor Cell. Intrinsic mechanisms like the asymmetric transmission of Cell-fate determinants during Cell division, and extrinsic Cell-interaction mechanisms, can mediate asymmetric divisions1,2,3. During embryonic development of the Drosophila central nervous system, neural stem Cells called neuroblasts divide asymmetrically to produce another multipotent neuroblast and a Ganglion Mother Cell (GMC) of more restricted developmental potential. Intrinsic mechanisms promote asymmetric division of neuroblasts: for example, the transcription factor Prospero localizes to the basal Cell cortex of mitotic neuroblasts and then segregates exclusively into the GMC, which buds off from the basal side of the neuroblast4,5,6. In the GMC, Prospero translocates to the nucleus, where it establishes differential gene expression between sibling Cells. Here we report the identification of a gene, miranda, which encodes a new protein that co-localizes with Prospero in mitotic neuroblasts, tethers Prospero to the basal cortex of mitotic neuroblasts, directing Prospero into the GMC, and releases Prospero from the Cell cortex within GMCs. miranda thus creates intrinsic differences between sibling Cells by mediating the asymmetric segregation of a transcription factor into only one daughter Cell during neural stem-Cell division.
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asymmetric segregation of the homeodomain protein prospero during drosophila development
Nature, 1995Co-Authors: Joe Hirata, Yoichi Nabeshima, Hideki Nakagoshi, Fumio MatsuzakiAbstract:ASYMMETRIC divisions that produce two distinct Cells play fundamental roles in generating different Cell types during development1,2. In the Drosophilacentral nervous system, neural stem Cells called neuroblasts divide unequally into another neuro-blast and a Ganglion Mother Cell which is subsequently cleaved into neurons. Correct gene expression of Ganglion Mother Cells requires the transcription factor Prospero3a¤-5. Here we demonstrate the asymmetric segregation of Prospero on neuroblast division. Prospero synthesized in neuroblasts is retained in the cytoplasm and at mitosis is exclusively partitioned to Ganglion Mother Cells, in which it is translocated to the nucleus. Differential segregation of Prospero was also found in the endoderm. We have identified a region in Prospero that is responsible for this event. The region shares a common motif with Numb6, which also shows unequal segregation7. We propose that asymmetric segregation of transcription factors is an intrinsic mechanism for establishing asymmetry in gene expression between sibling Cells.
F J Tejedor - One of the best experts on this subject based on the ideXlab platform.
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A Transient Expression of Prospero Promotes Cell Cycle Exit of Drosophila Postembryonic Neurons through the Regulation of Dacapo
2011Co-Authors: Jordi Colonques, J Ceron, Heinrich Reichert, F J TejedorAbstract:Cell proliferation, specification and terminal differentiation must be precisely coordinated during brain development to ensure the correct production of different neuronal populations. Most Drosophila neuroblasts (NBs) divide asymmetrically to generate a new NB and an intermediate progenitor called Ganglion Mother Cell (GMC) which divides only once to generate two postmitotic Cells called Ganglion Cells (GCs) that subsequently differentiate into neurons. During the asymmetric division of NBs, the homeodomain transcription factor PROSPERO is segregated into the GMC where it plays a key role as Cell fate determinant. Previous work on embryonic neurogenesis has shown that PROSPERO is not expressed in postmitotic neuronal progeny. Thus, PROSPERO is thought to function in the GMC by repressing genes required for Cell-cycle progression and activating genes involved in terminal differentiation. Here we focus on postembryonic neurogenesis and show that the expression of PROSPERO is transiently upregulated in the newly born neuronal progeny generated by most of the larval NBs of the OL and CB. Moreover, we provide evidence that this expression of PROSPERO in GCs inhibits their Cell cycle progression by activating the expression of the cyclin-dependent kinase inhibitor (CKI) DACAPO. These findings imply that PROSPERO, in addition to its known role as Cell fate determinant in GMCs, provides a transient signal to ensure a precise timing for Cell cycle exit of prospective neurons, and hence may link the mechanisms that regulate neurogenesis and thos
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A transient expression of Prospero promotes Cell cycle exit of Drosophila postembryonic neurons through the regulation of Dacapo.
Public Library of Science (PLoS), 2011Co-Authors: Jordi Colonques, J Ceron, Heinrich Reichert, F J TejedorAbstract:Cell proliferation, specification and terminal differentiation must be precisely coordinated during brain development to ensure the correct production of different neuronal populations. Most Drosophila neuroblasts (NBs) divide asymmetrically to generate a new NB and an intermediate progenitor called Ganglion Mother Cell (GMC) which divides only once to generate two postmitotic Cells called Ganglion Cells (GCs) that subsequently differentiate into neurons. During the asymmetric division of NBs, the homeodomain transcription factor PROSPERO is segregated into the GMC where it plays a key role as Cell fate determinant. Previous work on embryonic neurogenesis has shown that PROSPERO is not expressed in postmitotic neuronal progeny. Thus, PROSPERO is thought to function in the GMC by repressing genes required for Cell-cycle progression and activating genes involved in terminal differentiation. Here we focus on postembryonic neurogenesis and show that the expression of PROSPERO is transiently upregulated in the newly born neuronal progeny generated by most of the larval NBs of the OL and CB. Moreover, we provide evidence that this expression of PROSPERO in GCs inhibits their Cell cycle progression by activating the expression of the cyclin-dependent kinase inhibitor (CKI) DACAPO. These findings imply that PROSPERO, in addition to its known role as Cell fate determinant in GMCs, provides a transient signal to ensure a precise timing for Cell cycle exit of prospective neurons, and hence may link the mechanisms that regulate neurogenesis and those that control Cell cycle progression in postembryonic brain development
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patterns of Cell division and expression of asymmetric Cell fate determinants in postembryonic neuroblast lineages of drosophila
Developmental Biology, 2001Co-Authors: J Ceron, Cayetano Gonzalez, F J TejedorAbstract:Abstract We have studied the division of postembryonic neuroblasts (Nbs) in the outer proliferation center (OPC) and central brain anlagen of Drosophila. We focused our attention on three aspects of these processes: the pattern of Cellular division, the topological orientation of those divisions, and the expression of asymmetric Cell fate determinants. Although larval Nbs are of embryonic origin, our results indicate that their properties appear to be modified during development. Several conclusions can be summarized: (i) In early larvae, Nbs divide symmetrically to give rise to two Nbs while in the late larval brain most Nbs divide asymmetrically to bud off an intermediate Ganglion Mother Cell (GMC) that very rapidly divides into two Ganglion Cells (GC). (ii) Symmetric and asymmetric divisions of OPC Nbs show tangential and radial orientations, respectively. (iii) This change in the pattern of division correlates with the expression of inscuteable, which is apically localized only in asymmetric divisions. (iv) The spindle of asymmetrically dividing Nb is always oriented on an apical–basal axis. (v) Prospero does not colocalize with Miranda in the cortical crescent of mitotic Nbs. (vi) Prospero is transiently expressed in one of the two sibling GCs generated by the division of GMCs. The implications of these results on Cell fate specification and differentiation of adult brain neurons are discussed.
J Ceron - One of the best experts on this subject based on the ideXlab platform.
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A Transient Expression of Prospero Promotes Cell Cycle Exit of Drosophila Postembryonic Neurons through the Regulation of Dacapo
2011Co-Authors: Jordi Colonques, J Ceron, Heinrich Reichert, F J TejedorAbstract:Cell proliferation, specification and terminal differentiation must be precisely coordinated during brain development to ensure the correct production of different neuronal populations. Most Drosophila neuroblasts (NBs) divide asymmetrically to generate a new NB and an intermediate progenitor called Ganglion Mother Cell (GMC) which divides only once to generate two postmitotic Cells called Ganglion Cells (GCs) that subsequently differentiate into neurons. During the asymmetric division of NBs, the homeodomain transcription factor PROSPERO is segregated into the GMC where it plays a key role as Cell fate determinant. Previous work on embryonic neurogenesis has shown that PROSPERO is not expressed in postmitotic neuronal progeny. Thus, PROSPERO is thought to function in the GMC by repressing genes required for Cell-cycle progression and activating genes involved in terminal differentiation. Here we focus on postembryonic neurogenesis and show that the expression of PROSPERO is transiently upregulated in the newly born neuronal progeny generated by most of the larval NBs of the OL and CB. Moreover, we provide evidence that this expression of PROSPERO in GCs inhibits their Cell cycle progression by activating the expression of the cyclin-dependent kinase inhibitor (CKI) DACAPO. These findings imply that PROSPERO, in addition to its known role as Cell fate determinant in GMCs, provides a transient signal to ensure a precise timing for Cell cycle exit of prospective neurons, and hence may link the mechanisms that regulate neurogenesis and thos
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A transient expression of Prospero promotes Cell cycle exit of Drosophila postembryonic neurons through the regulation of Dacapo.
Public Library of Science (PLoS), 2011Co-Authors: Jordi Colonques, J Ceron, Heinrich Reichert, F J TejedorAbstract:Cell proliferation, specification and terminal differentiation must be precisely coordinated during brain development to ensure the correct production of different neuronal populations. Most Drosophila neuroblasts (NBs) divide asymmetrically to generate a new NB and an intermediate progenitor called Ganglion Mother Cell (GMC) which divides only once to generate two postmitotic Cells called Ganglion Cells (GCs) that subsequently differentiate into neurons. During the asymmetric division of NBs, the homeodomain transcription factor PROSPERO is segregated into the GMC where it plays a key role as Cell fate determinant. Previous work on embryonic neurogenesis has shown that PROSPERO is not expressed in postmitotic neuronal progeny. Thus, PROSPERO is thought to function in the GMC by repressing genes required for Cell-cycle progression and activating genes involved in terminal differentiation. Here we focus on postembryonic neurogenesis and show that the expression of PROSPERO is transiently upregulated in the newly born neuronal progeny generated by most of the larval NBs of the OL and CB. Moreover, we provide evidence that this expression of PROSPERO in GCs inhibits their Cell cycle progression by activating the expression of the cyclin-dependent kinase inhibitor (CKI) DACAPO. These findings imply that PROSPERO, in addition to its known role as Cell fate determinant in GMCs, provides a transient signal to ensure a precise timing for Cell cycle exit of prospective neurons, and hence may link the mechanisms that regulate neurogenesis and those that control Cell cycle progression in postembryonic brain development
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patterns of Cell division and expression of asymmetric Cell fate determinants in postembryonic neuroblast lineages of drosophila
Developmental Biology, 2001Co-Authors: J Ceron, Cayetano Gonzalez, F J TejedorAbstract:Abstract We have studied the division of postembryonic neuroblasts (Nbs) in the outer proliferation center (OPC) and central brain anlagen of Drosophila. We focused our attention on three aspects of these processes: the pattern of Cellular division, the topological orientation of those divisions, and the expression of asymmetric Cell fate determinants. Although larval Nbs are of embryonic origin, our results indicate that their properties appear to be modified during development. Several conclusions can be summarized: (i) In early larvae, Nbs divide symmetrically to give rise to two Nbs while in the late larval brain most Nbs divide asymmetrically to bud off an intermediate Ganglion Mother Cell (GMC) that very rapidly divides into two Ganglion Cells (GC). (ii) Symmetric and asymmetric divisions of OPC Nbs show tangential and radial orientations, respectively. (iii) This change in the pattern of division correlates with the expression of inscuteable, which is apically localized only in asymmetric divisions. (iv) The spindle of asymmetrically dividing Nb is always oriented on an apical–basal axis. (v) Prospero does not colocalize with Miranda in the cortical crescent of mitotic Nbs. (vi) Prospero is transiently expressed in one of the two sibling GCs generated by the division of GMCs. The implications of these results on Cell fate specification and differentiation of adult brain neurons are discussed.
Hiroko Ikeshimakataoka - One of the best experts on this subject based on the ideXlab platform.
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miranda localizes staufen and prospero asymmetrically in mitotic neuroblasts and epithelial Cells in early drosophila embryogenesis
Development, 1998Co-Authors: Fumio Matsuzaki, Hiroko Ikeshimakataoka, Tomokazu Ohshiro, Hitomi IzumiAbstract:When neuroblasts divide, prospero protein and mRNA segregate asymmetrically into the daughter neuroblast and sibling Ganglion Mother Cell. miranda is known to localize prospero protein to the basal Cell cortex of neuroblasts while the staufen RNA-binding protein mediates prospero mRNA localization. Here we show that miranda is required for asymmetric staufen localization in neuroblasts. Analyses using miranda mutants reveal that prospero and staufen interact with miranda under the same Cell-cycle-dependent control. miranda thus acts to partition both prospero protein and mRNA. Furthermore, miranda localizes prospero and staufen to the basolateral cortex in dividing epithelial Cells, which express the three proteins prior to neurogenesis. Our observations suggest that the epithelial Cell and neuroblast (both of epithelial origin) share the same molecular machinery for creating Cellular asymmetry.
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miranda directs prospero to a daughter Cell during drosophila asymmetric divisions
Nature, 1997Co-Authors: Hiroko Ikeshimakataoka, Chris Q. Doe, James B Skeath, Yoichi Nabeshima, Fumio MatsuzakiAbstract:Asymmetric Cell division is a general process used in many developmental contexts to create two differently fated Cells from a single progenitor Cell. Intrinsic mechanisms like the asymmetric transmission of Cell-fate determinants during Cell division, and extrinsic Cell-interaction mechanisms, can mediate asymmetric divisions1,2,3. During embryonic development of the Drosophila central nervous system, neural stem Cells called neuroblasts divide asymmetrically to produce another multipotent neuroblast and a Ganglion Mother Cell (GMC) of more restricted developmental potential. Intrinsic mechanisms promote asymmetric division of neuroblasts: for example, the transcription factor Prospero localizes to the basal Cell cortex of mitotic neuroblasts and then segregates exclusively into the GMC, which buds off from the basal side of the neuroblast4,5,6. In the GMC, Prospero translocates to the nucleus, where it establishes differential gene expression between sibling Cells. Here we report the identification of a gene, miranda, which encodes a new protein that co-localizes with Prospero in mitotic neuroblasts, tethers Prospero to the basal cortex of mitotic neuroblasts, directing Prospero into the GMC, and releases Prospero from the Cell cortex within GMCs. miranda thus creates intrinsic differences between sibling Cells by mediating the asymmetric segregation of a transcription factor into only one daughter Cell during neural stem-Cell division.
