Mind Bomb 1-Expressing Intermediate Progenitors Generate Notch Signaling to Maintain Radial Glial Cells

Yoon, Ki‐Jun; Koo, Bon–Kyoung; Im, Sun Kyoung; Jeong, Hyun‐Woo; Ghim, Jaewang; Kwon, Min-Chul; Moon, Jin-Sook; Miyata, Takaki; Kong, Young Yun

doi:10.1016/j.neuron.2008.03.018

Cited by 179 publications

(197 citation statements)

References 50 publications

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“…Its critical regulation of NotchDelta signaling alone incorporates it into almost every aspect of nervous system development (6,10,(55)(56)(57)(58)(59)(60). More recently, an interactome study revealed that it also plays a role in the equally vital Wnt signaling pathway (18).…”

Section: Discussionmentioning

confidence: 99%

Sequential Elution Interactome Analysis of the Mind Bomb 1 Ubiquitin Ligase Reveals a Novel Role in Dendritic Spine Outgrowth

Mertz¹,

Tan

Pagala

et al. 2015

Molecular & Cellular Proteomics

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The mind bomb 1 (Mib1) ubiquitin ligase is essential for controlling metazoan development by Notch signaling and possibly the Wnt pathway. It is also expressed in postmitotic neurons and regulates neuronal morphogenesis and synaptic activity by mechanisms that are largely unknown. We sought to comprehensively characterize the Mib1 interactome and study its potential function in neuron development utilizing a novel sequential elution strategy for affinity purification, in which Mib1 binding proteins were eluted under different stringency and then quantified by the isobaric labeling method. The strategy identified the Mib1 interactome with both deep coverage and the ability to distinguish high-affinity partners from low-affinity partners. A total of 817 proteins were identified during the Mib1 affinity purification, including 56 high-affinity partners and 335 low-affinity partners, whereas the remaining 426 proteins are likely copurified contaminants or extremely weak binding proteins. The analysis detected all previously known Mib1-interacting proteins and revealed a large number of novel components involved in Notch and Wnt pathways, endocytosis and vesicle transport, the ubiquitin-proteasome system, cellular morphogenesis, and synaptic activities. Immunofluorescence studies further showed colocalization of Mib1 with five selected proteins: the Usp9x (FAM) deubiquitinating enzyme, alpha-, beta-, and delta-catenins, and CDKL5. Mutations of CDKL5 are associated with early infantile epileptic encephalopathy-2 (EIEE2), a severe form of mental retardation. We found that the expression of Mib1 downregulated the protein level of CDKL5 by ubiquitination, and antagonized CDKL5 function during the formation of dendritic spines. Thus, the sequential elution strategy enables biochemical characterization of protein interac-

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Section: Discussionmentioning

confidence: 99%

Sequential Elution Interactome Analysis of the Mind Bomb 1 Ubiquitin Ligase Reveals a Novel Role in Dendritic Spine Outgrowth

Mertz¹,

Tan

Pagala

et al. 2015

Molecular & Cellular Proteomics

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“…IPC and migrating neurons activate Notch in RG cells via expressing mind bomb-1 (mib1) (Yoon et al, 2008), suggesting that IPC and daughter neurons may maintain RG proliferation ability through Notch signal activation by contacting RG radial fibers during migration. Interestingly, some studies have indicated that the proliferation of RG cells and IPC may be regulated by different Notch signal transductions.…”

Section: Rg Cell Division In Neocortical Developmentmentioning

confidence: 99%

Neuronal stem cells in the central nervous system and in human diseases

Wang

2012

Protein Cell

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The process of cortical expansion in the central nervous system is a key step of mammalian brain development to ensure its physiological function. Radial glial (RG) cells are a glial cell type contributing to this progress as intermediate neural progenitor cells responsible for an increase in the number of cortical neurons. In this review, we discuss the current understanding of RG cells during neurogenesis and provide further information on the mechanisms of neurodevelopmental diseases and stem cell-related brain tumorigenesis. Knowledge of neuronal stem cell and relative diseases will bridge benchmark research through translational studies to clinical therapeutic treatments of these diseases.

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“…Even if properties of neural precursors are normally modulated by short-and long-range signals coming from the embryonic structure they belong to [16,17], cardinal features of their behavior are largely controlled at single-cell level. This applies, for example, to the retention of their positional identity, the temporal order and precise timing by which their distinct neural cell progenies are laid down, the shapes of lineage trees connecting them to such progenies [18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Emx2 and Foxg1 Inhibit Gliogenesis and Promote Neuronogenesis

et al. 2010

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Neural stem cells (NSCs) give rise to all cell types forming the cortex: neurons, astrocytes, and oligodendrocytes. The transition from the former to the latter ones takes place via lineage-restricted progenitors in a highly regulated way. This process is mastered by large sets of genes, among which some implicated in central nervous system pattern formation. The aim of this study was to disentangle the kinetic and histogenetic roles exerted by two of these genes, Emx2 and Foxg1, in cortico-cerebral precursors. For this purpose, we set up a new integrated in vitro assay design. Embryonic cortical progenitors were transduced with lentiviral vectors driving overexpression of Emx2 and Foxg1 in NSCs and neuronal progenitors. Cells belonging to different neuronogenic and gliogenic compartments were labeled by spectrally distinguishable fluoroproteins driven by cell type-specific promoters and by cell type-specific antibodies and were scored via multiplex cytofluorometry and immunocytofluorescence. A detailed picture of Emx2 and Foxg1 activities in cortico-cerebral histogenesis resulted from this study. Unexpectedly, we found that both genes inhibit gliogenesis and promote neuronogenesis, through distinct mechanisms, and Foxg1 also dramatically stimulates neurite outgrowth. Remarkably, such activities, alone or combined, may be exploited to ameliorate the neuronal output obtainable from neural cultures, for purposes of cell-based brain repair. STEM CELLS

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Mind Bomb 1-Expressing Intermediate Progenitors Generate Notch Signaling to Maintain Radial Glial Cells

Cited by 179 publications

References 50 publications

Sequential Elution Interactome Analysis of the Mind Bomb 1 Ubiquitin Ligase Reveals a Novel Role in Dendritic Spine Outgrowth

Sequential Elution Interactome Analysis of the Mind Bomb 1 Ubiquitin Ligase Reveals a Novel Role in Dendritic Spine Outgrowth

Neuronal stem cells in the central nervous system and in human diseases

Emx2 and Foxg1 Inhibit Gliogenesis and Promote Neuronogenesis

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