Properly formed but improperly localized synaptic specializations in the absence of laminin α4

Patton, Bruce L.; Cunningham, Jeanette M.; Thyboll, Jill; Kortesmaa, Jarkko; Westerblad, Håkan; Edström, Lars; Tryggvason, Karl; Sanes, Joshua R.

doi:10.1038/88414

Cited by 174 publications

(242 citation statements)

References 36 publications

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“…Interestingly, studies using cultured hippocampal neurons showed that an extracellular domain of the AMPA receptor GluR2 subunit was important for induction of dendritic spines (Passafaro et al, 2003). In addition, analysis of mutant mice showed that the laminin ␣4 chain that can bind to presynaptic Ca 2ϩ channels was required for the apposition of active zones and junctional folds at the neuromuscular junction (Patton et al, 2001). Second, GluR␦2 may regulate the presynaptic active zone through the interaction between a postsynaptic GluR␦2-interacting molecule and an active zone component.…”

Section: Discussionmentioning

confidence: 99%

Control of Synaptic Connection by Glutamate Receptor δ2 in the Adult Cerebellum

Takeuchi

Miyazaki²,

Watanabe³

et al. 2005

J. Neurosci.

113

137

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Precise topological matching of presynaptic and postsynaptic specializations is essential for efficient synaptic transmission. Furthermore, synaptic connections are subjected to rearrangements throughout life. Here we examined the role of glutamate receptor (GluR) ␦2 in the adult brain by inducible and cerebellar Purkinje cell (PC)-specific gene targeting under the pure C57BL/6 genetic background. Concomitant with the decrease of postsynaptic GluR␦2 proteins, presynaptic active zones shrank progressively and postsynaptic density (PSD) expanded, resulting in mismatching between presynaptic and postsynaptic specializations at parallel fiber-PC synapses. Furthermore, GluR␦2 and PSD-93 proteins were concentrated at the contacted portion of mismatched synapses, whereas AMPA receptors were distributed in both the contacted and dissociated portions. When GluR␦2 proteins were diminished, PC spines lost their synaptic contacts. We thus identified postsynaptic GluR␦2 as a key regulator of the presynaptic active zone and PSD organization at parallel fiber-PC synapses in the adult brain.

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Section: Discussionmentioning

confidence: 99%

Control of Synaptic Connection by Glutamate Receptor δ2 in the Adult Cerebellum

Takeuchi

Miyazaki²,

Watanabe³

et al. 2005

J. Neurosci.

113

137

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“…[49][50] In vitro studies on several types of cells, including epithelial and endothelial cell lines, have established an important cell-adhesive role for laminin-10/11 20,51 and laminin-8. 21,22 We have previously shown that mouse multipotent hematopoietic FDCP-mix cells adhere to laminin-10/11, 35 suggesting that these laminins might also interact with hematopoietic progenitors.…”

Section: Discussionmentioning

confidence: 99%

Laminin isoform–specific promotion of adhesion and migration of human bone marrow progenitor cells

Kortesmaa

Tryggvason

et al. 2003

Blood

Self Cite

110

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Laminins are ␣␤␥ heterotrimeric extracellular proteins that regulate cellular functions by adhesion to integrin and nonintegrin receptors. Laminins containing ␣4 and ␣5 chains are expressed in bone marrow, but their interactions with hematopoietic progenitors are unknown. We studied human bone marrow cell adhesion to laminin-10/11 (␣5␤1␥1/␣5␤2␥1), laminin-8 (␣4␤1␥1), laminin-1 (␣1␤1␥1), and fibronectin. About 35% to 40% of CD34 ؉ and CD34 ؉ CD38 ؊ stem and progenitor cells adhered to laminin-10/11, and 45% to 50% adhered to fibronectin, whereas they adhered less to laminin-8 and laminin-1. Adhesion of CD34 ؉ CD38 ؊ cells to laminin-10/11 was maximal without integrin activation, whereas adhesion to other proteins was dependent on protein kinase C activation by 12-tetradecanoyl phorbol-13-acetate (TPA). Fluorescence-activated cell-sorting (FACS) analysis showed expression of integrin ␣6 chain on most CD34 ؉ and CD34 ؉ CD38 ؊ cells. Integrin ␣6 and ␤1 chains were involved in binding of both cell fractions to laminin-10/11 and laminin-8. Laminin-10/11 was highly adhesive to lineagecommitted myelomonocytic and erythroid progenitor cells and most lymphoid and myeloid cell lines studied, whereas laminin-8 was less adhesive. In functional assays, both laminin-8 and laminin-10/11 facilitated stromal-derived factor-1␣ (SDF-1␣)-stimulated transmigration of CD34 ؉ cells, by an integrin ␣6 receptor-mediated mechanism. In conclusion, we demonstrate laminin isoform-specific adhesive interactions with human bone marrow stem, progenitor, and more differentiated cells

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“…(Costell et al, 1999) Tenascin C Extracellular matrix Total NC cells fail to disperse laterally (Tucker, 2001) Laminin γ1 Extracellular matrix Total Death at E5.5, lack of basement membranes (Smyth et al, 1999) Laminin β2 Extracellular matrix Total Postnatal death between P15-30, neuromuscular junctions and glomerular defects (Noakes et al, 1995a;Noakes et al, 1995b;Patton et al, 1997) Laminin α2 Extracellular matrix Total Death by 5 weeks postnatal, severe muscular dystrophy and peripheral neurophathy (Miyagoe et al, 1997) Laminin α2 (dy/dy) Extracellular matrix Spontaneous Adult lethality, severe muscular dystrophy and peripheral nerve dysmyelination (Patton et al, 1999;Patton et al, 1997) Laminin α3 Extracellular matrix Total Death at P2-3, epithelial adhesion defect (Ryan et al, 1999) Laminin α4 Extracellular matrix Total Transient microvascular defect with hemorrhages and misalignment of neuromuscular junctions (Patton et al, 2001;Thyboll et al, 2002) Laminin α5 Extracellular matrix Total Death at E14-E17, with placental vessel, neural (Miner et al, 1998;Miner and Li, 2000) Protein Function Type Phenotype Reference tube, limb, and kidney defects Fibronectin Extracellular matrix Total Death before E14.5, shortened anterior-posterior axes, deformed neural tubes, and defects in mesodermally derived tissues. (George et al, 1993) Collagen XVIII Extracellular matrix Total Eye abnormalities modeling Knoblock syndrome (Fukai et al, 2002) Extracellular matrix Total Basement membrane defects (Utriainen et al, 2004) Collagen XV Extracellular matrix Total Skeletal myopathy and cardiovascular defects (Eklund et al, 2001) betaglycan Extracellular matrix Total Embryonic lethality of heart and liver defects (Stenvers et al, 2003) Connexin 43 Cell-cell adhesion In vitro studies of cells from knockout mice…”

Section: Note On Nomenclaturementioning

confidence: 99%

Cell biology of embryonic migration

Kurosaka¹,

Kashina²

2008

Birth Defects Research Pt C

117

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Cell migration is an evolutionarily conserved mechanism that underlies the development and functioning of uni-and multicellular organisms and takes place in normal and pathogenic processes, including various events of embryogenesis, wound healing, immune response, cancer metastases, and angiogenesis. Despite the differences in the cell types that take part in different migratory events, it is believed that all of these migrations occur by similar molecular mechanisms, whose major components have been functionally conserved in evolution and whose perturbation leads to severe developmental defects. These mechanisms involve intricate cytoskeleton-based molecular machines that can sense the environment, respond to signals, and modulate the entire cell behavior. A big question that has concerned the researchers for decades relates to the coordination of cell migration in situ and its relation to the intracellular aspects of the cell migratory mechanisms. Traditionally, this question has been addressed by researchers that considered the intra-and extracellular mechanisms driving migration in separate sets of studies. As more data accumulate researchers are now able to integrate all of the available information and consider the intracellular mechanisms of cell migration in the context of the developing organisms that contain additional levels of complexity provided by extracellular regulation. This review provides a broad summary of the existing and emerging data in the cell and developmental biology fields regarding cell migration during development.

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Properly formed but improperly localized synaptic specializations in the absence of laminin α4

Cited by 174 publications

References 36 publications

Control of Synaptic Connection by Glutamate Receptor δ2 in the Adult Cerebellum

Control of Synaptic Connection by Glutamate Receptor δ2 in the Adult Cerebellum

Laminin isoform–specific promotion of adhesion and migration of human bone marrow progenitor cells

Cell biology of embryonic migration

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