RanBP9 Plays a Critical Role in Neonatal Brain Development in Mice

RanBP9 is known to act as a scaffolding protein bringing together a variety of cell surface receptors and intracellular targets thereby regulating functions as diverse as neurite and axonal outgrowth, cell morphology, cell proliferation, myelination, gonad development, myofibrillogenesis and migrati...

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Veröffentlicht in:PloS one 2013-06, Vol.8 (6), p.e66908-e66908
Hauptverfasser: Palavicini, Juan Pablo, Lloyd, Brandon Noel, Hayes, Crystal D, Bianchi, Elisabetta, Kang, David E, Dawson-Scully, Ken, Lakshmana, Madepalli K
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container_issue 6
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container_title PloS one
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creator Palavicini, Juan Pablo
Lloyd, Brandon Noel
Hayes, Crystal D
Bianchi, Elisabetta
Kang, David E
Dawson-Scully, Ken
Lakshmana, Madepalli K
description RanBP9 is known to act as a scaffolding protein bringing together a variety of cell surface receptors and intracellular targets thereby regulating functions as diverse as neurite and axonal outgrowth, cell morphology, cell proliferation, myelination, gonad development, myofibrillogenesis and migration of neuronal precursors. Though RanBP9 is ubiquitously expressed in all tissues, brain is one of the organs with the highest expression levels of RanBP9. In the neurons, RanBP9 is localized mostly in the cytoplasm but also in the neurites and dendritic processes. We recently demonstrated that RanBP9 plays pathogenic role in Alzheimer's disease. To understand the role of RanBP9 in the brain, here we generated RanBP9 null mice by gene-trap based strategy. Most of Ran-/- mice die neonatally due to defects in the brain growth and development. The major defects include smaller cortical plate (CP), robustly enlarged lateral ventricles (LV) and reduced volume of hippocampus (HI). The lethal phenotype is due to a suckling defect as evidenced by lack of milk in the stomachs even several hours after parturition. The complex somatosensory system which is required for a behavior such as suckling appears to be compromised in Ran-/- mice due to under developed CP. Most importantly, RanBP9 phenotype is similar to ERK1/2 double knockout and the neural cell adhesion receptor, L1CAM knockout mice. Both ERK1 and L1CAM interact with RanBP9. Thus, RanBP9 appears to control brain growth and development through signaling mechanisms involving ERK1 and L1CAM receptor.
doi_str_mv 10.1371/journal.pone.0066908
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Though RanBP9 is ubiquitously expressed in all tissues, brain is one of the organs with the highest expression levels of RanBP9. In the neurons, RanBP9 is localized mostly in the cytoplasm but also in the neurites and dendritic processes. We recently demonstrated that RanBP9 plays pathogenic role in Alzheimer's disease. To understand the role of RanBP9 in the brain, here we generated RanBP9 null mice by gene-trap based strategy. Most of Ran-/- mice die neonatally due to defects in the brain growth and development. The major defects include smaller cortical plate (CP), robustly enlarged lateral ventricles (LV) and reduced volume of hippocampus (HI). The lethal phenotype is due to a suckling defect as evidenced by lack of milk in the stomachs even several hours after parturition. The complex somatosensory system which is required for a behavior such as suckling appears to be compromised in Ran-/- mice due to under developed CP. 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Though RanBP9 is ubiquitously expressed in all tissues, brain is one of the organs with the highest expression levels of RanBP9. In the neurons, RanBP9 is localized mostly in the cytoplasm but also in the neurites and dendritic processes. We recently demonstrated that RanBP9 plays pathogenic role in Alzheimer's disease. To understand the role of RanBP9 in the brain, here we generated RanBP9 null mice by gene-trap based strategy. Most of Ran-/- mice die neonatally due to defects in the brain growth and development. The major defects include smaller cortical plate (CP), robustly enlarged lateral ventricles (LV) and reduced volume of hippocampus (HI). The lethal phenotype is due to a suckling defect as evidenced by lack of milk in the stomachs even several hours after parturition. The complex somatosensory system which is required for a behavior such as suckling appears to be compromised in Ran-/- mice due to under developed CP. 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subjects Adaptor Proteins, Signal Transducing - deficiency
Adaptor Proteins, Signal Transducing - genetics
Adaptor Proteins, Signal Transducing - metabolism
Animal tissues
Animals
Animals, Newborn
Axon guidance
Axons
Biology
Body Weight
Brain
Brain - cytology
Brain - growth & development
Brain - metabolism
Brain-derived neurotrophic factor
Cell adhesion
Cell adhesion & migration
Cell Count
Cell cycle
Cell morphology
Cell proliferation
Cell surface
Cerebral Cortex - cytology
Cerebral Cortex - growth & development
Cortex
Cytology
Cytoplasm
Cytoskeletal Proteins - deficiency
Cytoskeletal Proteins - genetics
Cytoskeletal Proteins - metabolism
Defects
Dentate Gyrus - cytology
Dentate Gyrus - growth & development
Gene Knockout Techniques
Kinases
Localization
Mice
Milk
Mitogen-Activated Protein Kinase 3 - metabolism
Myelination
Neonates
Neural stem cells
Neurobiology
Neurosciences
Newborn babies
Nuclear Proteins - deficiency
Nuclear Proteins - genetics
Nuclear Proteins - metabolism
Organ Size
Organs
Parturition
Proliferating Cell Nuclear Antigen - metabolism
Proteins
Receptors
Rodents
Scaffolding
Signal Transduction
Signaling
Somatosensory system
Studies
Suckling behavior
Ventricle (lateral)
title RanBP9 Plays a Critical Role in Neonatal Brain Development in Mice
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