ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Concurrent Lpin1 and Nrcam mouse mutations result in severe peripheral neuropathy with transitory hindlimb paralysis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 24 citations in OpenAlex.
- Lipin phosphatidic acid phosphatases: Structure, function, regulation, and disease association.Advances in biological regulation · 2025Review
- Bi-allelic loss of function variant in the NRCAM gene is associated with motor-predominant axonal polyneuropathy; the second report.Molecular genetics & genomic medicine · 2023Article
- Bi-allelic variants in neuronal cell adhesion molecule cause a neurodevelopmental disorder characterized by developmental delay, hypotonia, neuropathy/spasticity.American journal of human genetics · 2022Article
- Whole-exome sequencing reveals common and rare variants in immunologic and neurological genes implicated in achalasia.American journal of human genetics · 2021Article
- Wrestling and Wrapping: A Perspective on SUMO Proteins in Schwann Cells.Biomolecules · 2021Review
- Crystal structure of a lipin/Pah phosphatidic acid phosphatase.Nature communications · 2020Article
- DDHD1, but Not DDHD2, Suppresses Neurite Outgrowth in SH-SY5Y and PC12 Cells by Regulating Protein Transport From Recycling Endosomes.Frontiers in cell and developmental biology · 2020Article
- Peripheral Neuropathy and Hindlimb Paralysis in a Mouse Model of Adipocyte-Specific Knockout of Lkb1.EBioMedicine · 2017Article
- Severity of Demyelinating and Axonal Neuropathy Mouse Models Is Modified by Genes Affecting Structure and Function of Peripheral Nodes.Cell reports · 2017Article
- Lipin1 Regulates Skeletal Muscle Differentiation through Extracellular Signal-regulated Kinase (ERK) Activation and Cyclin D Complex-regulated Cell Cycle Withdrawal.The Journal of biological chemistry · 2015Article
- A novel nondevelopmental role of the sax-7/L1CAM cell adhesion molecule in synaptic regulation in Caenorhabditis elegans.Genetics · 2015Article
- Gene structure and spatio-temporal expression of chicken LPIN2.Molecular biology reports · 2014Article
- Phosphatidic acid (PA)-preferring phospholipase A1 regulates mitochondrial dynamics.The Journal of biological chemistry · 2014Article
- Novel mouse model for Gardner syndrome generated by a large-scale N-ethyl-N-nitrosourea mutagenesis program.Cancer science · 2013Article
- A hypomorphic mutation in Lpin1 induces progressively improving neuropathy and lipodystrophy in the rat.The Journal of biological chemistry · 2011Article
- Lipins: multifunctional lipid metabolism proteins.Annual review of nutrition · 2010Review
- "CRASH"ing with the worm: insights into L1CAM functions and mechanisms.Developmental dynamics : an official publication of the American Association of Anatomists · 2010Review
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8 authors at 7 institutions in 3 countries.
Funding
Abstract
Peripheral neuropathy is a broad category of disorders with a diverse etiology, grouped together by their common pathogenic effect on the peripheral nervous system (PNS). Because of the heterogeneity observed to be responsible for these disorders, a forward genetics method of gene discovery was used to identify additional affected pathways. In this report, we describe the mutant mouse line 20884, generated by N-ethyl-N-nitrosourea mutagenesis, which is characterized by adult-onset transitory hindlimb paralysis. Linkage mapping revealed that two point mutations are responsible for the phenotype: a partial loss-of-function mutation in the gene for phosphatidate phosphatase Lpin1 and a truncation mutation in the gene that encodes the neuronal cell adhesion molecule NrCAM. To investigate how the 20884 Lpin1 and Nrcam mutations interact to produce the paralysis phenotype, the double mutant and both single mutants were analyzed by quantitative behavioral, histological, and electrophysiological means. The Lpin1(20884) mutant and the double mutant are characterized by similar levels of demyelination and aberrant myelin structures. Nevertheless, the double mutant exhibits more severe electrophysiological abnormalities than the Lpin1(20884) mutant. The Nrcam(20884) mutant is characterized by normal sciatic nerve morphology and a mild electrophysiological defect. Comparison of the double mutant phenotype with the two single mutants does not point to an additive relationship between the two defects; rather, the Lpin1(20884) and Nrcam(20884) defects appear to act synergistically to produce the 20884 phenotype. It is proposed that the absence of NrCAM in a demyelinating environment has a deleterious effect, possibly by impairing the process of remyelination.
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