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Homozygous Lmx1a mutant mice (Dreher) are deaf with dysmorphic ears with an abnormal morphogenesis and fused and misshapen sensory organs; however, computed tomography performed on a hearing-impaired family member did not reveal any cochleovestibular malformations.
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Data show that sustained expression of Lmx1a and Lmx1b is required for the survival of adult midbrain dopaminergic neurons.
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Lmx1a and Lmx1b regulate Plxnc1 expression.Lmx1a is required for the topographical organization of dopaminergic innervation in the striatum.
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Lmx1a is expressed in enterochromaffin cells and functions downstream of Nkx2.2.
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This study showed that spontaneous Lmx1a mutations causing cerebellar pathology are impaired in motor functions during the neonatal period.
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The data of this study that Oc-1 interacts with Lmx1a to promote ventral midbrain neural stem cells differentiation into dopamine neuron through Wnt1-Lmx1a pathway.
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Lmx1a signaling in mouse embryonic stem cells contributes to a molecular cascade establishing neuronal specification.
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our data demonstrate that key midbrain dopamine regulators (Nurr1, Pitx3, and Lmx1a) play overlapping as well as distinct roles during neurogenesis and neurotransmitter phenotype determination of mDA neurons
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The data of this study suggested that aberrant anlage patterning and granule cell development lead to Purkinje cell ectopia, which ultimately causes abnormal cerebellar architecture in dreher.
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dopamine transporter is a direct target of Lmx1a and emphasizes a novel role of Lmx1a as one of regulators of mature midbrain dopaminergic neurotransmitter phenotypes
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Lmx1a mutant (dr/dr) embryos demonstrate a clear decrease in expression of the genes Grb10 and Rgs4.
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The characterization of two new Lmx1a alleles highlights the critical role of this gene in the development of the cochlea and vestibular system.
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Data conclude that Lmx1a is a useful marker for the extraction of progenitors of GABAergic or dopaminergic neurons.
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The Lmx1a can induce desired neuronal lineages from most expressing neural progenitor cells by a mechanism resembling developmental binary cell-fate switching.
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This study demonstrated that Lmx1a and Lmx1b function cooperatively to regulate proliferation, specification, and differentiation of mDA progenitors, including their floor plate-like properties.
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data establish that Lmx1b influences the differentiation of multiple neuronal subtypes in the ventral midbrain, whereas Lmx1a appears to be exclusively devoted to the differentiation of the dopamine neuron lineage
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Generation of knockout mice expressing a GFP-reporter under the control of the Lmx1a locus.
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In the developing cerebellum, Lmx1a is expressed in the roof plate, where it is required to segregate the roof plate lineage from neuronal rhombic lip derivatives.
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obtained evidence that Lmx1a and Lmx1b cooperate with Foxa2 to specify mesDA neuron identity by gain-of-function approaches using transgenic mice
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Lmx1a/Lmx1b null mutant mice fail to generate a hindbrain roof plate. Both genes act in concert to direct normal hindbrain formation.
