Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ontogeny and cellular specificity of expression of beta-galactosidase activity and olfactory marker protein (OMP) are compared in olfactory tissue of the H-OMP-lacZ-3 line of transgenic mice. In this line the expression of lacZ is driven by a 0.3 kb fragment of the rat OMP promoter. During fetal development, lacZ expression is detectable in olfactory receptor neurons (ORNs) shortly after the initial appearance of endogenous OMP. The beta-galactosidase marker was observed only in mature olfactory receptor neurons where it co-localized with endogenous OMP. It was absent from immature neurons that express the growth associated phosphoprotein B50/GAP43. Lesion of the peripheral olfactory pathway by intranasal irrigation with Triton X-100 eliminated expression of both OMP and lacZ in the olfactory neuroepithelium. Subsequent regeneration of the full complement of olfactory receptor neurons was associated with co-expression of both OMP and beta-galactosidase activity. Neither OMP nor beta-galactosidase activity was induced in any other cell type of the regenerating olfactory mucosa. Thus, as little as 0.3 kb of the OMP promoter has the ability to target lacZ expression to olfactory receptor neurons in a temporally and spatially defined manner. We discuss the potential utility of this transgenic line for future studies of the olfactory system.
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PMID:LacZ and OMP are co-expressed during ontogeny and regeneration in olfactory receptor neurons of OMP promoter-lacZ transgenic mice. 901 Jul 27

The vertebrate olfactory system receives and discriminates a great variety of odorants. Many lines of evidence suggest that individual olfactory neuron expresses a single type or limited types of the olfactory receptor genes. However, the mechanism of selection of a single gene in the olfactory receptor family remains unclear. In the present study, we utilized zebrafish to identify the promoter element of the olfactory receptor genes in their 5'-upstream regions. First, we isolated a number of zebrafish olfactory receptor genes. These olfactory receptor genes were specifically expressed in the olfactory tissue as visualized by whole mount in situ hybridization analysis. Time of onset of the expression of each receptor clone varied from 24 h to 48 h postfertilization. Then, we injected various constructs containing the 5'-upstream regions of the olfactory receptor genes connected to beta-galactosidase reporter gene into fertilized zebrafish embryos. Constructs from two independent olfactory receptor genes exerted beta-galactosidase (promoter) activity that is specifically upregulated in the olfactory tissue. Use of either longer or deleted constructs of these two genes diminished the promoter activity in the olfactory tissue. From these results we discuss the mechanism of the transcription of the olfactory receptor genes in the olfactory neurons.
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PMID:Analysis of promoter activity of 5'-upstream regions of zebrafish olfactory receptor genes. 1070 79

The olfactory epithelium (OE) is unusual in its ability to regenerate and reinnervate its target, the olfactory bulb (OB), after deafferentation. To address the question of whether olfactory receptor neuron (ORN) axons preserve their topographic organization when they reestablish synaptic contact with the OB, the authors examined the pattern of ORN axon reinnervation into the bulb of adult H-OMP-lacZ-6 transgenic mice during and after recovery from chemical deafferentation. In the H-OMP-lacZ-6 mouse strain, lacZ expression is limited to a subset of ORNs that are distributed bilaterally in the OE and project primarily to a few glomeruli in the ventromedial region of the OB. The OE was lesioned by intranasal irrigation with Triton X-100, and the distribution of 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside (X-gal)-stained cells was examined in the OE along with beta-galactosidase-immunoreactive (beta-gal-ir) axonal processes in the OB after short (1 week), intermediate (3 week), and long (6-7 weeks) recovery times. One week after the lesion, immunostaining for beta-gal and olfactory marker protein was virtually eliminated in the bulb. After 3 weeks of recovery, beta-gal-containing axons appeared to target many of the same locations innervated in bulbs of unlesioned mice. The region that received the highest density of axonal innervation in controls, however, contained only a few processes at that time. After 6-7 week recovery periods, the pattern of X-gal staining in the OE and beta-gal-ir axons in the OB closely resembled that of unlesioned mice. These results demonstrate that the topographic distribution of ORNs in the OE and the pattern of axon innervation in the OB can be reconstituted after chemical deafferentation.
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PMID:Pattern of olfactory bulb innervation returns after recovery from reversible peripheral deafferentation. 1081 92

In transgenic neurotrophin-3 lacZ-neo (NT-3(lacZneo)) mice, in which the coding region for NT-3 is replaced by Eschericia coli lacZ, the expression of beta-galactosidase faithfully mimics the expression of NT-3 (Vigers AJ, Baquet ZC, Jones KR [2000], J Comp Neurol 416:398-416). During embryonic and early postnatal development, beta-galactosidase is detected in the olfactory system, beginning at embryonic day 11.5 in the nasal epithelium and at embryonic day 16.5 in the olfactory bulb. Levels of beta-galactosidase rise with age, reaching a peak during the second postnatal week, when beta-galactosidase reactivity is visible in up to 50% of the glomeruli. As the animal matures, the beta-galactosidase levels decline, but staining remains present in axons and cell bodies of a specific subset of olfactory receptor neurons (ORNs) projecting to a limited subset of glomeruli. The heavily labeled ORNs do not follow the typical OR expression zones in the epithelium but appear similar to the "patch" expression pattern of mOR37 receptors. The most heavily reactive glomeruli exhibit a striking reproducible pattern in the ventral olfactory bulb (OB). Some glomeruli of the OB contain calcitonin gene-related peptide (CGRP)-immunoreactive fibers of the trigeminal nerve. However, double-label immunocytochemistry for CGRP and beta-galactosidase rendered no correlation between trigeminal innervation and the degree of innervation by NT-3-expressing ORNs. Thus, the timing and presence of beta-galactosidase in a subset of ORNs suggests that NT-3 plays a role in synaptogenesis and/or synapse function in a specific subset of ORNs within the olfactory bulb.
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PMID:Neurotrophin-3 is expressed in a discrete subset of olfactory receptor neurons in the mouse. 1281 59

Previously, we identified PHR1 as an abundantly expressed gene in photoreceptors and showed that it encodes four isoforms, each with N-terminal pleckstrin homology (PH) and C-terminal transmembrane domains. To better understand PHR1 function and expression, we made a Phr1 null mouse by inserting a beta-galactosidase/neor cassette into exon 3. In addition to photoreceptors, we found abundant expression of specific Phr1 splice forms in olfactory receptor neurons and vestibular and cochlear hair cells. We also found Phr1 expression in cells with a possible sensory function, including peripheral retinal ganglion cells, cochlear interdental cells, and neurons of the circumventricular organ. Despite this discrete expression in known and putative sensory neurons, mice lacking PHR1 do not have overt sensory deficits.
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PMID:PHR1, a PH domain-containing protein expressed in primary sensory neurons. 1545 85

Ciliary neurotrophic factor (CNTF) has been implicated in processes of neuroprotection, axonal regeneration and synaptogenesis in the lesioned CNS. In the olfactory system, which is characterized by particularly robust neuroplasticity throughout life, the concentration of CNTF is high even under physiological conditions. In the present study, the cellular localization of CNTF-immunoreactivity was studied in the rat and mouse olfactory epithelium. In both species, individual olfactory sensory neurons (ONs) displayed intense CNTF-immunoreactivity. The number of CNTF-ir ONs varied interindividually in rats and was lower in mice than in rats. In olfactory epithelia of mice expressing beta-galactosidase under control of the CNTF promoter, cells of the ON layer were immunoreactive for the reporter protein. CNTF-ir ONs were olfactory marker protein-positive and growth associated protein 43-negative. CNTF-ir ONs lacked apoptotic markers, and the number of specifically labeled ONs was apparently unchanged after light chemical lesioning of the epithelium, indicating that CNTF-immunoreactivity was not associated with ON death. Electron microscopy of CNTF-ir ON axons in innervated olfactory bulb glomeruli documented that they formed typical ON axonal synapses with target neurons. Three dimensional reconstructions of bulb pairs showed a striking similarity of the positions of glomeruli innervated by CNTF-ir ON axons in left and right bulbs of individual animals and interindividually. The number of innervated glomeruli differed interindividually in rats and was lower in mice than in rats. The results show that in rodents CNTF-immunoreactivity occurs in a subset of mature, functionally competent ONs. The localization of target glomeruli suggests that CNTF-immunoreactivity may be associated with the expression and/or activation of specific olfactory receptor proteins.
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PMID:Ciliary neurotrophic factor-immunoreactivity in olfactory sensory neurons. 1603 89

Trace amine-associated receptors (TAARs) are a class of G-protein-coupled receptors found in mammals. While TAAR1 is expressed in several brain regions, all the other TAARs have been described mainly in the olfactory epithelium and the glomerular layer of the olfactory bulb and are believed to serve as a new class of olfactory receptors sensing innate odors. However, there is evidence that TAAR5 could play a role also in the central nervous system. In this study, we characterized a mouse line lacking TAAR5 (TAAR5 knockout, TAAR5-KO) expressing beta-galactosidase mapping TAAR5 expression. We found that TAAR5 is expressed not only in the glomerular layer in the olfactory bulb but also in deeper layers projecting to the limbic brain olfactory circuitry with prominent expression in numerous limbic brain regions, such as the anterior olfactory nucleus, the olfactory tubercle, the orbitofrontal cortex (OFC), the amygdala, the hippocampus, the piriform cortex, the entorhinal cortex, the nucleus accumbens, and the thalamic and hypothalamic nuclei. TAAR5-KO mice did not show gross developmental abnormalities but demonstrated less anxiety- and depressive-like behavior in several behavioral tests. TAAR5-KO mice also showed significant decreases in the tissue levels of serotonin and its metabolite in several brain areas and were more sensitive to the hypothermic action of serotonin 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propilamino)tetralin (8-OH-DPAT). These observations indicate that TAAR5 is not just innate odor-sensing olfactory receptor but also serves to provide olfactory input into limbic brain areas to regulate emotional behaviors likely via modulation of the serotonin system. Thus, anxiolytic and/or antidepressant action of future TAAR5 antagonists could be predicted. In general, "olfactory" TAAR-mediated brain circuitry may represent a previously unappreciated neurotransmitter system involved in the transmission of innate odors into emotional behavioral responses.
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PMID:Trace Amine-Associated Receptor 5 Provides Olfactory Input Into Limbic Brain Areas and Modulates Emotional Behaviors and Serotonin Transmission. 3219 74