Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 myelin basic protein (MBP) gene produces two families of structurally related proteins from three different promoters-the golli products, generated from the most upstream promoter, and the MBPs, produced from the two downstream promoters. In this report we describe the expression of golli proteins within some of the earliest neuronal populations of the brain, including Cajal-Retzius cells and preplate neurons of the forebrain, representing a new marker for these cells. To identify elements responsible for neuronal expression of the golli products, we generated transgenic animals from constructs containing different portions of the upstream promoter. A construct containing 1.1 kb immediately upstream of the golli transcription start site targeted expression of beta-galactosidase to preplate neurons and a subset of Cajal-Retzius cells in transgenic mice-the first reported genetic element to target expression to these pioneer cortical populations. Although expression in Cajal-Retzius cells declined with embryonic development, preplate cells continued to express the transgene after arriving at their final destination in the subplate. Interestingly, expression persisted in subplate neurons found within a distinct layer between the white matter and cortical layer VI well into postnatal life. Birth dating studies with bromodeoxyuridine indicated that these neurons were born between E10.5 and E12.5. Thus, the transgene marked subplate neurons from their birth, providing a fate marker for these cells. This work suggests a role for the MBP gene in the early developing brain long before myelination and especially in the pioneer cortical neurons important in the formation of the cortical layers.
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PMID:Embryonic expression of the myelin basic protein gene: identification of a promoter region that targets transgene expression to pioneer neurons. 973 52

The plp gene encodes the proteolipid protein and its alternatively spliced product DM-20, major proteins of CNS myelin. In the mouse, plp/dm-20 transcripts are expressed beginning at embryonic day 9.5 (E9.5) by restricted foci of germinative neuroepithelial cells. To determine the identity of the neural precursors expressing plp/dm- 20, a zeomycin resistance gene fused to the lacZ reporter was expressed in transgenic mice under the control of the plp regulatory sequences. In the three different lines generated, the pattern of beta-galactosidase expression was similar and superimposable on the expression pattern of endogenous plp/dm-20. Both in vivo and in vitro, the transgene was expressed by O4(+) pre-oligodendrocytes, and later by RIP+ differentiated oligodendrocytes, but not by neuronal cells, astrocytes, or radial glial cells. After zeomycin selection, a dramatic enrichment in O4(+) pre-oligodendrocytes was observed in cultures derived from E12.5 transgenic embryos. This enrichment indicates the oligodendroglial specification of neural precursors that continuously express plp/dm-20. Early plp/dm-20-expressing precursors, however, appear to be a separate population from previously described PDGFRalpha oligodendrocyte precursors, as shown by the striking differences in their (1) patterns of distribution and (2) responsiveness to PDGF. These data suggest that oligodendrocytes have a plural origin and that early plp/dm-20 defines one of the neural lineages generating oligodendrocytes.
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PMID:Multiple restricted origin of oligodendrocytes. 976 77

The retinal pigment epithelium (RPE) is essential for eye development by interacting with the overlaying neuroepithelium. Regulatory sequences of the gene encoding for tyrosinase-related protein 1 (TRP-1), linked to the lacZ reporter gene, lead to strong and specific beta-galactosidase expression in the RPE. We asked how the oncogene ret would affect this epithelial cell type during mouse development. We used the TRP-1 promoter to express ret in the developing RPE, and obtained transgenic mouse lines, which showed mild to severe microphthalmia. During development, the RPE changed to a stratified epithelium with reduced or absent pigmentation from E10.5 onward. In addition, proliferation of RPE cells and tumor formation were observed from E12.5 onward. These early events prevent closure of choroid fissure and lead to microphthalmia and secondary malformations after birth. We conclude that ret transgene expression in the RPE prevents normal differentiation of this epithelial layer and induces proliferation and tumor formation. The appearance of the microphthalmic phenotype underlines the requirement of a normally developed RPE for eye development.
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PMID:Ectopic expression of RET results in microphthalmia and tumors in the retinal pigment epithelium. 993 63

The biological activity of mouse kappa opioid receptor (KOR) gene promoter was examined in transgenic mice using a beta-galactosidase (lacZ) reporter strategy for the first time. A lacZ cDNA was inserted at the 5th amino acid in the coding region of a mouse KOR genomic segment containing 3 kb of the 5' regulatory region, to generate a Kor-lacZ fusion gene which was then used to generate transgenic mice. The expression of transgene was demonstrated at the RNA level by reverse transcription-polymerase chain reaction (RT-PCR), and at the protein level by in situ lacZ enzyme assay. From studying three independent transgenic mouse lines that express this transgene, it is concluded that Kor-lacZ expression begins at embryonic day 9.5 (E9.5) and increases in several brain areas and neural tube as embryos develop. At E12.5 and E13.5, Kor-lacZ expression is found primarily in the mantle layer of midbrain, hindbrain and medulla oblongata, cranial ganglion and vagus nerve. At E15.5 and E17.5, the transgene is expressed in eye, ear, neopallial cortex, caudate putamen, lateral ventricle, thalamus, hypothalamus and pons. Therefore, the 3 kb 5' regulatory sequence of the mouse KOR gene is functional in transgenic animals and directs a specific expression pattern recapitulating that of the endogenous KOR gene expression during developmental stages. However, in adult animals, this transgene is only expressed in the brain, indicating that the regulatory information for peripheral expression in the adult is not encoded within this 3 kb upstream sequence.
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PMID:Promoter activity of mouse kappa opioid receptor gene in transgenic mouse. 1035 Jun 35

A mouse gene, designated prtb (proline codon-rich transcript, brain expressed) was identified and characterized from a gene trap embryonic stem cell line. It encodes a proline-rich protein of 168 amino acids that shares 99% amino acid sequence identity with its human homologue and is located on the distal region of mouse chromosome 15. To determine the expression pattern and function of prtb, mice that carry the prtb(gt) allele were generated. During embryogenesis,prtb gene expression as revealed by beta-galactosidase (beta-gal) marker gene activity was highly regulated. Between embryonic day (E) 11.5 and E12.5, beta-gal activity was restricted to the developing heart. From E13.5 on, expression in the heart was extinguished. However, very strong beta-gal activity could be detected in the brains of adult mice, suggesting a role for this gene in brain function. Mice homozygous for the mutation were viable, fertile, and did not display any obvious abnormalities. This could be due to functional redundancy as Northern blot hybridization analysis clearly demonstrated that prtb(gt) is likely to be a null allele.
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PMID:Expression and genetic analysis of prtb, a gene that encodes a highly conserved proline-rich protein expressed in the brain. 1037 15

Vessel formation in the lung has been described as occurring by two mechanisms: proximal, or branch, pulmonary arteries develop via angiogenesis; and distal, smaller vessels form by vasculogenesis. Connections between the proximal and distal vessels establish the final vascular network. The preponderance of vessel formation has been suspected to occur during the canalicular stage of lung development. To test these hypotheses, reporter gene expression under control of the regulatory domain of fetal liver kinase-1 (flk), an early endothelial cell-specific marker, was used to evaluate mouse lungs from embryonic day 10.5 (E10.5) through 2 wk postnatal age. Morphologic assessment was performed after histochemical staining, and quantification of vessel development by a chemiluminescent assay was compared with overall embryonic lung growth. LacZ expression under flk promoter control allowed: (1) early identification of differentiating endothelial cells of the branch pulmonary arteries; (2) visualization of distal vessels forming in the lung mesenchyme (primary capillary network) with subsequent remodeling; (3) recognition of early continuity between proximal and distal vessels, occurring by E10.5; and (4) assessment of developing pulmonary veins and venous confluence. Quantitative analysis revealed increased flk regulated beta-galactosidase (beta-gal) activity of 12 ng beta-gal/lung at E12.5 to 3,215 ng beta-gal/lung at 2 wk, which corresponded to overall lung growth during this period as shown by an increase in total protein content per lung from 35 microg at E12.5 to 6,456 microg at 2 wk after birth. We identified endothelial cell precursors of the developing pulmonary vasculature before vessel lumen formation. Continuity between the proximal pulmonary artery and vessels forming in the distal mesenchyme was present even at the earliest stage evaluated, suggesting endothelial cell differentiation at the site of vessel formation (i.e., vasculogenesis) as occurs with development of the aorta. Finally, we demonstrated that lung vessel development was not accentuated during the canalicular stage, but occurred at all stages and directly corresponded to overall lung growth.
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PMID:Qualitative and quantitative analysis of embryonic pulmonary vessel formation. 1065 36

There are three subtypes of alpha2 adrenoceptor, i.e., alpha2A, alpha2B, and alpha2C, mediating the specific effect of epinephrine and norepinephrine in various tissues by means of G protein-coupled signal transduction pathways. In an attempt to delineate the regulatory mechanism of the alpha2B receptor subtype (encoded by subtype gene Adra2b) expression in the central nervous system (CNS), we have established transgenic (Tg) mice lines in which the transgene (NN-lacZ) was composed of the promoter region of Adra2b (NcoI fragment, 4.7 kb immediately upstream from receptor coding region) and a reporter gene lacZ (encoding beta-galactosidase). The selective expression of alpha2B in brain as indexed by beta-galactosidase, under the direction of this promoter region, may be traced in situ by using X-gal staining. The expression pattern of Adra2b-NN-lacZ in CNS of Tg mice during development was examined. The temporal course of examination was from gestation day 9.5 (E9.5) to postnatal day 28 (P28). Significant X-gal staining was detected in the dorsal root ganglion and cranial nerves V and VII at E12.5. By E18.5, expression was noted in the cerebral cortex, anterior olfactory nucleus, hypothalamus, brainstem, and cerebellar Purkinje cells, among others, and persisted through postnatal development. Adra2b-NN-directed reporter expression was detected in the hippocampal dentate gyrus first at P4. The temporal course of expression up to P28 in this area is in accordance with the developmental profiles of granule neurons of dentate gyrus. From P7 on, transgene expression was detected in additional brain areas, including the septum and thalamus. The expression correlates well with the noradrenergic innervations as evidenced by colocalization by using tyrosine hydroxylase or dopamine-beta-hydroxylase immunocytochemistry.
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PMID:Regulated expression of alpha2B adrenoceptor during development. 1224 14

Mutations in the genes encoding endothelin receptor-B (Ednrb) and its ligand endothelin-3 (Edn3) affect the development of two neural crest-derived cell types, melanocytes and enteric neurons. EDNRB signaling is exclusively required between E10.5 and E12.5 during the migratory phase of melanoblast and enteric neuroblast development. To determine the fate of Ednrb-expressing cells during this critical period, we generated a strain of mice with the bacterial beta-galactosidase (lacZ) gene inserted downstream of the endogenous Ednrb promoter. The expression of the lacZ gene was detected in melanoblasts and precursors of the enteric neuron system (ENS), as well as other neural crest cells and nonneural crest-derived lineages. By comparing Ednrb(lacZ)/+ and Ednrb(lacZ)/Ednrb(lacZ) embryos, we determined that the Ednrb pathway is not required for the initial specification and dispersal of melanoblasts and ENS precursors from the neural crest progenitors. Rather, the EDNRB-mediated signaling is required for the terminal migration of melanoblasts and ENS precursors, and this pathway is not required for the survival of the migratory cells.
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PMID:The endothelin receptor-B is required for the migration of neural crest-derived melanocyte and enteric neuron precursors. 1281 96

There is increasing interest into the extent to which epithelial differentiation can be altered by mesenchymal influence, and the molecular basis for these changes. In this study, we investigated whether amnion epithelium could be transformed into skin and hair follicles by associating E12.5 to E14.5 mouse amnion from the ROSA 26 strain, with mouse embryonic hair-forming dermis from a wild-type strain. These associations were able to produce fully formed hair follicles with associated sebaceous glands, and skin epidermis. Using beta-galactosidase staining we were able to demonstrate that the follicular epithelium and skin epidermis, but not the associated dermal cells, originated from the amnion. As Noggin and Sonic hedgehog (Shh) were recently shown to be required for early chick ventral skin formation, and able to trigger skin and feather formation from chick amnion, we associated cells engineered to produce those two factors with mouse amnion. In a few cases, we obtained hair buds connected to a pluristratified epithelium; however, the transformation of the amnion was impeded by uncontrolled fibroblastic proliferation. In contrast to an earlier report, none of our control amnion specimens autonomously transformed into skin and hair follicles, indicating that specific influences are necessary to elicit follicle formation from the mouse amnion. The ability to turn amnion into skin and its appendages has practical potential for the tissue engineering of replacement skin, and related biotechnological approaches.
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PMID:Transformation of amnion epithelium into skin and hair follicles. 1561 66

Genetic disruption of Hoxa3 results in bilateral defects of the common carotid artery, which is derived from the third branchial arch artery. The tunica media of the great arteries derived from the arch arteries is formed by the ectomesenchymal neural crest cells. To examine the etiology of the regression of the third arch artery, we generated Hoxa3 homozygous null mutant embryos that expressed a lacZ marker transgene driven by a connexin43 (Cx43): promoter in the neural crest cells. The expression of beta-galactosidase in these mouse embryos was examined by both whole-mount X-gal staining and immunohistochemistry with the monoclonal beta-galactosidase antibody on sections. The migration of neural crest cells from the neural tube to the third branchial arch was not affected in the Hoxa3 homozygotes. The initial formation of the third arch artery was also not disturbed. The artery, however, regressed at embryonic day 11.5 (E11.5), when differentiation of the third pharyngeal arch began. The internal and external carotid arteries arose from the dorsal aorta in E12.5 null mutants, which showed an abnormal persistence of the ductus caroticus. The third pharyngeal arch of wild-type mice fuses with the fourth and second arches at E12.0. In the Hoxa3 null mutants, however, the fusion was delayed, and the hypoplastic third pharyngeal arch was still discerned at E12.5. Moreover, the number of proliferating cells in the third arch of the null mutants was small compared with that in the wild-type. Thus, Hoxa3 is required for the growth and differentiation of the third pharyngeal arch. The defective development of the third pharyngeal arch may induce the anomalies of the carotid artery system.
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PMID:Hoxa3 regulates the proliferation and differentiation of the third pharyngeal arch mesenchyme in mice. 1571 86


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