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Journal articles on the topic 'LacZ'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

Kroupskaya, I. V., and E. B. Paton. "Influence of rare codons in the 5'-terminal regions on the expression of genes rplJ'-lacZ and rplL'-lacZ." Biopolymers and Cell 6, no. 4 (July 20, 1990): 102–5. http://dx.doi.org/10.7124/bc.000286.

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2

Itoh, S., M. Miura, and H. Shimada. "Lack of mutagenicity of levofloxacin in lacZ transgenic mice." Mutagenesis 13, no. 1 (January 1, 1998): 51–55. http://dx.doi.org/10.1093/mutage/13.1.51.

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3

EBARA, Fumio, and Noboru FUJIHARA. "Successful Transfer of Exogenously Introduced Gene (lacZ/MiwZ and lacZ&GFP/pkkv4-lacZ) for Generations in Chicken." Journal of Reproduction and Development 46, no. 3 (2000): 177–82. http://dx.doi.org/10.1262/jrd.46.177.

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4

Zhang, Guo-Jun, Tsing-Bau Chen, Brett Connolly, Shu-An Lin, Richard Hargreaves, Amy Vanko, Bohumil Bednar, Douglas J. MacNeil, Cyrille Sur, and David L. Williams. "In Vivo Optical Imaging of LacZ Expression Using lacZ Transgenic Mice." ASSAY and Drug Development Technologies 7, no. 4 (August 2009): 391–99. http://dx.doi.org/10.1089/adt.2009.0195.

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5

Sanzgiri, Vibhav R., Suhas H. Mangoli, Jyoti Ramchandani, and Suresh K. Mahajan. "A simple method for studying lacZ fusions in lacZ+ Escherichia coli hosts." Technical Tips Online 2, no. 1 (January 1997): 67–69. http://dx.doi.org/10.1016/s1366-2120(08)70037-0.

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6

Subbarao, M. N., and D. Kennell. "Evidence for endonucleolytic cleavages in decay of lacZ and lacI mRNAs." Journal of Bacteriology 170, no. 6 (1988): 2860–65. http://dx.doi.org/10.1128/jb.170.6.2860-2865.1988.

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7

Mathis, L., C. Bonnerot, L. Puelles, and J. F. Nicolas. "Retrospective clonal analysis of the cerebellum using genetic laacZ/lacZ mouse mosaics." Development 124, no. 20 (October 15, 1997): 4089–104. http://dx.doi.org/10.1242/dev.124.20.4089.

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Analysis of lacZ neuronal clones in the mouse cerebellum demonstrates genealogical independence of the primary and secondary germinal epithelia (PGE and SGE) from early development. PGE precursors and their neuronal descendants are organised into two polyclonal groups of similar sizes that exhibit parasagittal patterning and generally respect the midline. The relationship between these two groups cannot be traced back in time to less than 80 independent cells, which were probably recruited following a period of non-coherent growth that distributes unrelated cells into distinct territories of the neural tube. A lateromedial clonal organisation is observed in the mature cerebellum, suggesting the existence of many small parasagittal domains of clonal restriction and/or of cell dispersion in the rostrocaudal but not in the mediolateral dimension. The organisation is orthogonal with respect to the cellular organisation in the neural tube as is the genetic organisation. Cellular and genetic patterning of the cerebellum therefore share similarities. A possible hypothesis is that distinct cell behaviours create the different clonal domains observed in this study and that the cellular and genetic organisation of the cerebellum are coordinated.

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8

Gaunt, Stephen J., Deborah Drage, and Richard C. Trubshaw. "cdx4/lacZ and cdx2/lacZ protein gradients formed by decay during gastrulation in the mouse." International Journal of Developmental Biology 49, no. 8 (2005): 901–8. http://dx.doi.org/10.1387/ijdb.052021sg.

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9

Marsh, Jon. "Kinetic determination of cellular LacZ expression." Genetic Analysis: Biomolecular Engineering 11, no. 1 (January 1994): 20–23. http://dx.doi.org/10.1016/1050-3862(94)90005-1.

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10

Jain, Chaitanya. "New improved lacZ gene fusion vectors." Gene 133, no. 1 (October 1993): 99–102. http://dx.doi.org/10.1016/0378-1119(93)90231-q.

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11

Tinwell, H., U. Liegibel, O. Krebs, P. Schmezer, J. Favor, and J. Ashby. "Comparison of lacI and lacZ transgenic mouse mutation assays: an EU-sponsored interlaboratory study." Mutation Research/Environmental Mutagenesis and Related Subjects 335, no. 2 (October 1995): 185–90. http://dx.doi.org/10.1016/0165-1161(95)90054-3.

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12

Hayes, Beth M., Mollie W. Jewett, and Patricia A. Rosa. "lacZ Reporter System for Use in Borrelia burgdorferi." Applied and Environmental Microbiology 76, no. 22 (September 17, 2010): 7407–12. http://dx.doi.org/10.1128/aem.01389-10.

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ABSTRACT Regulation of gene expression is critical for the ability of Borrelia burgdorferi to adapt to different environments during its natural infectious cycle. Reporter genes have been used successfully to study gene regulation in multiple organisms. We have introduced a lacZ gene into B. burgdorferi, and we show that B. burgdorferi produces a protein with detectable β-galactosidase activity in both liquid and solid media when lacZ is expressed from a constitutive promoter. Furthermore, when lacZ is expressed from the ospC promoter, β-galactosidase activity is detected only in B. burgdorferi clones that express ospC, and it accurately monitors endogenous gene expression. The addition of lacZ to the repertoire of genetic tools available for use in B. burgdorferi should contribute to a better understanding of how B. burgdorferi gene expression is regulated during the infectious cycle.

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13

Bharatan, Shanti M., Manjula Reddy, and J. Gowrishankar. "Distinct Signatures for Mutator Sensitivity of lacZ Reversions and for the Spectrum of lacI/lacO Forward Mutations on the Chromosome of Nondividing Escherichia coli." Genetics 166, no. 2 (February 1, 2004): 681–92. http://dx.doi.org/10.1093/genetics/166.2.681.

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Abstract A conditional lethal galE(Ts)-based strategy was employed in Escherichia coli, first to eliminate all growth-associated chromosomal reversions in lacZ or forward mutations in lacI/lacO by incubation at the restrictive temperature and subsequently to recover (as papillae) spontaneous mutations that had arisen in the population of nondividing cells after shift to the permissive temperature. Data from lacZ reversion studies in mutator strains indicated that the products of all genes for mismatch repair (mutHLS, dam, uvrD), of some for oxidative damage repair (mutMT), and of that for polymerase proofreading (dnaQ) are required in dividing cells; some others for oxidative damage repair (mutY, nth nei) are required in both dividing and nondividing cells; and those for alkylation damage repair (ada ogt) are required in nondividing cells. The spectrum of lacI/lacO mutations in nondividing cells was distinguished both by lower frequencies of deletions and IS1 insertions and by the unique occurrence of GC-to-AT transitions at lacO +5. In the second approach to study mutations that had occurred in nondividing cells, lacI/lacO mutants were selected as late-arising papillae from the lawn of a galE+ strain; once again, transitions at lacO +5 were detected among the mutants that had been obtained from populations initially grown on poor carbon sources such as acetate, palmitate, or succinate. Our results indicate that the lacO +5 site is mutable only in nondividing cells, one possible mechanism for which might be that random endogenous alkylation (or oxidative) damage to DNA in these cells is efficiently corrected by the Ada Ogt (or Nth Nei) repair enzymes at most sites but not at lacO +5. Furthermore, the late-arising papillae from the second approach were composed almost exclusively of dominant lacI/lacO mutants. This finding lends support to “instantaneous gratification” models in which a spontaneous lesion, occurring at a random site in DNA of a nondividing cell, is most likely to be fixed as a mutation if it allows the cell to immediately exit the nondividing state.

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14

Hendrikx, P. J., J. Vermeulen, A. Hagenbeek, M. Vermey, and A. C. Martens. "LacZ staining in paraffin-embedded tissue sections." Journal of Histochemistry & Cytochemistry 44, no. 11 (November 1996): 1323–29. http://dx.doi.org/10.1177/44.11.8918907.

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Femora and tibiae of rats carrying leukemia from a LacZ-marked acute promyelocytic leukemia-derived leukemic cell line (LT12NL15) were decalcified using EDTA and routinely embedded in paraffin. Sections were used to develop for the first time an immunostaining method for LacZ, employing catalyzed reporter deposition (CARD) based on the deposition of biotinylated tyramine. This method was used to study homing and adhesion of leukemic cells.

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15

Josephy, P. David. "The Escherichia coli lacZ reversion mutagenicity assay." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 455, no. 1-2 (November 2000): 71–80. http://dx.doi.org/10.1016/s0027-5107(00)00063-4.

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16

Moosmann, P. "Alpha complementation of LacZ in mammalian cells." Nucleic Acids Research 24, no. 6 (March 15, 1996): 1171–72. http://dx.doi.org/10.1093/nar/24.6.1171.

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17

Pessi, Gabriella, Caroline Blumer, and Dieter Haas. "lacZ fusions report gene expression, don't they?" Microbiology 147, no. 8 (August 1, 2001): 1993–95. http://dx.doi.org/10.1099/00221287-147-8-1993.

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18

Warner, Jessica B., and Juke S. Lolkema. "LacZ-promoter fusions: the effect of growth." Microbiology 148, no. 5 (May 1, 2002): 1241–43. http://dx.doi.org/10.1099/00221287-148-5-1241.

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19

Tomich, C.-S. C., P. S. Kaytes, M. K. Olsen, and H. Patel. "Use of lacZ expression to monitor transcription." Plasmid 20, no. 2 (September 1988): 167–70. http://dx.doi.org/10.1016/0147-619x(88)90022-4.

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20

Lassak, Jürgen, Luitpold Fried, and Kirsten Jung. "Angestaubt, aber nicht eingerostet — der Bioreporter LacZ." BIOspektrum 20, no. 5 (September 2014): 510–13. http://dx.doi.org/10.1007/s12268-014-0473-7.

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21

Foster, Patricia L., and John Cairns. "Adaptive Mutation of a lacZ Amber Allele." Genetics 150, no. 3 (November 1, 1998): 1329–30. http://dx.doi.org/10.1093/genetics/150.3.1329.

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22

MATSUTANI, SACHIKO. "THE INTERNAL SEQUENCE OF IS1STIMULATES RNA SYNTHESIS FROM THE IS1OWN AND EXOGENOUS PROMOTERS." Journal of Biological Systems 13, no. 03 (September 2005): 313–29. http://dx.doi.org/10.1142/s0218339005001513.

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The bacterial IS1 contains the genes insA and B′-insB encoding transposition related-proteins. The expression of these genes is driven by a promoter within the left end of IS1. Using IS1-lacZ constructs in which lacZs were fused in-frame at various sites of IS1 genes, it was found that the presence of the internal region of insA results in about a 100-fold increase in lacZ expression. The lacZ expression of the fusion constructs in which the IS1 own promoter was displaced by an exogenous promoter, was also stimulated by the presence of the IS1 internal region. Similarly, when lacZ was transcriptionally fused to the internal region of IS1, the lacZ expression from an exogenous promoter was stimulated. This result shows that the IS1 internal region acts as a cis-element to stimulate RNA synthesis from the upstream promoter. This was confirmed by Northern blot analyses. Furthermore, the gene which encodes the factor working with the IS1 internal sequence to stimulate transcription, was cloned. The gene was artA in the transfer region of the Escherichia coli F factor. Interestingly, the cis-element for transcription stimulation is found downstream, whereas many such elements are located upstream, of the promoter.

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23

Yu, C. C., L. C. Tsui, and M. L. Breitman. "Homologous and heterologous enhancers modulate spatial expression but not cell-type specificity of the murine gamma F-crystallin promoter." Development 110, no. 1 (September 1, 1990): 131–39. http://dx.doi.org/10.1242/dev.110.1.131.

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Previous studies have shown that mouse gamma F-crystallin sequences −759 to +45, which include the core promoter and two upstream enhancer elements, contain sufficient information for directing gene expression to terminally differentiated fiber cells of the ocular lens. To investigate the role that proximal sequences of the mouse gamma F-crystallin promoter play in the developmental regulation of gene expression, we generated transgenic mice containing the lacZ gene driven by either mouse gamma F-crystallin sequences −171 to +45, which lack functional enhancers, or a hybrid hamster alpha A-/mouse gamma F-crystallin promoter, which contains the hamster alpha A-crystallin enhancer instead of operational gamma F-crystallin enhancers. In situ analysis of lacZ expression in these mice revealed that the mouse gamma F-crystallin promoter segment −171 to +45, which shows low activity in vitro, is able to direct gene expression to the fiber cells in the nucleus of the lens. However, animals expressing gamma 171-lacZ show both a lower level of expression of the lacZ gene and a narrower pattern of staining in the lens nucleus than mice expressing gamma 759-lacZ, which contains the two enhancer elements located between −392 and −278 and −226 to −123.(ABSTRACT TRUNCATED AT 250 WORDS)

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24

Jung, Hyo Sun, and Dong Soo Kim. "Availability of the lacZ gene as a Reporter Gene for Production of Transgenic Artemia franciscana." Korean Journal of Fisheries and Aquatic Sciences 46, no. 6 (December 31, 2013): 901–6. http://dx.doi.org/10.5657/kfas.2013.0901.

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25

Fernandez, Nielsen Q., Jörg Grosshans, Jason S. Goltz, and David Stein. "Separable and redundant regulatory determinants in Cactus mediate its dorsal group dependent degradation." Development 128, no. 15 (August 1, 2001): 2963–74. http://dx.doi.org/10.1242/dev.128.15.2963.

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Dorsal-ventral polarity within the Drosophila syncytial blastoderm embryo is determined by the maternally encoded dorsal group signal transduction pathway that regulates nuclear localization of the transcription factor Dorsal. Nuclear uptake of Dorsal, a Rel/NFκB homolog, is controlled by the interaction with its cognate IκB inhibitor protein Cactus, which is degraded on the ventral side of the embryo in response to dorsal group signaling. Previous studies have suggested that an N-terminally located kinase target motif similar to that found in IκB proteins is involved in the spatially controlled degradation of Cactus. We report studies of the in vivo function and distribution of fusion proteins comprising segments of Cactus attached to Escherichia coli β-galactosidase (lacZ). Full-length Cactus-lacZ expressed in vivo normalizes the ventralized phenotype of embryos that lack Cactus and faithfully reconstitutes dorsal group-regulated degradation, while fusion protein constructs that lack the first 125 amino acids of Cactus escape dorsal group-dependent degradation. Furthermore, Cactus-lacZ constructs that lack only the putative IκB-dependent kinase target-like motif can nevertheless undergo spatially regulated dorsal group-dependent degradation and we have identified the regulatory determinant responsible for dorsal group-dependent degradation of Cactus in the absence of this motif. Taken together, our studies indicate the presence of two distinct redundantly acting determinants in the N terminus of Cactus that direct dorsal group-dependent degradation. Strikingly, the regulatory domain of human IκBα can also direct polarized degradation of Cactus-lacZ fusion protein.

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26

Walters, Eric, Mary Grillo, A. Beate Oestreicher, and Frank L. Margolis. "LacZ andOMP are co-expressed during ontogeny and regeneration in olfactory receptor neurons of omp promoter-lacZ transgenic mice." International Journal of Developmental Neuroscience 14, no. 7-8 (November 1996): 813–22. http://dx.doi.org/10.1016/s0736-5748(96)00063-9.

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27

Soares, Holly D., Shu-Cheng Chen, and James I. Morgan. "Differential and Prolonged Expression of Fos–lacZ and Jun–lacZ in Neurons, Glia, and Muscle Following Sciatic Nerve Damage." Experimental Neurology 167, no. 1 (January 2001): 1–14. http://dx.doi.org/10.1006/exnr.2000.7558.

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28

Tan, Seong-Seng. "Liver-specific and position-effect expression of a retinol-binding protein-lacZ fusion gene (RBP-lacZ) in transgenic mice." Developmental Biology 146, no. 1 (July 1991): 24–37. http://dx.doi.org/10.1016/0012-1606(91)90443-7.

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29

Wilkie, Alison L., Siobhán A. Jordan, and Ian J. Jackson. "Neural crest progenitors of the melanocyte lineage: coat colour patterns revisited." Development 129, no. 14 (July 15, 2002): 3349–57. http://dx.doi.org/10.1242/dev.129.14.3349.

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Neural crest-derived melanoblasts are the progenitors of melanocytes, the pigment cells of the skin, hair and choroid. Previous studies of adult chimaeric mice carrying different coat colour markers have suggested that the total melanocyte population is derived from a small number of melanoblast progenitors, each of which generates a discrete unilateral transverse band of colour. This work also suggested minimal mixing of cells between clones. We have used two complementary approaches to assess the behaviour of migrating clones of melanoblasts directly in the developing embryo. First, we made aggregation chimaeras between transgenic Dct-lacZ and non-transgenic embryos, in which lacZ is a marker for melanoblasts. Second, we generated transgenic mice carrying a modified lacZ reporter construct containing a 289 base pair duplication (laacZ) under the control of the Dct promoter. The laacZ transgene is normally inactive, but reverts to wild-type lacZ at low frequency, labelling a cell and all of its progeny at random. Mosaic embryos containing labelled melanoblast clones were generated. In contrast to previous data, chimaeric and mosaic embryonic melanoblast patterns suggest that: (1) there is a large number of melanoblast progenitors; (2) there is a pool of melanoblasts in the cervical region; (3) different cell dispersion mechanisms may operate in the head and trunk regions; and (4) there is extensive axial mixing between clones.

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30

SLOWINSKI, Torsten, Norma SCHULZ, Frank T. RUSCHITZKA, Thomas QUASCHNING, Christian BAUER, Franz THEURING, Hans-H. NEUMAYER, Max GASSMANN, and Berthold HOCHER. "Pattern of prepro-endothelin-1 expression revealed by reporter-gene activity in kidneys of erythropoietin-overexpressing mice." Clinical Science 103, s2002 (September 1, 2002): 44S—47S. http://dx.doi.org/10.1042/cs103s044s.

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Transgenic overexpression of erythropoietin (Epo) in mice increases haematocrit to a mean of 80% in adult mice, leading to an increase in blood viscosity and volume. As a consequence, renal tissue endothelin-1 (ET-1) concentrations are significantly elevated in erythropoietin-overexpressing (Epo+) mice (mean±S.E.M; Epo+, 798±71; Epo-, 400±25pg/g tissue; P<0.01). To investigate the pattern of expression of the primary translation product of the ET-1 gene, prepro-ET-1, in kidneys of (Epo+) mice, we generated crossbred mice overexpressing the human EPO gene with mice carrying a reporter gene construct expressing the LacZ gene under the control of the human prepro-ET-1 promotor sequence (LacZ+/Epo+). For comparison, we generated (LacZ+/Epo-) mice from the same strains. After Bluo-Gal staining of frozen kidney sections (n = 10 in each group), intracellular blue precipitates as indicators of prepro-ET-1 promotor activity were detectable in tubular and vascular endothelium and glomerular cells in (LacZ+/Epo-) as well as (LacZ+/Epo+) mice. Comparison of the amount of blue precipitates by semiquantitative scoring showed a significant increase in reporter gene activity in tubular epithelium of (LacZ+/Epo+) mice (mean±S.E.M.; LacZ+/Epo+, 1.64±0.18; LacZ+/Epo-, 1.00±0.19; P<0.05). Reporter gene activity was not significantly elevated in epithelium of small intrarenal arteries of (LacZ+/Epo+) mice (mean±S.E.M.; LacZ+/Epo+, 0.86±0.14; LacZ+/Epo-, 0.38±0.21; P = 0.08) and was similar in glomerular cells (mean±S.E.M.; LacZ+/Epo+, 1.28±0.16; LacZ+/Epo-, 1.14±0.21; P = 0.6). The main source of elevated ET-1 tissue concentration in kidneys of (Epo+) mice therefore seems more likely to be tubular than vascular endothelium or glomerular cells.

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31

Bollag, W. B., Y. Xiong, J. Ducote, and C. S. Harmon. "Regulation of fos-lacZ fusion gene expression in primary mouse epidermal keratinocytes isolated from transgenic mice." Biochemical Journal 300, no. 1 (May 15, 1994): 263–70. http://dx.doi.org/10.1042/bj3000263.

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The expression of a fos-lacZ fusion gene was studied in primary mouse epidermal keratinocytes obtained from transgenic mice. This gene construct contains the entire upstream regulatory sequence of c-fos, and expression of the endogenous and fusion gene was shown by Northern analysis to correlate upon induction with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA). Using a chromogenic substrate of beta-galactosidase, we also demonstrated that expression of the fusion gene product, like that of Fos, was localized to the cell nucleus. In addition, we showed that epidermal keratinocytes responded to dialysed fetal bovine serum (FBS), TPA and high-calcium medium with enhanced Fos-lacZ expression and an inhibition of proliferation. The time course of induction of Fos-lacZ expression was similar for dialysed FBS and TPA, with a peak approximately 2 h after exposure. Exposure for approximately 24 h to an elevated extracellular calcium concentration was required to elicit an increase in Fos-lacZ expression. The lack of an immediate effect of raising medium calcium levels on Fos-lacZ expression contrasted with the rapidity of its effect on DNA synthesis, which was significantly inhibited within 6-8 h. In addition, we found that the protein kinase C inhibitor Ro 31-7549 blocked Fos-lacZ expression induced by TPA but had little or no effect on that elicited by high calcium levels. Thus, although our results indicate that the fos gene product may be involved in mediating epidermal keratinocyte growth arrest in response to differentiative agents such as FBS, TPA and high medium calcium levels, the exact role of this gene product remains unclear.

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32

Vaughan, Elaine E., R. David Pridmore, and Beat Mollet. "Transcriptional Regulation and Evolution of Lactose Genes in the Galactose-Lactose Operon of Lactococcus lactisNCDO2054." Journal of Bacteriology 180, no. 18 (September 15, 1998): 4893–902. http://dx.doi.org/10.1128/jb.180.18.4893-4902.1998.

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ABSTRACT The genetics of lactose utilization within the slow-lactose-fermenting Lactococcus lactis strain NCDO2054 was studied with respect to the organization, expression, and evolution of the lac genes. Initially the β-galactosidase gene (lacZ) was cloned by complementation of an Escherichia coli mutant on a 7-kb HpaI fragment. Nucleotide sequence analysis of the complete fragment revealed part of a gal-lac operon, and the genes were characterized by inactivation and complementation analyses and in vitro enzyme activity measurements. The gene order isgalK-galT-lacA-lacZ-galE; the gal genes encode enzymes of the Leloir pathway for galactose metabolism, andlacA encodes a galactoside acetyltransferase. ThegalT and galE genes of L. lactisLM0230 (a lactose plasmid-cured derivative of the fast-lactose-fermenting L. lactis C2) were highly similar at the nucleotide sequence level to their counterparts in strain NCDO2054 and, furthermore, had the same gene order except for the presence of the intervening lacA-lacZ strain NCDO2054. Analysis of mRNA for the gal and lac genes revealed an unusual transcriptional organization for the operon, with a surprisingly large number of transcriptional units. The regulation of the lac genes was further investigated by using fusions consisting of putative promoter fragments and the promoterless β-glucuronidase gene (gusA) from E. coli, which identified three lactose-inducible intergenic promoters in the gal-lac operon. The greater similarity of thelacA and lacZ genes to homologs in gram-negative organisms than to those of gram-positive bacteria, in contrast to the homologies of the gal genes, suggests that the genes within the gal operon of L. lactisNCDO2054 have been recently acquired. Thus, thelacA-lacZ genes appear to have engaged the promoters of thegal operon in order to direct and control their expression.

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33

GOTO, HIDEYUKI, FRANKLIN D. SHULER, CHANIN LAMSAM, HANS D. MOLLER, CHRISTOPHER NIYIBIZI, FREDDIE H. FU, PAUL D. ROBBINS, and CHRISTOPHER H. EVANS. "Transfer of LacZ Marker Gene to the Meniscus*." Journal of Bone & Joint Surgery 81, no. 7 (July 1999): 918–25. http://dx.doi.org/10.2106/00004623-199907000-00003.

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34

Sanderson, Sarah, and Nilabh Shastri. "LacZ inducible, antigen/MHC-specific T cell hybrids." International Immunology 6, no. 3 (1994): 369–76. http://dx.doi.org/10.1093/intimm/6.3.369.

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35

Miljkovic, Marijana, and Branka Vasiljevic. "In trans regulation of the sgm::lacZ fusion." Archives of Biological Sciences 54, no. 1-2 (2002): 1P—2P. http://dx.doi.org/10.2298/abs0202001m.

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36

Cohen-Tannoudji, Michel, Sandrine Vandormael-Pournin, Jean-Michel Drezen, Pascale Mercier, Charles Babinet, and Dominique Morello. "lacZ sequences prevent regulated expression of housekeeping genes." Mechanisms of Development 90, no. 1 (January 2000): 29–39. http://dx.doi.org/10.1016/s0925-4773(99)00226-9.

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37

Li, Li, Roger J. Zemp, Gina Lungu, George Stoica, and Lihong V. Wang. "Photoacoustic imaging of lacZ gene expression in vivo." Journal of Biomedical Optics 12, no. 2 (2007): 020504. http://dx.doi.org/10.1117/1.2717531.

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38

Williams, C. V., K. Fletcher, H. Tinwell, and J. Ashby. "Mutagenicity of ethyl carbamate to lacZ− transgenic mice." Mutagenesis 13, no. 2 (1998): 133–37. http://dx.doi.org/10.1093/mutage/13.2.133.

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39

Stroud, Dina Myers, Bruce J. Darrow, Sang Do Kim, Jie Zhang, Monique R. M. Jongbloed, Stacey Rentschler, Ivan P. G. Moskowitz, Jonathan Seidman, and Glenn I. Fishman. "Complex genomic rearrangement in CCS-LacZ transgenic mice." genesis 45, no. 2 (2007): 76–82. http://dx.doi.org/10.1002/dvg.20267.

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40

Dwyer, R. S., J. C. Malinverni, D. Boyd, J. Beckwith, and T. J. Silhavy. "Folding LacZ in the Periplasm of Escherichia coli." Journal of Bacteriology 196, no. 18 (July 7, 2014): 3343–50. http://dx.doi.org/10.1128/jb.01843-14.

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41

Nagy, A., M. Gertsenstein, K. Vintersten, and R. Behringer. "Staining Whole Mouse Embryos for -Galactosidase (lacZ) Activity." Cold Spring Harbor Protocols 2007, no. 8 (April 1, 2007): pdb.prot4725. http://dx.doi.org/10.1101/pdb.prot4725.

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42

Parsot, C. "Identification of a lacZ gene in Vibrio cholerae." Research in Microbiology 143, no. 1 (January 1992): 27–36. http://dx.doi.org/10.1016/0923-2508(92)90031-i.

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Prentki, Pierre. "Nucleotide sequence of the classical lacZ deletion ΔM15." Gene 122, no. 1 (December 1992): 231–32. http://dx.doi.org/10.1016/0378-1119(92)90056-u.

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Herzing, Laura B. K., and M. Stephen Meyn. "Novel lacZ-based recombination vectors for mammalian cells." Gene 137, no. 2 (December 1993): 163–69. http://dx.doi.org/10.1016/0378-1119(93)90002-k.

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Kroupskaya, I. V., A. N. Zhyvoloup, and E. B. Paton. "Construction of hybrid lacZ genes to study the E. coli rpljl operon genes expression mechanisms." Biopolymers and Cell 6, no. 2 (March 20, 1990): 91–100. http://dx.doi.org/10.7124/bc.000262.

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Domino, S. E. "LacZ expression in Fut2-LacZ reporter mice reveals estrogen-regulated endocervical glandular expression during estrous cycle, hormone replacement, and pregnancy." Glycobiology 14, no. 2 (September 26, 2003): 169–75. http://dx.doi.org/10.1093/glycob/cwh019.

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Hou, L., J. J. Panthier, and H. Arnheiter. "Signaling and transcriptional regulation in the neural crest-derived melanocyte lineage: interactions between KIT and MITF." Development 127, no. 24 (December 15, 2000): 5379–89. http://dx.doi.org/10.1242/dev.127.24.5379.

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Abstract:

Genetic and cell culture analyses have shown that the development of melanocytes from neural crest-derived precursor cells critically depends on the tyrosine kinase receptor KIT and the basic-helix-loop-helix-leucine zipper transcription factor MITF. KIT and MITF show complex interactions in that MITF is needed for the maintenance of Kit expression in melanoblasts and KIT signaling modulates MITF activity and stability in melanocyte cell lines. Using primary neural crest cell cultures from embryos homozygous for a Kit null allele marked by an inserted LacZ gene (Kit(W-LacZ)), we show that the onset of Mitf expression in melanoblasts does not require KIT. In fact, provided that the melanocyte growth factor endothelin-3 is present, a small number of MITF/beta-Gal-positive cells can be maintained for at least 2 weeks in Kit(W-LacZ)/Kit(W-LacZ) cultures. These cells express several pigment cell-specific genes that are thought or have been shown to be activated by MITF, including dautochrome tautomerase, pMel 17/Silver and tyrosinase-related protein-1, but lack expression of the MITF target gene tyrosinase, which encodes the rate-limiting enzyme in melanin synthesis. Consequently, the cells remain unpigmented. Addition of cholera toxin, which elevates cAMP levels and mimics part of the KIT signaling pathway, increases the number of MITF-positive cells in Kit(W-LacZ)/Kit(W-LacZ) cultures, leads to tyrosinase expression, and induces the differentiation of melanoblasts into mature, pigmented melanocytes. Even when added on day 5–6 of culture, cholera toxin still rescues tyrosinase expression and differentiation. The results thus demonstrate that the presence of MITF is not sufficient for tyrosinase expression in melanoblasts and that KIT signaling influences gene expression during melanocyte development in a gene-selective manner.

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Isensee, Jörg, Luca Meoli, Valeria Zazzu, Christoph Nabzdyk, Henning Witt, Dian Soewarto, Karin Effertz, et al. "Expression Pattern of G Protein-Coupled Receptor 30 in LacZ Reporter Mice." Endocrinology 150, no. 4 (December 18, 2008): 1722–30. http://dx.doi.org/10.1210/en.2008-1488.

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Multiple reports implicated the function of G protein-coupled receptor (GPR)-30 with nongenomic effects of estrogen, suggesting that GPR30 might be a G-protein coupled estrogen receptor. However, the findings are controversial and the expression pattern of GPR30 on a cell type level as well as its function in vivo remains unclear. Therefore, the objective of this study was to identify cell types that express Gpr30 in vivo by analyzing a mutant mouse model that harbors a lacZ reporter (Gpr30-lacZ) in the Gpr30 locus leading to a partial deletion of the Gpr30 coding sequence. Using this strategy, we identified the following cell types expressing Gpr30: 1) an endothelial cell subpopulation in small arterial vessels of multiple tissues, 2) smooth muscle cells and pericytes in the brain, 3) gastric chief cells in the stomach, 4) neuronal subpopulations in the cortex as well as the polymorph layer of the dentate gyrus, 5) cell populations in the intermediate and anterior lobe of the pituitary gland, and 6) in the medulla of the adrenal gland. In further experiments, we aimed to decipher the function of Gpr30 by analyzing the phenotype of Gpr30-lacZ mice. The body weight as well as fat mass was unchanged in Gpr30-lacZ mice, even if fed with a high-fat diet. Flow cytometric analysis revealed lower frequencies of T cells in both sexes of Gpr30-lacZ mice. Within the T-cell cluster, the amount of CD62L-expressing cells was clearly reduced, suggesting an impaired production of T cells in the thymus of Gpr30-lacZ mice.

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Gomi, Hiroshi, Airi Hinata, Tadashi Yasui, Seiji Torii, and Masahiro Hosaka. "Expression Pattern of the LacZ Reporter in Secretogranin III Gene-trapped Mice." Journal of Histochemistry & Cytochemistry 69, no. 4 (February 23, 2021): 229–43. http://dx.doi.org/10.1369/0022155421996845.

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Secretogranin III (SgIII) is a granin protein involved in secretory granule formation in peptide-hormone-producing endocrine cells. In this study, we analyzed the expression of the LacZ reporter in the SgIII knockout mice produced by gene trapping ( SgIII-gtKO) for the purpose of comprehensively clarifying the expression patterns of SgIII at the cell and tissue levels. In the endocrine tissues of SgIII-gtKO mice, LacZ expression was observed in the pituitary gland, adrenal medulla, and pancreatic islets, where SgIII expression has been canonically revealed. LacZ expression was extensively observed in brain regions, especially in the cerebral cortex, hippocampus, hypothalamic nuclei, cerebellum, and spinal cord. In peripheral nervous tissues, LacZ expression was observed in the retina, optic nerve, and trigeminal ganglion. LacZ expression was particularly prominent in astrocytes, in addition to neurons and ependymal cells. In the cerebellum, at least four cell types expressed SgIII under basal conditions. The expression of SgIII in the glioma cell lines C6 and RGC-6 was enhanced by excitatory glutamate treatment. It also became clear that the expression level of SgIII varied among neuron and astrocyte subtypes. These results suggest that SgIII is involved in glial cell function, in addition to neuroendocrine functions, in the nervous system:

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Sung, Hoon Ki, Yong-Woon Kim, Soo Jeong Choi, Jong-Yeon Kim, Kyung Hee Jeune, Kyu-Chang Won, Jason K. Kim, Gyu Young Koh, and So-Young Park. "COMP-angiopoietin-1 enhances skeletal muscle blood flow and insulin sensitivity in mice." American Journal of Physiology-Endocrinology and Metabolism 297, no. 2 (August 2009): E402—E409. http://dx.doi.org/10.1152/ajpendo.00122.2009.

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To test whether chronic enhanced blood flow alters insulin-stimulated glucose uptake, we measured skeletal muscle glucose uptake in chow-fed and high-fat-fed mice injected with adenovirus containing modified angiopoietin-1, COMP-Ang1, via euglycemic-hyperinsulinemic clamp. Blood flow rates and platelet endothelial cell adhesion molecule-1 positive endothelial cells in the hindlimb skeletal muscle were elevated in COMP-Ang1 compared with control LacZ. Whole body glucose uptake and whole body glycogen/lipid synthesis were elevated in COMP-Ang1 compared with LacZ in chow diet. High-fat diet significantly reduced whole body glucose uptake and whole body glycolysis in LacZ mice, whereas high-fat-fed COMP-Ang1 showed a level of whole body glucose uptake that was comparable with chow-fed LacZ and showed increased glucose uptake compared with high-fat-fed LacZ. Glucose uptake and glycolysis in gastrocnemius muscle of chow-fed COMP-Ang1 were increased compared with chow-fed LacZ. High-fat diet-induced whole body insulin resistance in the LacZ was mostly due to ∼40% decrease in insulin-stimulated glucose uptake in skeletal muscle. In contrast, COMP-Ang1 prevented diet-induced skeletal muscle insulin resistance compared with high-fat-fed LacZ. Akt phosphorylation in skeletal muscle was increased in COMP-Ang1 compared with LacZ in both chow-fed and high-fat-fed groups. These results suggest that increased blood flow by COMP-Ang1 increases insulin-stimulated glucose uptake and prevents high-fat diet-induced insulin resistance in skeletal muscle.

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