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Journal articles on the topic 'Mutants de type-1'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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1

Nikolaitchik, Olga, Terence D. Rhodes, David Ott, and Wei-Shau Hu. "Effects of Mutations in the Human Immunodeficiency Virus Type 1 gag Gene on RNA Packaging and Recombination." Journal of Virology 80, no. 10 (2006): 4691–97. http://dx.doi.org/10.1128/jvi.80.10.4691-4697.2006.

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ABSTRACT Human immunodeficiency virus type 1 (HIV-1) recombination occurs during reverse transcription when parts of the two copackaged RNAs are used as templates for DNA synthesis. It was previously hypothesized that HIV-1 Gag polyproteins preferentially encapsidate the RNA from which they were translated (cis-packaging hypothesis). This hypothesis implies that mutants encoding Gag that cannot efficiently package viral RNA are selected against at two levels: these mutants do not generate infectious virus, and these mutants are not efficiently rescued by the wild-type virus because the mutant

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2

Operario, Darwin J., Mini Balakrishnan, Robert A. Bambara, and Baek Kim. "Reduced dNTP Interaction of Human Immunodeficiency Virus Type 1 Reverse Transcriptase Promotes Strand Transfer." Journal of Biological Chemistry 281, no. 43 (2006): 32113–21. http://dx.doi.org/10.1074/jbc.m604665200.

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We have recently demonstrated that HIV-1 RT mutants characterized by low dNTP binding affinity display significantly reduced dNTP incorporation kinetics in comparison to wild-type RT. This defect is particularly emphasized at low dNTP concentrations where WT RT remains capable of efficient synthesis. Kinetic interference in DNA synthesis can induce RT pausing and slow down the synthesis rate. RT stalling and slow synthesis rate can enhance RNA template cleavage by RT-RNase H, facilitating transfer of the primer to a homologous template. We therefore hypothesized that reduced dNTP binding RT mu

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3

LA RAGIONE, R. M., A. R. SAYERS, and M. J. WOODWARD. "The role of fimbriae and flagella in the colonization, invasion and persistence of Escherichia coli O78[ratio ]K80 in the day-old-chick model." Epidemiology and Infection 124, no. 3 (2000): 351–63. http://dx.doi.org/10.1017/s0950268899004045.

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To understand the role of flagella and fimbriae of Escherichia coli O78[ratio ]K80 in avian colibacillosis, day-old chicks were dosed orally with defined afimbriate and or aflagellate mutants and colonization, invasion and persistence compared with that of the wild-type. In an invasion model, chicks were dosed with 1 × 105 c.f.u. of a single strain and mutants defective for type 1 fimbriae, curli fimbriae or flagella colonized livers by 24 h although the numbers of bacteria present were significantly less than the wild-type. Mutants colonized between 50 and 75% of spleens whereas the wild-type

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4

Martinez-Picado, Javier, Anu V. Savara, Lorraine Sutton, and Richard T. D’Aquila. "Replicative Fitness of Protease Inhibitor-Resistant Mutants of Human Immunodeficiency Virus Type 1." Journal of Virology 73, no. 5 (1999): 3744–52. http://dx.doi.org/10.1128/jvi.73.5.3744-3752.1999.

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ABSTRACT The relative replicative fitness of human immunodeficiency virus type 1 (HIV-1) mutants selected by different protease inhibitors (PIs) in vivo was determined. Each mutant was compared to wild type (WT), NL4-3, in the absence of drugs by several methods, including clonal genotyping of cultures infected with two competing viral variants, kinetics of viral antigen production, and viral infectivity/virion particle ratios. A nelfinavir-selected protease D30N substitution substantially decreased replicative capacity relative to WT, while a saquinavir-selected L90M substitution moderately d

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5

Baker, Stefanie H., Debra L. Frederick, Andrew Bloecher, and Kelly Tatchell. "Alanine-Scanning Mutagenesis of Protein Phosphatase Type 1 in the Yeast Saccharomyces cerevisiae." Genetics 145, no. 3 (1997): 615–26. http://dx.doi.org/10.1093/genetics/145.3.615.

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Protein phosphatase type 1, encoded by GLC7 in Saccharomyces cerevisiae, is an essential serine/threonine phosphatase implicated in the regulation of a diverse array of physiological functions. We constructed and examined 20 mutant alleles of GLC7 in which codons encoding clusters of charged residues were changed to alanine codons. Three of 20 mutant alleles alter residues in the active site of the phosphatase and are unable to rescue the lethality of a glc7::LEU2 disruption. The 17 alleles that support growth confer a range of mutant traits including cell cycle arrest, 2-deoxyglucose resistan

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6

Toppaldoddi, Katte Rao, Maira da Costa Cacemiro, Olivier Bluteau, et al. "Rare type 1-like and type 2-like calreticulin mutants induce similar myeloproliferative neoplasms as prevalent type 1 and 2 mutants in mice." Oncogene 38, no. 10 (2018): 1651–60. http://dx.doi.org/10.1038/s41388-018-0538-z.

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7

Bjerke, Susan L., John M. Cowan, Jelani K. Kerr, Ashley E. Reynolds, Joel D. Baines, and Richard J. Roller. "Effects of Charged Cluster Mutations on the Function of Herpes Simplex Virus Type 1 UL34 Protein." Journal of Virology 77, no. 13 (2003): 7601–10. http://dx.doi.org/10.1128/jvi.77.13.7601-7610.2003.

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ABSTRACT Herpes simplex virus type 1 (HSV-1) is a DNA virus that acquires an envelope by budding into the inner nuclear membrane of an infected cell. Recombinant HSV-1 lacking the UL34 gene cannot undergo this event. UL34 and UL31, another viral protein, colocalize in an infected cell and are necessary and sufficient to target both proteins to the inner nuclear envelope. In order to define and characterize sequences of UL34 that are necessary for primary envelopment to occur, a library of 19 UL34 charged cluster mutants and a truncation mutant lacking the putative transmembrane domain (ΔTM) we

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8

Ying, Baoling, Kimberley Smith, and Katherine R. Spindler. "Mouse Adenovirus Type 1 Early Region 1A Is Dispensable for Growth in Cultured Fibroblasts." Journal of Virology 72, no. 8 (1998): 6325–31. http://dx.doi.org/10.1128/jvi.72.8.6325-6331.1998.

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ABSTRACT Mouse adenovirus type 1 (MAV-1) mutants with deletions of conserved regions of early region 1A (E1A) or with point mutations that eliminate translation of E1A were used to determine the role of E1A in MAV-1 replication. MAV-1 E1A mutants expressing no E1A protein grew to titers comparable to wild-type MAV-1 titers on mouse fibroblasts (3T6 fibroblasts and fibroblasts derived from Rb+/+,Rb+/−, and Rb−/− transgenic embryos). To test the hypothesis that E1A could induce a quiescent cell to reenter the cell cycle, fibroblasts were serum starved to stop DNA replication and cellular replica

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9

Silverman, Jessica L., Sapna Sharma, Tina M. Cairns, and Ekaterina E. Heldwein. "Fusion-Deficient Insertion Mutants of Herpes Simplex Virus Type 1 Glycoprotein B Adopt the Trimeric Postfusion Conformation." Journal of Virology 84, no. 4 (2009): 2001–12. http://dx.doi.org/10.1128/jvi.01791-09.

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ABSTRACT Glycoprotein B (gB) enables the fusion of viral and cell membranes during entry of herpesviruses. However, gB alone is insufficient for membrane fusion; the gH/gL heterodimer is also required. The crystal structure of the herpes simplex virus type 1 (HSV-1) gB ectodomain, gB730, has demonstrated similarities between gB and other viral fusion proteins, leading to the hypothesis that gB is a fusogen, presumably directly involved in bringing the membranes together by refolding from its initial or prefusion form to its final or postfusion form. The only available crystal structure likely

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10

Collins, Jennifer A., M. Gregory Thompson, Elijah Paintsil, Melisa Ricketts, Joanna Gedzior, and Louis Alexander. "Competitive Fitness of Nevirapine-Resistant Human Immunodeficiency Virus Type 1 Mutants." Journal of Virology 78, no. 2 (2004): 603–11. http://dx.doi.org/10.1128/jvi.78.2.603-611.2004.

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ABSTRACT Determining the fitness of drug-resistant human immunodeficiency virus type 1 (HIV-1) strains is necessary for the development of population-based studies of resistance patterns. For this purpose, we have developed a reproducible, systematic assay to determine the competitive fitness of HIV-1 drug-resistant mutants. To demonstrate the applicability of this assay, we tested the fitness of the five most common nevirapine-resistant mutants (103N, 106A, 181C, 188C, and 190A), with mutations in HIV-1 reverse transcriptase (RT), singly and in combination (for a total of 31 variants) in a de

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11

Tatsuno, Ichiro, Hiroshi Kimura, Akiko Okutani, et al. "Isolation and Characterization of Mini-Tn5Km2 Insertion Mutants of Enterohemorrhagic Escherichia coliO157:H7 Deficient in Adherence to Caco-2 Cells." Infection and Immunity 68, no. 10 (2000): 5943–52. http://dx.doi.org/10.1128/iai.68.10.5943-5952.2000.

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ABSTRACT Adherence of enterohemorrhagic Escherichia coli (EHEC) to intestinal epithelium is essential for initiation of the infection. To identify genes involved in adherence, an EHEC O157:H7 strain (O157Sakai) was mutagenized by mini-Tn5Km2, where Km refers to kanamycin resistance, and 4,677 insertion mutants were screened for their ability to form microcolonies (MC) on Caco-2 cells. The less adherent mutants were divided into three groups: those with no adherent ability (designated as class 1 mutants, n = 10), those less adherent than the wild type (class 2 mutants, n = 16), and those unable

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12

Chen, Steve S. L., Sheau-Fen Lee, Huey-Jong Hao, and Chin-Kai Chuang. "Mutations in the Leucine Zipper-Like Heptad Repeat Sequence of Human Immunodeficiency Virus Type 1 gp41 Dominantly Interfere with Wild-Type Virus Infectivity." Journal of Virology 72, no. 6 (1998): 4765–74. http://dx.doi.org/10.1128/jvi.72.6.4765-4774.1998.

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ABSTRACT It has been previously shown that a proline substitution for any of the conserved leucine or isoleucine residues located in the leucine zipper-like heptad repeat sequence of human immunodeficiency virus type 1 (HIV-1) gp41 renders viruses noninfectious and envelope (Env) protein unable to mediate membrane fusion (S. S.-L. Chen, C.-N. Lee, W.-R. Lee, K. McIntosh, and T.-M. Lee, J. Virol. 67:3615–3619, 1993; S. S.-L. Chen, J. Virol. 68:2002–2010, 1994). To understand whether these variants could act as trans-dominant inhibitory mutants, the ability of these mutants to inhibit wild-type

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13

Lu, Qiaosheng, Ying T. Hwang, and Charles B. C. Hwang. "Mutation Spectra of Herpes Simplex Virus Type 1 Thymidine Kinase Mutants." Journal of Virology 76, no. 11 (2002): 5822–28. http://dx.doi.org/10.1128/jvi.76.11.5822-5828.2002.

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ABSTRACT To examine whether the exonuclease activity intrinsic to the polymerase (Pol) of herpes simplex virus type 1 can influence the mutational spectra, we applied the denaturing gradient gel electrophoresis (DGGE) system combined with sequencing to characterize thymidine kinase mutants isolated from both the wild-type virus and a mutant deficient in exonuclease activity, Y7. Wild-type viruses produced predominately frameshift mutations (67%), whereas Y7 replicated a significantly lower proportion of frameshifts (21%; P < 0.005). Furthermore, the majority of substitutions were transition

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14

Wang, Kening, Gowtham Mahalingam, Susan E. Hoover, et al. "Diverse Herpes Simplex Virus Type 1 Thymidine Kinase Mutants in Individual Human Neurons and Ganglia." Journal of Virology 81, no. 13 (2007): 6817–26. http://dx.doi.org/10.1128/jvi.00166-07.

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ABSTRACT Mutations in the thymidine kinase gene (tk) of herpes simplex virus type 1 (HSV-1) explain most cases of virus resistance to acyclovir (ACV) treatment. Mucocutaneous lesions of patients with ACV resistance contain mixed populations of tk mutant and wild-type virus. However, it is unknown whether human ganglia also contain mixed populations since the replication of HSV tk mutants in animal neurons is impaired. Here we report the detection of mutated HSV tk sequences in human ganglia. Trigeminal and dorsal root ganglia were obtained at autopsy from an immunocompromised woman with chroni

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15

Jeng, Chung-Jiuan, Yu-Ting Chen, Yi-Wen Chen, and Chih-Yung Tang. "Dominant-negative effects of human P/Q-type Ca2+ channel mutations associated with episodic ataxia type 2." American Journal of Physiology-Cell Physiology 290, no. 4 (2006): C1209—C1220. http://dx.doi.org/10.1152/ajpcell.00247.2005.

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Episodic ataxia type 2 (EA2) is an inherited autosomal dominant disorder related to cerebellar dysfunction and is associated with mutations in the pore-forming α1A-subunits of human P/Q-type Ca2+ channels (Cav2.1 channels). The majority of EA2 mutations result in significant loss-of-function phenotypes. Whether EA2 mutants may display dominant-negative effects in human, however, remains controversial. To address this issue, five EA2 mutants in the long isoform of human α1A-subunits were expressed in Xenopus oocytes to explore their potential dominant-negative effects. Upon coexpressing the cRN

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16

Lu, Richard, Hina Z. Ghory, and Alan Engelman. "Genetic Analyses of Conserved Residues in the Carboxyl-Terminal Domain of Human Immunodeficiency Virus Type 1 Integrase." Journal of Virology 79, no. 16 (2005): 10356–68. http://dx.doi.org/10.1128/jvi.79.16.10356-10368.2005.

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ABSTRACT Results of in vitro assays identified residues in the C-terminal domain (CTD) of human immunodeficiency virus type 1 (HIV-1) integrase (IN) important for IN-IN and IN-DNA interactions, but the potential roles of these residues in virus replication were mostly unknown. Sixteen CTD residues were targeted here, generating 24 mutant viruses. Replication-defective mutants were typed as class I (blocked at integration) or class II (additional reverse transcription and/or assembly defects). Most defective viruses (15 of 17) displayed reverse transcription defects. In contrast, replication-de

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17

Arita, Minetaro, Hiroyuki Shimizu, and Tatsuo Miyamura. "Characterization of in vitro and in vivo phenotypes of poliovirus type 1 mutants with reduced viral protein synthesis activity." Journal of General Virology 85, no. 7 (2004): 1933–44. http://dx.doi.org/10.1099/vir.0.19768-0.

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Sabin vaccine strains of poliovirus (PV) contain major attenuation determinants in the internal ribosomal entry site (IRES), an area that directs viral protein synthesis. To examine the effect of reduced viral protein synthesis on PV neurovirulence, spacer sequences, consisting of short open reading frames of different lengths, were introduced between the IRES and the initiation codon of viral polyprotein, resulting in PV mutants with reduced viral protein synthesis. These PV mutants had a viral protein synthesis activity 8·8–55 % of that of the parental Mahoney strain as measured in HeLa S3 c

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18

de Pace, Fernanda, Gerson Nakazato, Alline Pacheco, Jacqueline Boldrin de Paiva, Vanessa Sperandio, and Wanderley Dias da Silveira. "The Type VI Secretion System Plays a Role in Type 1 Fimbria Expression and Pathogenesis of an Avian Pathogenic Escherichia coli Strain." Infection and Immunity 78, no. 12 (2010): 4990–98. http://dx.doi.org/10.1128/iai.00531-10.

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ABSTRACT Avian pathogenic Escherichia coli (APEC) strains frequently cause extraintestinal infections and are responsible for significant economic losses in the poultry industry worldwide. APEC isolates are closely related to human extraintestinal pathogenic E. coli (ExPEC) strains and may also act as pathogens for humans. Known APEC virulence factors include adhesins such as type 1 fimbriae and curli, iron acquisition systems, and cytotoxins. Here we show that APEC strain SEPT362, isolated from a septicemic hen, expresses a type VI secretion system (T6SS); causes cytoskeleton rearrangements;

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19

Ansari-Lari, M. Ali, Lawrence A. Donehower, and Richard A. Gibbs. "Analysis of Human Immunodeficiency Virus Type 1 Integrase Mutants." Virology 211, no. 1 (1995): 332–35. http://dx.doi.org/10.1006/viro.1995.1412.

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20

Cisar, J. O., A. E. Vatter, W. B. Clark, S. H. Curl, S. Hurst-Calderone, and A. L. Sandberg. "Mutants of Actinomyces viscosus T14V lacking type 1, type 2, or both types of fimbriae." Infection and Immunity 56, no. 11 (1988): 2984–89. http://dx.doi.org/10.1128/iai.56.11.2984-2989.1988.

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21

Koleilat, Alaa, Joseph A. Dugdale, Trace A. Christenson, et al. "L-type voltage-gated calcium channel agonists mitigate hearing loss and modify ribbon synapse morphology in the zebrafish model of Usher syndrome type 1." Disease Models & Mechanisms 13, no. 11 (2020): dmm043885. http://dx.doi.org/10.1242/dmm.043885.

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ABSTRACTThe mariner (myo7aa−/−) mutant is a zebrafish model for Usher syndrome type 1 (USH1). To further characterize hair cell synaptic elements in myo7aa−/− mutants, we focused on the ribbon synapse and evaluated ultrastructure, number and distribution of immunolabeled ribbons, and postsynaptic densities. By transmission electron microscopy, we determined that myo7aa−/− zebrafish have fewer glutamatergic vesicles tethered to ribbon synapses, yet maintain a comparable ribbon area. In myo7aa−/− hair cells, immunolocalization of Ctbp2 showed fewer ribbon-containing cells in total and an altered

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Llano, Manuel, Tara Kelly, Maria Vanegas, et al. "Blockade of Human Immunodeficiency Virus Type 1 Expression by Caveolin-1." Journal of Virology 76, no. 18 (2002): 9152–64. http://dx.doi.org/10.1128/jvi.76.18.9152-9164.2002.

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ABSTRACT Caveolin-1 (Cav-1) is a major protein constituent of caveolae, a type of plasma membrane raft. We observed that coexpression of human Cav-1 with human immunodeficiency virus type 1 (HIV-1) blocked virion production from cells that are ordinarily highly permissive. Further investigation showed that this effect is specific, occurs at low ratios of Cav-1 to HIV-1 DNA, depends on expression of Cav-1 protein, and involves severely impaired expression of HIV-1 proteins. Cav-1 also blocked HIV-2 expression. In contrast, Cav-1 did not inhibit protein expression by a paramyxovirus and did not

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Conzelmann, A., A. Spiazzi, C. Bron, and R. Hyman. "No glycolipid anchors are added to Thy-1 glycoprotein in Thy-1-negative mutant thymoma cells of four different complementation classes." Molecular and Cellular Biology 8, no. 2 (1988): 674–78. http://dx.doi.org/10.1128/mcb.8.2.674.

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Recent evidence shows that the mature Thy-1 surface glycoprotein lacks the C-terminal amino acids 113 to 143 predicted from the cDNA sequence and is anchored in the plasma membrane by a complex, phosphatidylinositol-containing glycolipid attached to the alpha-carboxyl group of amino acid 112. Here we studied the biosynthesis of Thy-1 in two previously described and two newly isolated Thy-1-deficient mutant cell lines. Somatic cell hybridization indicated that their mutations affected some processing step rather than the Thy-1 structural gene. The Thy-1 made by mutants of classes C, F, and H bo

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Conzelmann, A., A. Spiazzi, C. Bron, and R. Hyman. "No glycolipid anchors are added to Thy-1 glycoprotein in Thy-1-negative mutant thymoma cells of four different complementation classes." Molecular and Cellular Biology 8, no. 2 (1988): 674–78. http://dx.doi.org/10.1128/mcb.8.2.674-678.1988.

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Recent evidence shows that the mature Thy-1 surface glycoprotein lacks the C-terminal amino acids 113 to 143 predicted from the cDNA sequence and is anchored in the plasma membrane by a complex, phosphatidylinositol-containing glycolipid attached to the alpha-carboxyl group of amino acid 112. Here we studied the biosynthesis of Thy-1 in two previously described and two newly isolated Thy-1-deficient mutant cell lines. Somatic cell hybridization indicated that their mutations affected some processing step rather than the Thy-1 structural gene. The Thy-1 made by mutants of classes C, F, and H bo

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25

Fujiwara, Mamoru, Junko Tanuma, Hirokazu Koizumi, et al. "Different Abilities of Escape Mutant-Specific Cytotoxic T Cells To Suppress Replication of Escape Mutant and Wild-Type Human Immunodeficiency Virus Type 1 in New Hosts." Journal of Virology 82, no. 1 (2007): 138–47. http://dx.doi.org/10.1128/jvi.01452-07.

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ABSTRACT There is much evidence that in human immunodeficiency virus type 1 (HIV-1)-infected individuals, strong cytotoxic T lymphocyte (CTL)-mediated immune pressure results in the selection of HIV-1 mutants that have escaped from wild-type-specific CTLs. If escape mutant-specific CTLs are not elicited in new hosts sharing donor HLA molecules, the transmission of these mutants results in the accumulation of escape mutants in the population. However, whether escape mutant-specific CTLs are definitively not elicited in new hosts sharing donor HLA molecules still remains unclear. A previous stud

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DeLuca, N. A., and P. A. Schaffer. "Activation of immediate-early, early, and late promoters by temperature-sensitive and wild-type forms of herpes simplex virus type 1 protein ICP4." Molecular and Cellular Biology 5, no. 8 (1985): 1997–2008. http://dx.doi.org/10.1128/mcb.5.8.1997.

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To better define the activities on herpes simplex virus type 1 gene expression of temperature-sensitive and wild-type forms of the transcriptional regulatory protein ICP4, regulatory sequences from immediate-early, early, and late herpes simplex virus genes were fused to the gene for chloramphenicol acetyltransferase (CAT). These constructs were used in trans induction and cotransfection experiments with wild-type and temperature-sensitive mutant alleles of ICP4. The ICP4 genes used in this study were cloned from the KOS strain (wild type) and two phenotypically distinct temperature-sensitive

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DeLuca, N. A., and P. A. Schaffer. "Activation of immediate-early, early, and late promoters by temperature-sensitive and wild-type forms of herpes simplex virus type 1 protein ICP4." Molecular and Cellular Biology 5, no. 8 (1985): 1997–2008. http://dx.doi.org/10.1128/mcb.5.8.1997-2008.1985.

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To better define the activities on herpes simplex virus type 1 gene expression of temperature-sensitive and wild-type forms of the transcriptional regulatory protein ICP4, regulatory sequences from immediate-early, early, and late herpes simplex virus genes were fused to the gene for chloramphenicol acetyltransferase (CAT). These constructs were used in trans induction and cotransfection experiments with wild-type and temperature-sensitive mutant alleles of ICP4. The ICP4 genes used in this study were cloned from the KOS strain (wild type) and two phenotypically distinct temperature-sensitive

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Johnson, Welkin E., Jennifer M. Sauvron, and Ronald C. Desrosiers. "Conserved, N-Linked Carbohydrates of Human Immunodeficiency Virus Type 1 gp41 Are Largely Dispensable for Viral Replication." Journal of Virology 75, no. 23 (2001): 11426–36. http://dx.doi.org/10.1128/jvi.75.23.11426-11436.2001.

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ABSTRACT The transmembrane subunit (TM) of human immunodeficiency virus type 1 (HIV-1) envelope protein contains four well-conserved sites for the attachment of N-linked carbohydrates. To study the contribution of these N-glycans to the function of TM, we systematically mutated the sites individually and in all combinations and measured the effects of each on viral replication in culture. The mutants were derived from SHIV-KB9, a simian immunodeficiency virus/HIV chimera with an envelope sequence that originated from a primary HIV-1 isolate. The attachment site mutants were generated by replac

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Eversole, P., J. J. DiGangi, T. Menees, and R. H. Davis. "Structural gene for ornithine decarboxylase in Neurospora crassa." Molecular and Cellular Biology 5, no. 6 (1985): 1301–6. http://dx.doi.org/10.1128/mcb.5.6.1301.

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To define the structural gene for ornithine decarboxylase (ODC) in Neurospora crassa, we sought mutants with kinetically altered enzyme. Four mutants, PE4, PE7, PE69, and PE85, were isolated. They were able to grow slowly at 25 degrees C on minimal medium but required putrescine or spermidine supplementation for growth at 35 degrees C. The mutants did not complement with one another or with ODC-less spe-1 mutants isolated in earlier studies. In all of the mutants isolated to date, the mutations map at the spe-1 locus on linkage group V. Strains carrying mutations PE4, PE7, and PE85 displayed a

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Eversole, P., J. J. DiGangi, T. Menees, and R. H. Davis. "Structural gene for ornithine decarboxylase in Neurospora crassa." Molecular and Cellular Biology 5, no. 6 (1985): 1301–6. http://dx.doi.org/10.1128/mcb.5.6.1301-1306.1985.

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To define the structural gene for ornithine decarboxylase (ODC) in Neurospora crassa, we sought mutants with kinetically altered enzyme. Four mutants, PE4, PE7, PE69, and PE85, were isolated. They were able to grow slowly at 25 degrees C on minimal medium but required putrescine or spermidine supplementation for growth at 35 degrees C. The mutants did not complement with one another or with ODC-less spe-1 mutants isolated in earlier studies. In all of the mutants isolated to date, the mutations map at the spe-1 locus on linkage group V. Strains carrying mutations PE4, PE7, and PE85 displayed a

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Murphy, Caitlin N., Martin S. Mortensen, Karen A. Krogfelt, and Steven Clegg. "Role of Klebsiella pneumoniae Type 1 and Type 3 Fimbriae in Colonizing Silicone Tubes Implanted into the Bladders of Mice as a Model of Catheter-Associated Urinary Tract Infections." Infection and Immunity 81, no. 8 (2013): 3009–17. http://dx.doi.org/10.1128/iai.00348-13.

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ABSTRACTCatheter-associated urinary tract infections are biofilm-mediated infections that cause a significant economic and health burden in nosocomial environments. Using a newly developed murine model of this type of infection, we investigated the role of fimbriae in implant-associated urinary tract infections by the Gram-negative bacteriumKlebsiella pneumoniae, which is a proficient biofilm former and a commonly isolated nosocomial pathogen. Studies have shown that type 1 and type 3 fimbriae are involved in attachment and biofilm formationin vitro, and these fimbrial types are suspected to b

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Spormann, Alfred M., and Dale Kaiser. "Gliding Mutants of Myxococcus xanthuswith High Reversal Frequencies and Small Displacements." Journal of Bacteriology 181, no. 8 (1999): 2593–601. http://dx.doi.org/10.1128/jb.181.8.2593-2601.1999.

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ABSTRACT Myxococcus xanthus cells move on a solid surface by gliding motility. Several genes required for gliding motility have been identified, including those of the A- and S-motility systems as well as the mgl and frz genes. However, the cellular defects in gliding movement in many of these mutants were unknown. We conducted quantitative, high-resolution single-cell motility assays and found that mutants defective inmglAB or in cglB, an A-motility gene, reversed the direction of gliding at frequencies which were more than 1 order of magnitude higher than that of wild type cells (2.9 min−1fo

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Wang, Chin-Tien, Hsiu-Yu Lai, and Jue-Jyh Li. "Analysis of Minimal Human Immunodeficiency Virus Type 1 gag Coding Sequences Capable of Virus-Like Particle Assembly and Release." Journal of Virology 72, no. 10 (1998): 7950–59. http://dx.doi.org/10.1128/jvi.72.10.7950-7959.1998.

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ABSTRACT We have constructed a series of human immunodeficiency virus (HIV)gag mutants by progressive truncation of thegag coding sequence from the C terminus and have combined these mutants with an assembly-competent matrix domain deletion mutation (ΔMA). By using several methods, the particle-producing capabilities of each mutant were examined. Our analysis indicated that truncated Gag precursors lacking most of C-terminal gaggene products assembled and were released from 293T cells. Additionally, a mutant with a combined deletion of the MA (ΔMA) and p6 domains even produced particles at lev

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de Jonge, Ramon, Zarmina Durrani, Sjoerd G. Rijpkema, Ernst J. Kuipers, Arnoud H. M. van Vliet, and Johannes G. Kusters. "Role of the Helicobacter pylori outer-membrane proteins AlpA and AlpB in colonization of the guinea pig stomach." Journal of Medical Microbiology 53, no. 5 (2004): 375–79. http://dx.doi.org/10.1099/jmm.0.45551-0.

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The human gastric pathogen Helicobacter pylori expresses several putative outer-membrane proteins (OMPs), but the role of individual OMPs in colonization of the stomach by H. pylori is still poorly understood. The role of four such OMPs (AlpA, AlpB, OipA and HopZ) in a guinea pig model of H. pylori infection has been investigated. Single alpA, alpB, hopZ and oipA isogenic mutants were constructed in the guinea pig-adapted, wild-type H. pylori strain GP15. Guinea pigs were inoculated intragastrically with the wild-type strain, single mutants or a mixture of the wild-type and a single mutant in

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Qi, Mingli, Ruifeng Yang, and Christopher Aiken. "Cyclophilin A-Dependent Restriction of Human Immunodeficiency Virus Type 1 Capsid Mutants for Infection of Nondividing Cells." Journal of Virology 82, no. 24 (2008): 12001–8. http://dx.doi.org/10.1128/jvi.01518-08.

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ABSTRACT Among retroviruses, lentiviruses are unusual in their ability to efficiently infect both dividing and nondividing cells, such as activated T cells and macrophages, respectively. Recent studies implicate the viral capsid protein (CA) as a key determinant of cell-cycle-independent infection by human immunodeficiency virus type 1 (HIV-1). We investigated the effects of the host cell protein cyclophilin A (CypA), which binds to HIV-1 CA, on HIV-1 infection of nondividing cells. The HIV-1 CA mutants A92E, T54A, and R132K were impaired for infection of aphidicolin-arrested HeLa cells, but n

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Loewen, Peter C., Jacek Switala, Mark Smolenski, and Barbara L. Triggs-Raine. "Molecular characterization of three mutations in katG affecting the activity of hydroperoxidase I of Escherichia coli." Biochemistry and Cell Biology 68, no. 7-8 (1990): 1037–44. http://dx.doi.org/10.1139/o90-153.

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Hydroperoxidase I (HPI) of Escherichia coli is a bifunctional enzyme exhibiting both catalase and peroxidase activities. Mutants lacking appreciable HPI have been generated using nitrosoguanidine and the gene encoding HPI, katG, has been cloned from three of these mutants using either classical probing methods or polymerase chain reaction amplification. The mutant genes were sequenced and the changes from wild-type sequence identified. Two mutants contained G to A changes in the coding strand, resulting in glycine to aspartate changes at residues 119 (katG15) and 314 (katG16) in the deduced am

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Lu, Richard, Ana Limón, Eric Devroe, Pamela A. Silver, Peter Cherepanov, and Alan Engelman. "Class II Integrase Mutants with Changes in Putative Nuclear Localization Signals Are Primarily Blocked at a Postnuclear Entry Step of Human Immunodeficiency Virus Type 1 Replication." Journal of Virology 78, no. 23 (2004): 12735–46. http://dx.doi.org/10.1128/jvi.78.23.12735-12746.2004.

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ABSTRACT Integrase has been implicated in human immunodeficiency virus type 1 (HIV-1) nuclear import. Integrase analyses, however, can be complicated by the pleiotropic nature of mutations: whereas class I mutants are integration defective, class II mutants display additional assembly and/or reverse transcription defects. We previously determined that HIV-1V165A, originally reported as defective for nuclear import, was a class II mutant. Here we analyzed mutants containing changes in other putative nuclear localization signals, including 186KRK188/211KELQKQITK219 and Cys-130. Previous work est

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Chan, Woan-Eng, Hui-Hua Lin, and Steve S. L. Chen. "Wild-Type-Like Viral Replication Potential of Human Immunodeficiency Virus Type 1 Envelope Mutants Lacking Palmitoylation Signals." Journal of Virology 79, no. 13 (2005): 8374–87. http://dx.doi.org/10.1128/jvi.79.13.8374-8387.2005.

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ABSTRACT Palmitoylation of the cytoplasmic domain of the human immunodeficiency type virus type 1 (HIV-1) envelope (Env) transmembrane protein, gp41, has been implicated in Env targeting to detergent-resistant lipid rafts, Env incorporation into the virus, and viral infectivity. In contrast, we provide evidence here to show that HIV-1 infectivity, Env targeting to lipid rafts, and Env incorporation into the virus are independent of cytoplasmic tail palmitoylation. The T-cell (T)-tropic HXB2-based virus, which utilizes CXCR4 as the entry coreceptor, carrying a Cys-to-Ser mutation at residue 764

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Razani, Babak, and Michael P. Lisanti. "Two distinct caveolin-1 domains mediate the functional interaction of caveolin-1 with protein kinase A." American Journal of Physiology-Cell Physiology 281, no. 4 (2001): C1241—C1250. http://dx.doi.org/10.1152/ajpcell.2001.281.4.c1241.

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Numerous components of the cAMP-based signaling cascade, namely G-proteins and G- protein coupled receptors, adenylyl cyclase, and protein kinase A (PKA) have been localized to caveolae and shown to be regulated by the caveolar marker proteins, the caveolins. In order to gain mechanistic insights into these processes in vivo, we have assessed the functional interaction of caveolin-1 (Cav-1) with PKA using mutational analysis. As two regions of Cav-1 had previously been implicated in PKA signaling in vitro, we constructed Cav-1 molecules with mutations/deletions in one or both of these domains.

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Oide, Shinichi, Jinyuan Liu, Sung-Hwan Yun, et al. "Histidine Kinase Two-Component Response Regulator Proteins Regulate Reproductive Development, Virulence, and Stress Responses of the Fungal Cereal Pathogens Cochliobolus heterostrophus and Gibberella zeae." Eukaryotic Cell 9, no. 12 (2010): 1867–80. http://dx.doi.org/10.1128/ec.00150-10.

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ABSTRACT Histidine kinase (HK) phosphorelay signaling is a major mechanism by which fungi sense their environment. The maize pathogen Cochliobolus heterostrophus has 21 HK genes, 4 candidate response regulator (RR) genes (SSK1, SKN7, RIM15, REC1), and 1 gene (HPT1) encoding a histidine phosphotransfer domain protein. Because most HKs are expected to signal through RRs, these were chosen for deletion. Except for pigment and slight growth alterations for rim15 mutants, no measurable altered phenotypes were detected in rim15 or rec1 mutants. Ssk1p is required for virulence and affects fertility a

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Hamam, Ahmed, and Roger R. Lew. "Electrical Phenotypes of Calcium Transport Mutant Strains of a Filamentous Fungus, Neurospora crassa." Eukaryotic Cell 11, no. 5 (2012): 694–702. http://dx.doi.org/10.1128/ec.05329-11.

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ABSTRACT We characterized the electrical phenotypes of mutants with mutations in genes encoding calcium transporters—a mechanosensitive channel homolog ( MscS ), a Ca 2+ /H + exchange protein ( cax ), and Ca 2+ -ATPases ( nca-1 , nca-2 , nca-3 )—as well as those of double mutants (the nca-2 cax , nca-2 nca-3 , and nca-3 cax mutants). The electrical characterization used dual impalements to obtain cable-corrected current-voltage measurements. Only two types of mutants (the MscS mutant; the nca-2 mutant and nca-2 -containing double mutants) exhibited lower resting potentials. For the nca-2 mutan

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Milne, Richard S. B., Sheri L. Hanna, Ann H. Rux, Sharon H. Willis, Gary H. Cohen, and Roselyn J. Eisenberg. "Function of Herpes Simplex Virus Type 1 gD Mutants with Different Receptor-Binding Affinities in Virus Entry and Fusion." Journal of Virology 77, no. 16 (2003): 8962–72. http://dx.doi.org/10.1128/jvi.77.16.8962-8972.2003.

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ABSTRACT We have studied the receptor-specific function of four linker-insertion mutants of herpes simplex virus type 1 glycoprotein D (gD) representing each of the functional regions of gD. We used biosensor analysis to measure binding of the gD mutants to the receptors HVEM (HveA) and nectin-1 (HveC). One of the mutants, gD(∇34t), failed to bind HVEMt but showed essentially wild-type (WT) affinity for nectin-1t. The receptor-binding kinetics and affinities of the other three gD mutants varied over a 1,000-fold range, but each mutant had the same affinity for both receptors. All of the mutant

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Iglesias-Ussel, Maria Dolores, Concepción Casado, Eloísa Yuste, Isabel Olivares, and Cecilio López-Galíndez. "In vitro analysis of human immunodeficiency virus type 1 resistance to nevirapine and fitness determination of resistant variants." Journal of General Virology 83, no. 1 (2002): 93–101. http://dx.doi.org/10.1099/0022-1317-83-1-93.

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Nevirapine-resistant variants were generated by serial passages in MT-2 cells in the presence of increasing drug concentrations. In passage 5, mutations V106A, Y181C and G190A were detected in the global population, associated with a 100-fold susceptibility decrease. Sequence analysis of biological clones obtained from passage 5 and subsequent passages showed that single mutants, detected in first passages, were progressively replaced in passage 15 by double mutants, correlating with a 500-fold increase in phenotypic resistance. Fitness determination of single mutants confirmed that, in the pr

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Lambert, P. F., B. C. Monk, and P. M. Howley. "Phenotypic analysis of bovine papillomavirus type 1 E2 repressor mutants." Journal of Virology 64, no. 2 (1990): 950–56. http://dx.doi.org/10.1128/jvi.64.2.950-956.1990.

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Armstrong, Kimberly L., Tun-Hou Lee, and M. Essex. "Replicative Capacity Differences of Thymidine Analog Resistance Mutations in Subtype B and C Human Immunodeficiency Virus Type 1." Journal of Virology 83, no. 9 (2009): 4051–59. http://dx.doi.org/10.1128/jvi.02645-08.

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ABSTRACT In order to understand the impact of zidovudine resistance and thymidine analog mutations (TAMs) on subtype C human immunodeficiency virus type 1, we created mutants in subtype C reverse transcriptase (RT). The subtype B RT was placed in a subtype C backbone to act as a control. Mutants and wild-type (WT) virus were competed in a head-to-head competition assay to determine how different clones grew in the same culture. Different viruses were distinguished by sequence tags in nef and a quantitative-PCR assay. The 67N and 70R accessory mutations gave an advantage over the WT in subtype

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D’Aloja, Paola, Anna Claudia Santarcangelo, Stefan Arold, Andreas Baur, and Maurizio Federico. "Genetic and functional analysis of the human immunodeficiency virus (HIV) type 1-inhibiting F12-HIVnef allele." Journal of General Virology 82, no. 11 (2001): 2735–45. http://dx.doi.org/10.1099/0022-1317-82-11-2735.

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The primary human immunodeficiency virus type 1 (HIV-1) Nef mutant F12-HIVNef is characterized by three rare amino acid substitutions, G140E, V153L and E177G. It was reported previously that the expression of F12-HIVNef in the context of the highly productive NL4-3 HIV-1 strain blocks virus replication at the level of virus assembly and/or release by a mechanism depending on the presence of the CD4 intracytoplasmic tail. Here, it is reported that NL4-3 HIV-1 strains expressing F12-HIVnef alleles that were back-mutated in each amino acid substitution readily replicated in CD4+ cells. Attempting

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Yin, Lei, Douglas Braaten, and Jeremy Luban. "Human Immunodeficiency Virus Type 1 Replication Is Modulated by Host Cyclophilin A Expression Levels." Journal of Virology 72, no. 8 (1998): 6430–36. http://dx.doi.org/10.1128/jvi.72.8.6430-6436.1998.

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ABSTRACT Human immunodeficiency virus type 1 (HIV-1) Gag and the cellular protein cyclophilin A form an essential complex in the virion core: virions produced by proviruses encoding Gag mutants with decreased cyclophilin A affinity exhibit attenuated infectivity, as do virions produced in the presence of the competitive inhibitor cyclosporine. The A224E Gag mutant has no effect on cyclophilin A affinity but renders HIV-1 replication cyclosporine resistant in Jurkat T cells. In contrast, A224E mutant virus is dead in H9 T cells, although replication is rescued by cyclosporine or by expression i

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Miettinen, H. M., S. N. Edwards, and M. Jalkanen. "Analysis of transport and targeting of syndecan-1: effect of cytoplasmic tail deletions." Molecular Biology of the Cell 5, no. 12 (1994): 1325–39. http://dx.doi.org/10.1091/mbc.5.12.1325.

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Madin-Darby canine kidney (MDCK) cells and Chinese hamster ovary (CHO) cells were transfected with wild-type and cytoplasmic deletion mutants of mouse syndecan-1 to study the requirements for transport and polarized expression of this proteoglycan. Expression in MDCK cells revealed that wild-type syndecan-1 is directed to the basolateral surface via a brefeldin A-insensitive route. A deletion of the last 12 amino acids of the syndecan-1 cytoplasmic tail (CT22) was sufficient to result in the appearance of mutant proteoglycans at both the basolateral and apical cell surfaces. Treatment with bre

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van Swinderen, Bruno, Laura B. Metz, Laynie D. Shebester, Jane E. Mendel, Paul W. Sternberg та C. Michael Crowder. "Goα Regulates Volatile Anesthetic Action in Caenorhabditis elegans". Genetics 158, № 2 (2001): 643–55. http://dx.doi.org/10.1093/genetics/158.2.643.

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Abstract To identify genes controlling volatile anesthetic (VA) action, we have screened through existing Caenorhabditis elegans mutants and found that strains with a reduction in Go signaling are VA resistant. Loss-of-function mutants of the gene goa-1, which codes for the α-subunit of Go, have EC50s for the VA isoflurane of 1.7- to 2.4-fold that of wild type. Strains overexpressing egl-10, which codes for an RGS protein negatively regulating goa-1, are also isoflurane resistant. However, sensitivity to halothane, a structurally distinct VA, is differentially affected by Go pathway mutants. T

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Snyder, Jennifer A., Amanda L. Lloyd, C. Virginia Lockatell, David E. Johnson, and Harry L. T. Mobley. "Role of Phase Variation of Type 1 Fimbriae in a Uropathogenic Escherichia coli Cystitis Isolate during Urinary Tract Infection." Infection and Immunity 74, no. 2 (2006): 1387–93. http://dx.doi.org/10.1128/iai.74.2.1387-1393.2006.

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ABSTRACT Type 1 fimbrial phase-locked mutants of uropathogenic Escherichia coli cystitis isolate F11 were used to assess the role of the invertible element during urinary tract infection. Compared to the wild type, the phase-locked off mutant was attenuated, and constitutive production of type 1 fimbriae by the phase-locked on mutant did not provide a competitive advantage.

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