Janet E. Rinehart

University of Chicago Medical Center

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Berl R. Oakley

University of Kansas

C. Elizabeth Oakley

University of Kansas

Raymond P. Roos

University of Chicago

Ricardo M. Gómez

Consejo Nacional de Investigaciones Científicas y Técnicas

Brenda Mitchell

Marshall University

Edith A. Leonhardt

University of California, San Francisco

Gregory S. May

The University of Texas MD Anderson Cancer Center

Gregory L. Gray

University of Colorado Boulder

James B. Boyd

University of California, Davis

David G. Watson

University of Strathclyde

Cooperative Institutions

The Ohio State University

University of California, Davis

University of Southern California

National Institutes of Health

Rutgers, The State University of New Jersey

University of Chicago

University of Chicago Medical Center

University of Kansas

University of British Columbia

Chia Nan University of Pharmacy and Science

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Characterization of the mus308 gene in Drosophila melanogaster.

Genetics (1993)

Edith A. Leonhardt Daryl S. Henderson Janet E. Rinehart James B. Boyd

Among the available mutagen-sensitive mutations in Drosophila, those at the mus308 locus are unique in conferring hypersensitivity to DNA cross-linking agents but not to monofunctional agents. Those mutations are also associated with an elevated frequency of chromosomal aberrations, altered DNA metabolism and the modification of a deoxyribonuclease. This spectrum of phenotypes is shared with selected mammalian mutations including Fanconi anemia in humans. In anticipation of the molecular characterization of the mus308 gene, it has been localized cytogenetically to 87C9-87D1,2 on the right arm of chromosome three. Nine new mutant alleles of the gene have been generated by X-ray mutagenesis and one was recovered following hybrid dysgenesis. Characterization of these new alleles has uncovered additional phenotypes of mutations at this locus. Homozygous mus308 flies that have survived moderate mutagen treatment exhibit an altered wing position that is correlated with reduced flight ability and an altered mitochondrial morphology. In addition, observations of elevated embryo mortality are potentially explained by an aberrant distribution of nuclear material in early embryos which is similar to that seen in the mutant giant nuclei.

10.1093/genetics/133.1.87

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Citations (29)

Detection of serotypic variants in viral preparations: Sensitivity of a procedure for selection

Journal of Virological Methods (1989)

David G. Watson L. Jean Patterson Janet E. Rinehart John H. Hughes Vincent V. Hamparian

Polyclonal antibodies

Rhinovirus

10.1016/0166-0934(89)90165-1

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Conditionally lethal tubA α-tubulin mutations in Aspergillus nidulans

MGG Molecular & General Genetics (1987)

Berl R. Oakley C. Elizabeth Oakley Janet E. Rinehart

Aspergillus nidulans

Cold sensitivity

Wild type

Heat sensitive

10.1007/bf00330434

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Citations (29)

Development of HeLa cell lines that differentiate human rhinoviruses using the major cellular receptor

Janet E. Rinehart

HeLa

Rhinovirus

Human cell

Source

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Molecular determinants for virulence in coxsackievirus B1 infection

Journal of Virology (1997)

Janet E. Rinehart Ricardo M. Gómez Raymond P. Roos

Studies demonstrated that a strain derived from an infectious clone of coxsackievirus B1 (CVB1N) (N. Iizuka, H. Yonekawa, and A. Nomoto, J. Virol. 65:4867-4873, 1991) was 3 to 4 log10 less virulent than the myotropic Tucson strain of CVB1 (CVB1T) following intraperitoneal inoculation of newborn mice. Replacement of nucleotides (nt) 69 to 804 from the 5' untranslated region (5' UTR) and 1A coding region of CVB1N or nt 117 to 161 from the 5' UTR with the corresponding part from CVB1T restored greater than 90% of the virulence. Sequencing of the 5' UTR of CVB1T demonstrated areas with a greater similarity to particular echoviruses than to CVB1N, suggesting that recombination events might have occurred, perhaps influencing the virulence phenotype.

Coxsackievirus

Coding region

clone (Java method)

10.1128/jvi.71.5.3986-3991.1997

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Citations (46)

Theiler's murine encephalomyelitis virus-induced cardiac and skeletal muscle disease

Journal of Virology (1996)

Ricardo M. Gómez Janet E. Rinehart Robert L. Wollmann Raymond P. Roos

The DA strain of Theiler's murine encephalomyelitis virus, a member of the cardiovirus genus of picornaviruses, induces a restricted and persistent infection associated with a demyelinating process following intracerebral inoculation of mice; both virus infection and the immune response are believed to contribute to the late white matter disease. We now report that intraperitoneal inoculation with DA produces an acute myositis that progresses to a chronic inflammatory muscle disease in CD-1 mice as well as several inbred mouse strains. Some mouse strains also develop central nervous system white matter disease and a focal myocarditis. Infectious virus in skeletal muscle falls to undetectable levels 3 weeks postinoculation (p.i.), although viral genome persists for at least 12 weeks p.i., the longest period of observation. Severe combined immunodeficient animals have evidence of muscle pathology as long as 5 weeks p.i., suggesting that DA virus is capable of inducing chronic muscle disease in the absence of an immune response. The presence in immunocompetent mice, however, of prominent muscle inflammation in the absence of infectious virus suggests that the immune system also contributes to the pathology. T lymphocytes are the predominant cell type infiltrating the skeletal muscle during the chronic disease. This murine model may further our understanding of virus-induced chronic myositis and help to clarify the pathogenesis of human inflammatory myopathies.

Picornavirus

Pathogenesis

Encephalomyelitis

10.1128/jvi.70.12.8926-8933.1996

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Citations (25)

Isolation and characterization of cold-sensitive mutations at the benA, β-tubulin, locus of Aspergillus nidulans

MGG Molecular & General Genetics (1985)

Berl R. Oakley C. Elizabeth Oakley Kimberly S. Kniepkamp Janet E. Rinehart

Reversion

Aspergillus nidulans

Suppressor mutation

10.1007/bf00397987

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Citations (22)

Cloning, mapping and molecular analysis of the pyrG (orotidine-5'-phosphate decarboxylase) gene of Aspergillus nidulans

Gene (1987)

Berl R. Oakley Janet E. Rinehart Brenda Mitchell C. Elizabeth Oakley Cynthia Cannona

Aspergillus nidulans

Cloning (programming)

10.1016/0378-1119(87)90201-0

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Citations (164)

Mitochondria and nuclei move by different mechanisms in Aspergillus nidulans.

The Journal of Cell Biology (1985)

Berl R. Oakley Janet E. Rinehart

We have examined the effects of the antimicrotubule agent benomyl and several mutations on nuclear and mitochondrial movement in germlings of the filamentous fungus Aspergillus nidulans. While, as previously reported, benomyl inhibited nuclear division and movement, it did not inhibit mitochondrial movement. To test the effects of benomyl more rigorously, we germinated two benomyl super-sensitive, beta-tubulin mutants at a benomyl concentration 50-100 times greater than that required to inhibit colony formation completely. Again nuclear division and movement were inhibited, but mitochondrial movement was not. We also examined conditionally lethal beta-tubulin mutations that disrupt microtubule function under restrictive conditions. Nuclear division and movement were inhibited but, again, mitochondrial movement was not. Finally we examined the effects of five heat-sensitive mutations that inhibit nuclear movement but not nuclear division at restrictive temperatures. These mutations strongly inhibited nuclear movement at a restrictive temperature but did not inhibit mitochondrial movement. These data demonstrate that the mechanisms of nuclear and mitochondrial movement in Aspergillus nidulans are not identical and suggest that mitochondrial movement does not require functional microtubules.

Aspergillus nidulans

Benomyl

10.1083/jcb.101.6.2392

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Citations (70)