This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The obligate intracellular infectious agent Toxoplasma gondii is a member of the phylum Apicomplexa, which includes the organisms responsible for malaria and coccidiosis. Although most Toxoplasma infections are asymptomatic, they can lead to severe disease and even death in utero and in individuals immunocompromised by AIDS or cancer. Some of the devastating effects of a Toxoplasma infection are a direct consequence of its lytic cycle, which consists of attachment to the host cell, invasion, intracellular replication and egress. Both invasion and egress involve fluctuation in intracellular calcium concentration, morphological rearrangements and modifications to the host cell. The specific genes and cues involved in these rapid and active events are not known. It has been observed, however, that a decrease in potassium concentration within the host cell can serve as a signal for Toxoplasma egress. It is the goal of this proposal to elucidate the unknown genetic and molecular mechanisms utilized by this pathogen to sense changes in the environment as it specifically regards to potassium fluxes. This will be accomplished by isolating and characterizing mutants with an altered sensitivity to potassium concentration changes. The phenotypic and molecular analysis of these mutants will identify the genes involved in perceiving the pivotal changes in potassium concentration important during egress as well shed light to events critical to host-pathogen communication.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Exploratory Grants (P20)
Project #
5P20RR015587-07
Application #
7381182
Study Section
Special Emphasis Panel (ZRR1-RI-8 (01))
Project Start
2006-06-01
Project End
2007-05-31
Budget Start
2006-06-01
Budget End
2007-05-31
Support Year
7
Fiscal Year
2006
Total Cost
$199,069
Indirect Cost
Name
University of Idaho
Department
Microbiology/Immun/Virology
Type
Schools of Earth Sciences/Natur
DUNS #
075746271
City
Moscow
State
ID
Country
United States
Zip Code
83844
Kuan, Man I; O'Dowd, John M; Fortunato, Elizabeth A (2016) The absence of p53 during Human Cytomegalovirus infection leads to decreased UL53 expression, disrupting UL50 localization to the inner nuclear membrane, and thereby inhibiting capsid nuclear egress. Virology 497:262-278
Zavala, Anamaria G; O'Dowd, John M; Fortunato, Elizabeth A (2016) Infection of a Single Cell Line with Distinct Strains of Human Cytomegalovirus Can Result in Large Variations in Virion Production and Facilitate Efficient Screening of Virus Protein Function. J Virol 90:2523-35
Kuan, Man I; O'Dowd, John M; Chughtai, Kamila et al. (2016) Human Cytomegalovirus nuclear egress and secondary envelopment are negatively affected in the absence of cellular p53. Virology 497:279-293
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Kashyap, Bhavani; Pegorsch, Laurel; Frey, Ruth A et al. (2014) Eye-specific gene expression following embryonic ethanol exposure in zebrafish: roles for heat shock factor 1. Reprod Toxicol 43:111-24
Kulkarni, Amit S; Fortunato, Elizabeth A (2014) Modulation of homology-directed repair in T98G glioblastoma cells due to interactions between wildtype p53, Rad51 and HCMV IE1-72. Viruses 6:968-85
Duan, Ying-Liang; Ye, Han-Qing; Zavala, Anamaria G et al. (2014) Maintenance of large numbers of virus genomes in human cytomegalovirus-infected T98G glioblastoma cells. J Virol 88:3861-73

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