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P J Dillon

Publications and source records attributed to P J Dillon.

26 records · Page 2Linked to original sources
PubMed1990

A cDNA for a protein that interacts with the human immunodeficiency virus Tat transactivator.

The human immunodeficiency virus (HIV) tat protein (Tat) is a positive regulator of virus gene expression and replication. Biotinylated Tat was used as a probe to screen a lambda gt11 fusion protein library, and a complementary DNA encoding a protein that interacts with Tat was cloned. Expression of this protein, designated TBP-1 (for Tat binding protein-1), was observed in a variety of cell lines, with expression being highest in human cells. TBP-1 was localized predominantly in the nucleus, which is consistent with the nuclear localization of Tat. In cotransfection experiments, expression of TBP-1 was able to specifically suppress Tat-mediated transactivation. The strategy described may be useful for direct identification and cloning of genes encoding proteins that associate with other proteins to modulate their activity in a positive or negative fashion.

ATPases Associated with Diverse Cellular Activitie↗
PubMed1990

Interaction of the human immunodeficiency virus type 1 Rev protein with a structured region in env mRNA is dependent on multimer formation mediated through a basic stretch of amino acids.

Interaction of the human immunodeficiency virus type 1 (HIV-1) Rev protein with a structured region within env mRNA (termed RRE) mediates the export of virus structural mRNAs from the nucleus to the cytoplasm. We show that the region encompassing the basic stretch of amino acids is essential for the ability of Rev to bind to RRE RNA and function in vivo. By use of a functional truncated Rev protein in conjunction with authentic Rev, effects on gel mobilities of the Rev-RRE RNA complex attributable to multimerization of Rev protein were observed. Rev proteins, unable to multimerize, failed to bind RRE RNA. Identification of Rev mutants capable of forming multimers, but unable to bind RRE RNA, suggests that the multimerization and RNA-binding domains can be distinguished and that multimerization is likely a prerequisite for formation of the RRE RNA-binding site. A mutant Rev protein, shown previously to function as a trans-dominant inhibitor of Rev function, bound to RRE RNA as a multimer to a similar extent as wild-type Rev. This observation is consistent with the hypothesis that regulation of HIV gene expression by Rev involves the interaction with cellular factors and that the trans-dominant Rev is probably defective in this function.

Amino Acid Sequence↗
PubMed1990

Function of the human immunodeficiency virus types 1 and 2 Rev proteins is dependent on their ability to interact with a structured region present in env gene mRNA.

The interaction of the human immunodeficiency virus type 1 (HIV-1) Rev protein with a structured region in env mRNA (the Rev-responsive element [RRE]) mediates the export of structural mRNAs from the nucleus to the cytoplasm. We demonstrated that unlike HIV-1 Rev, which functions with both the HIV-1 and HIV-2 RREs, HIV-2 Rev functions only with the HIV-2 RRE. Rev-RRE binding studies suggested that the lack of nonreciprocal complementation stems from the inability of HIV-2 Rev to interact with HIV-1 RRE RNA. Maintenance of RNA secondary structure, rather than the primary nucleotide sequence, appeared to be the major determinant for interaction of both HIV-1 and HIV-2 Rev with the HIV-2 RRE. Moreover, the binding domain of the HIV-2 RRE recognized by HIV-1 Rev was dissimilar to the binding domain of the HIV-1 RRE, in terms of both secondary structure and primary nucleotide sequence. Our results support the hypothesis that function of HIV Rev proteins and possibly the functionally similar Rex proteins encoded by the human T-cell leukemia viruses (HTLVs) HTLV-I and HTLV-II is controlled by the presence of RNA secondary structure generated within the RRE RNA.

Base Sequence↗
PubMed1989

Expression of five proteins from the Sendai virus P/C mRNA in infected cells.

The polycistronic P/C mRNA of Sendai virus is translated under cell-free conditions into five proteins (P, C', C, Y1, and Y2) from overlapping reading frames. In this study, we showed that in addition to the P, C', and C proteins, Y1 and Y2 were expressed by six different Sendai virus strains in infected cells. The Y proteins exhibited strain-specific variation in their gel mobility which corresponds to the variation seen in the cognate C proteins. While the relative levels of the P, C', and C proteins were consistent among various cell lines, the levels of Y1 and Y2 proteins varied among the cell lines used for viral infection.

Cell Line↗
PubMed1988

Early steps in the assembly of vesicular stomatitis virus nucleocapsids in infected cells.

The assembly of nucleocapsids is an essential step in the replicative cycle of vesicular stomatitis virus (VSV). In this study, we have examined the early events of vesicular stomatitis virus nucleocapsid assembly in BHK-21 cells. Nuclease-resistant intracellular nucleocapsids were isolated at various stages of assembly and analyzed for RNA and protein contents. The smallest ribonucleoprotein complex formed during nucleocapsid assembly contains the 5'-terminal 65 nucleotides of nascent viral RNA complexed with the viral proteins N and NS. Elongation of the assembling nucleocapsids proceeds unidirectionally towards the 3' terminus by the sequential addition of viral proteins which incrementally protect short stretches of the growing RNA chain. Pulse-chase studies show that the assembling nucleocapsids can be chased into full-length nucleocapsids which are incorporated into mature virions. Our results also suggest an involvement of the cytoskeletal framework during nucleocapsid assembly.

Animals↗
PubMedDate not supplied

Monitoring the results of Canada/U.S.A. acid rain control programs: some lake responses.

Aquatic acidification by deposition of airborne pollutants emerged as an environmental issue in southeastern Canada during the 1970s. Drawing information from the extensive research and monitoring programs, a sequence of issue assessments demonstrated the necessity of reducing the anthropogenic emissions of acidifying pollutants, particularly sulphur dioxide (SO2). The 1991 Canada-U.S. Air Quality Agreement (AQA) was negotiated to reduce North American SO2 emissions by approximately 40% relative to 1980 levels by 2010, and at present, both countries have reduced emissions beyond their AQA commitment. In response to reduced SO2 emissions, atmospheric deposition of sulphate (SO4(2-)) and SO4(2-) concentrations in many lakes have declined, particularly in south-central Ontario and southern Québec. Sulphate deposition still exceeds aquatic critical loads throughout southeastern Canada however. Increasing pH or alkalinity (commonly deemed 'recovery') has been observed in only some lakes. Several biogeochemical factors have intervened to modify the lake chemistry response to reduced SO4(2-) input, notably release of stored SO4(2-) from wetlands following periods of drought and reduction in the export of base cations from terrestrial soils. Three examples from Ontario are presented to illustrate these responses. Significant increases in pH and alkalinity have been observed in many lakes in the Sudbury area of Ontario due to the large reductions in local SO2 emissions; 'early-stage' biological recovery is evident in these lakes. An integrated assessment model predicts that AQA emission reductions will not be sufficient to promote widespread chemical or biological recovery of Canadian lakes. Monitoring and modeling are mutually supporting assessment activities and both must continue.

Acid Rain↗