Source, concentration, and distribution of elemental mercury in the atmosphere in Toronto, Canada.

Atmospheric gaseous elemental mercury [GEM] at 1.8, 4, and 59 m above ground, in parking lots, and in indoor and outdoor air was measured in Toronto City, Canada from May 2008-July 2009. The average GEM value at 1.8 m was 1.89 ± 0.62 ng m(-3). The GEM values increased with elevation. The average GEM in underground parking lots ranged from 1.37 to 7.86 ng m(-3) and was higher than those observed from the surface parking lots. The GEM in the indoor air ranged from 1.21 to 28.50 ng m(-3), was higher in the laboratories than in the offices, and was much higher than that in the outdoor air. All these indicate that buildings serve as sources of mercury to the urban atmosphere. More studies are needed to estimate the contribution of urban areas to the atmospheric mercury budget and the impact of indoor air on outdoor air quality and human health.

The QUTA activator and QUTR repressor proteins of Aspergillus nidulans interact to regulate transcription of the quinate utilization pathway genese.

Genetic evidence suggests that the activity of the native QUTA transcription activator protein is negated by the action of the QUTR transcription repressor protein. When Aspergillus nidulans was transformed with plasmids containing the wild-type qutA gene, transformants that constitutively expressed the quinate pathway enzymes were isolated. The constitutive phenotype of these transformants was associated with an increased copy number of the transforming qutA gene and elevated qutA mRNA levels. Conversely, when A. nidulans was transformed with plasmids containing the qutR gene under the control of the constitutive pgk promoter, transformants with a super-repressed phenotype (unable to utilize quinate as a carbon source) were isolated. The super-repressed phenotype of these transformants was associated with an increased copy number of the transforming qutR gene and elevated qutR mRNA levels. These copy-number-dependent phenotypes argue that the levels of the QUTA and QUTR proteins were elevated in the high-copy-number transformants. When diploid strains were formed by combining haploid strains that contained high copy numbers of either the qutA gene (constitutive phenotype) or the qutR gene (super-repressing; non-inducible phenotype), the resulting diploid phenotype was one of quinate-inducible production of the quinate pathway enzymes, in a manner similar to wild-type. The simplest interpretation of these observations is that the QUTR repressor protein mediates its repressing activity through a direct interaction with the QUTA activator protein. Other possible interpretations are discussed in the text. Experiments in which truncated versions of the QUTA protein were produced in the presence of a wild-type QUTA protein indicate that the QUTR repressor protein recognizes and binds to the C-terminal half of the QUTA activator protein.