A global view of the selectivity of zinc deprivation and excess on genes expressed in human THP-1 mononuclear cells.

Among the micronutrients required by humans, zinc has particularly divergent modes of action. cDNA microarray and quantitative PCR technologies were used to investigate the zinc responsiveness of known genes that influence zinc homeostasis and to identify, through global screening, genes that may relate to phenotypic outcomes of altered dietary zinc intake. Human monocytic/macrophage THP-1 cells were either acutely zinc depleted, using a cell-permeable zinc-specific chelator, or were supplemented with zinc to alter intracellular zinc concentrations. Initially, genes associated with zinc homeostasis were evaluated by quantitative PCR to establish ranges for fold changes in transcript abundance that might be expected with global screening. Zinc transporter-1 and zinc transporter-7 expression increased when cellular zinc increased, whereas Zip-2 expression, the most zinc-responsive gene examined, was markedly increased by zinc depletion. Microarrays composed of approximately 22,000 elements were used to identify those genes responsive to either zinc depletion, zinc supplementation, or both conditions. Hierarchal clustering and ANOVA revealed that approximately 5% or 1,045 genes were zinc responsive. Further sorting based on this pattern of the zinc responsiveness of these genes into seven groups revealed that 104 genes were linearly zinc responsive in a positive mode (i.e., increased expression as cellular zinc increases) and 86 genes that were linearly zinc responsive in a negative mode (i.e., decreased expression as cellular zinc increases). Expression of some genes was responsive to only zinc depletion or supplementation. Categorization by function revealed numerous genes needed for host defense were among those identified as zinc responsive, including cytokine receptors and genes associated with amplification of the Th1 immune response.

Potato yellow mosaic virus: a synonym of tomato yellow mosaic virus.

Tomato yellow mosaic was first described in 1963, as a disease caused by a geminivirus transmitted by the whitefly Bemisia tabaci in Venezuela. In 1981 and 1985, Tomato yellow mosaic virus (ToYMV) was reported to occasionally infect potato plants growing in the proximity of tomato plantings affected by this virus. Despite these previous reports, a virus isolated from yellow mosaic-affected potato plants in Venezuela, was described in 1986 as a "new geminivirus" called potato yellow mosaic virus (PYMV). In recent years, different geminiviruses related to PYMV have been described from tomato fields in Venezuela and other countries in the Caribbean Basin, including Panama. Comparative nucleotide and amino acid sequence analyses of a 1698 bp fragment amplified from the common region and part of the AV1 and AC1 ORFs of ToYMV from Venezuela, yielded 95.7% sequence identity with the corresponding regions of PYMV. Nucleotide and amino acid sequence identities between ToYMV and PYMV, were 96.3% and 95.1% for AC1, and 95.7% and 100% for AV1, respectively. The identity of the nucleotide sequence for the common region of ToYMV and PYMV was 96.5%. Comparative sequence analyses conducted with ToYMV and other tomato begomoviruses present in the Caribbean region, showed only distant relationships. It is concluded here that PYMV is a synonym of ToYMV.