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<jats:p> The steady state of histone acetylation is established and maintained by multiple histone acetyltransferases and deacetylases, and this steady state affects chromatin structure and function. The identification of a maize complementary DNA encoding the chromatin-bound deacetylase HD2 is reported. This protein was not homologous to the yeast <jats:italic>RPD3</jats:italic> transcriptional regulator. It was expressed throughout embryo germination in correlation with the proliferative activity of cells. Antibodies against recombinant HD2-p39 immunoprecipitated the native enzyme complex, which was composed of phosphorylated p39 subunits. Immunofluorescence microscopy and sequence homologies suggested nucleolar localization. HD2 is an acidic nucleolar phosphoprotein that might regulate ribosomal chromatin structure and function. </jats:p>

<jats:p> The plant growth regulator gibberellin (GA) has a profound effect on shoot development and promotes developmental transitions such as flowering. Little is known about any analogous effect GA might have on root development. In a screen for mutants, <jats:italic>Arabidopsis</jats:italic> plants carrying a mutation designated <jats:italic>pickle</jats:italic> ( <jats:italic>pkl</jats:italic> ) were isolated in which the primary root meristem retained characteristics of embryonic tissue. Expression of this aberrant differentiation state was suppressed by GA. Root tissue from plants carrying the <jats:italic>pkl</jats:italic> mutation spontaneously regenerated new embryos and plants. </jats:p>

<jats:p>Bovine spongiform encephalopathy (BSE) has become a public health issue because a recently evolved BSE agent has infected people, yielding an unusual form of Creutzfeld-Jakob disease (CJD). A new CJD agent that provokes similar amyloid plaques and cerebellar pathology was serially propagated. First-passage rats showed obvious clinical signs and activated microglia but had negligible PrP-res (the more protease-resistant form of host PrP) or cerebellar lesions. Microglia and astrocytes may participate in strain selection because the agent evolved, stabilized, and reproducibly provoked BSE-like disease in subsequent passages. Early vacuolar change involving activated microglia and astrocytes preceded significant PrP-res accumulation by more than 50 days. These studies reveal several inflammatory host reactions to an exogenous agent.</jats:p>

<jats:p> The immunosuppressant rapamycin interferes with G <jats:sub>1</jats:sub> -phase progression in lymphoid and other cell types by inhibiting the function of the mammalian target of rapamycin (mTOR). mTOR was determined to be a terminal kinase in a signaling pathway that couples mitogenic stimulation to the phosphorylation of the eukaryotic initiation factor (eIF)-4E–binding protein, PHAS-I. The rapamycin-sensitive protein kinase activity of mTOR was required for phosphorylation of PHAS-I in insulin-stimulated human embryonic kidney cells. mTOR phosphorylated PHAS-I on serine and threonine residues in vitro, and these modifications inhibited the binding of PHAS-I to eIF-4E. These studies define a role for mTOR in translational control and offer further insights into the mechanism whereby rapamycin inhibits G <jats:sub>1</jats:sub> -phase progression in mammalian cells. </jats:p>

<jats:p>The importance of terrestrial-aquatic linkages was evaluated by a large-scale, 3-year exclusion of terrestrial leaf litter inputs to a forest stream. Exclusion of leaf litter had a strong bottom-up effect that was propagated through detritivores to predators. Most invertebrate taxa in the predominant habitat declined in either abundance, biomass, or both, compared with taxa in a nearby reference stream. However, fauna in moss habitats changed little, indicating that different food webs exist in habitats of different geomorphology. Thus, the ecosystem-level consequences of excluding detrital inputs to an ecosystem were demonstrated. Inputs of riparian detritus are essential for conservation or restoration of diverse stream food webs.</jats:p>

<jats:p> The pathogenic yeast <jats:italic>Candida albicans</jats:italic> regulates its cellular morphology in response to environmental conditions. Ellipsoidal, single cells (blastospores) predominate in rich media, whereas filaments composed of elongated cells that are attached end-to-end form in response to starvation, serum, and other conditions. The <jats:italic>TUP1</jats:italic> gene, which encodes a general transcriptional repressor in <jats:italic>Saccharomyces cerevisiae</jats:italic> , was isolated from <jats:italic>C. albicans</jats:italic> and disrupted. The resulting <jats:italic>tup1</jats:italic> mutant strain of <jats:italic>C. albicans</jats:italic> grew exclusively as filaments under all conditions tested. <jats:italic>TUP1</jats:italic> was epistatic to the transcriptional activator <jats:italic>CPH1</jats:italic> , previously found to promote filamentous growth. The results suggest a model where <jats:italic>TUP1</jats:italic> represses genes responsible for initiating filamentous growth and this repression is lifted under inducing environmental conditions. </jats:p>

<jats:p>Hepatocyte nuclear factors 1 and 4 (HNF-1 and HNF-4) are liver-enriched transcription factors that function in the regulation of several liver-specific genes. HNF-1 activates genes containing promoters with HNF-1 binding sites. However, this factor negatively regulates its own expression and that of other HNF-4–dependent genes that lack HNF-1 binding sites in their promoter region. This repression is exerted by a direct interaction of HNF-1 with AF2, the main activation domain of HNF-4. The dual functions of gene activation and repression suggest that HNF-1 is a global regulator of the transcriptional network involved in the maintenance of hepatocyte-specific phenotype.</jats:p>

<jats:p> Highly active antiretroviral therapy (HAART) increases CD4 <jats:sup>+</jats:sup> cell numbers, but its ability to correct the human immunodeficiency virus (HIV)–induced immune deficiency remains unknown. A three-phase T cell reconstitution was demonstrated after HAART, with: (i) an early rise of memory CD4 <jats:sup>+</jats:sup> cells, (ii) a reduction in T cell activation correlated to the decreasing retroviral activity together with an improved CD4 <jats:sup>+</jats:sup> T cell reactivity to recall antigens, and (iii) a late rise of “naı̈ve” CD4 <jats:sup>+</jats:sup> lymphocytes while CD8 <jats:sup>+</jats:sup> T cells declined, however, without complete normalization of these parameters. Thus, decreasing the HIV load can reverse HIV-driven activation and CD4 <jats:sup>+</jats:sup> T cell defects in advanced HIV-infected patients. </jats:p>

<jats:p> A major fraction of ambient particulate matter arises from atmospheric gas-to-particle conversion. Attempts to reduce particulate matter levels require control of the same organic and nitrogen oxide (NO <jats:sub> <jats:italic>x</jats:italic> </jats:sub> ) emissions that are precursors to urban and regional ozone formation. Modeling of the gas-aerosol chemical interactions that govern levels of particulate components showed that control of gas-phase organic and NO <jats:sub> <jats:italic>x</jats:italic> </jats:sub> precursors does not lead to proportionate reductions of the gas-phase–derived components of atmospheric particles. The chemical coupling between ozone and particulate matter has implications for strategies to achieve the new ozone and particulate matter standards proposed by the U.S. Environmental Protection Agency. </jats:p>