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<jats:p>Despite myriads of biological activities ascribed to uteroglobin (UG), a steroid-inducible secreted protein, its physiological functions are unknown. Mice in which the uteroglobin gene was disrupted had severe renal disease that was associated with massive glomerular deposition of predominantly multimeric fibronectin (Fn). The molecular mechanism that normally prevents Fn deposition appears to involve high-affinity binding of UG with Fn to form Fn-UG heteromers that counteract Fn self-aggregation, which is required for abnormal tissue deposition. Thus, UG is essential for maintaining normal renal function in mice, which raises the possibility that an analogous pathogenic mechanism may underlie genetic Fn-deposit human glomerular disease.</jats:p>

<jats:p>A human nuclear protein that specifically interacts with the constitutive transport element (CTE) of simian retrovirus was identified as adenosine 5′-triphosphate–dependent RNA helicase A. This protein could bind to functional CTE but not to inactive CTE mutants. The interaction of helicase A with CTE was distinct from previously described helicase activity of this protein. Helicase A shuttled from the nucleus to the cytoplasm in the presence of a transcription inhibitor or in cells transiently overexpressing CTE-containing RNA. In vivo colocalization of helicase A and CTE was observed in experiments that combined in situ hybridization and immunostaining. These results suggest that helicase A plays a role in the nuclear export of CTE-containing RNA.</jats:p>

<jats:p>Expansins are extracellular proteins that increase plant cell wall extensibility in vitro. Beads loaded with purified expansin induced bulging on the leaf-generating organ, the apical meristem, of tomato plants. Some of these bulges underwent morphogenesis to produce leaflike structures, resulting in a reversal of the direction of phyllotaxis. Thus, expansin can induce tissue expansion in vivo, and localized control of tissue expansion may be sufficient to induce leaf formation. These results suggest a role for biophysical forces in the regulation of plant development.</jats:p>

<jats:p>STAT (signal transducers and activators of transcription) proteins undergo cytokine-dependent phosphorylation on serine and tyrosine. STAT3, a transcription factor for acute phase response genes, was found to act as an adapter molecule in signal transduction from the type I interferon receptor. STAT3 bound to a conserved sequence in the cytoplasmic tail of the IFNAR1 chain of the receptor and underwent interferon-dependent tyrosine phosphorylation. The p85 regulatory subunit of phosphatidylinositol 3-kinase, which activates a series of serine kinases, bound to phosphorylated STAT3 and subsequently underwent tyrosine phosphorylation. Thus, STAT3 acts as an adapter to couple another signaling pathway to the interferon receptor.</jats:p>

<jats:p> The dominant exported proteins and protective antigens of <jats:italic>Mycobacterium tuberculosis</jats:italic> are a triad of related gene products called the antigen 85 (Ag85) complex. Each has also been implicated in disease pathogenesis through its fibronectin-binding capacities. A carboxylesterase domain was found within the amino acid sequences of Ag85A, B, and C, and each protein acted as a mycolyltransferase involved in the final stages of mycobacterial cell wall assembly, as shown by direct enzyme assay and site-directed mutagenesis. Furthermore, the use of an antagonist (6-azido-6-deoxy-α,α′-trehalose) of this activity demonstrates that these proteins are essential and potential targets for new antimycobacterial drugs. </jats:p>

<jats:p>No growth factors specific for the lymphatic vascular system have yet been described. Vascular endothelial growth factor (VEGF) regulates vascular permeability and angiogenesis, but does not promote lymphangiogenesis. Overexpression of VEGF-C, a ligand of the VEGF receptors VEGFR-3 and VEGFR-2, in the skin of transgenic mice resulted in lymphatic, but not vascular, endothelial proliferation and vessel enlargement. Thus, VEGF-C induces selective hyperplasia of the lymphatic vasculature, which is involved in the draining of interstitial fluid and in immune function, inflammation, and tumor metastasis. VEGF-C may play a role in disorders involving the lymphatic system and may be of potential use in therapeutic lymphangiogenesis.</jats:p>

<jats:p>Human and bovine capillary endothelial cells were switched from growth to apoptosis by using micropatterned substrates that contained extracellular matrix-coated adhesive islands of decreasing size to progressively restrict cell extension. Cell spreading also was varied while maintaining the total cell-matrix contact area constant by changing the spacing between multiple focal adhesion-sized islands. Cell shape was found to govern whether individual cells grow or die, regardless of the type of matrix protein or antibody to integrin used to mediate adhesion. Local geometric control of cell growth and viability may therefore represent a fundamental mechanism for developmental regulation within the tissue microenvironment.</jats:p>

<jats:p>In the vertebrate brain, neurons grouped in parallel laminae receive distinct sets of synaptic inputs. In the avian optic tectum, arbors and synapses of most retinal axons are confined to 3 of 15 laminae. The adhesion molecule N-cadherin and cell surface glycoconjugates recognized by a plant lectin are selectively associated with these “retinorecipient” laminae. The lectin and a monoclonal antibody to N-cadherin perturbed laminar selectivity in distinct fashions. In contrast, neurotrophins increased the complexity of retinal arbors without affecting their laminar distribution. Thus, cell surface molecules and soluble trophic factors may collaborate to shape lamina-specific arbors in the brain, with the former predominantly affecting their position and the latter their size.</jats:p>

<jats:p> Ecologists have fiercely debated for many decades whether populations are self-regulated by density-dependent biological mechanisms or are controlled by exogenous environmental forces. Here, a stochastic mechanistic model is used to show that the interaction of these two forces can explain observed large fluctuations in Dungeness crab ( <jats:italic>Cancer magister</jats:italic> ) numbers. Relatively small environmental perturbations interact with realistic nonlinear (density dependent) biological mechanisms, to produce dynamics that are similar to observations. This finding has implications throughout population biology, suggesting both that the study of deterministic density-dependent models is highly problematic and that stochastic models must include biologically relevant nonlinear mechanisms. </jats:p>