Nonrandom integration of human U4 RNA pseudogenes.

Four loci for human U4 RNA have been characterized by DNA sequence analysis. The results show that all four loci represent pseudogenes, which are flanked by direct repeats. Three of the pseudogenes, designated U4/5, U4/6, and U4/8, have very similar structures; they are all truncated and contain the first 67 to 68 nucleotides of the U4 RNA sequence. Their properties suggest that they were created by integration of truncated cDNA copies of the U4 RNA into new chromosomal sites. An interesting observation was that their flanking regions exhibit sequence homology. A purine-rich 5'-flanking sequence 12 to 13 nucleotides long is almost perfectly conserved in all three loci. Boxes of homology were also found on the 3' side when the U4/6 and U4/8 loci were compared. The U4/4 locus has a slightly different structure; the pseudogene matches the first 79 nucleotides of U4 RNA, but contains a greater number of mutations than the other pseudogenes. Taken together, the results suggest that a frequently occurring type of pseudogene for human U4 was created by a RNA-mediated mechanism and that the integration sites have features in common.     

Human U1 small nuclear RNA pseudogenes do not map to the site of the U1 genes in 1p36 but are clustered in 1q12-q22.

Human U1 small nuclear RNA is encoded by approximately 30 gene copies. All of the U1 genes share several kilobases of essentially perfect flanking homology both upstream and downstream from the U1 coding region, but remarkably, for many U1 genes excellent flanking homology extends at least 24 kilobases upstream and 20 kilobases downstream. Class I U1 RNA pseudogenes are abundant in the human genome. These pseudogenes contain a complete but imperfect U1 coding region and possess extensive flanking homology to the true U1 genes. We mapped four class I pseudogenes by in situ hybridization to the long arm of chromosome 1, bands q12-q22, a region distinct from the site on the distal short arm of chromosome 1 to which the U1 genes have been previously mapped (Lund et al., Mol. Cell. Biol. 3:2211-2220, 1983; Naylor et al., Somat. Cell Mol. Genet. 10:307-313, 1984). We confirmed our in situ hybridization results by genomic blotting experiments with somatic cell hybrid lines with translocation products of human chromosome 1. These experiments provide further evidence that class I U1 pseudogenes and the true U1 genes are not interspersed. The results, along with those published elsewhere (Bernstein et al., Mol. Cell. Biol. 5:2159-2171, 1985), suggest that gene amplification may be responsible for the sequence homogeneity of the human U1 gene family.     

Cyclic AMP-induced inhibition of collagen lattice contraction by fibroblasts may be attenuated by both cyclic AMP dependent and independent mechanisms

The contraction of collagen lattices made with forskin fibroblasts in medium containing 1% fetal bovine serum was inhibited by intracelluar cyclic AMP raising drugs including cholera toxin (CT), forskolin, and dibutyryl-cAMP. The inhibition by CT was attenuated by insulin, acidic fibroblast growth factor (aFGF), and transforming growth factor-β (TGF-β). All three peptide factors have previously been reported to promote collagen lattice contraction by arterial smooth muscle cells and/or fibroblasts. Incubation of cells suspended in collagen gels with CT and forskolin resulted in a transient rise of the intracellular cyclic AMP levels, which peaked at 2 hr and 30 min, respectively, after drug exposure. Cholera toxin-induced intracellular cyclic AMP increase was attenuated by TGF-β, but not by aFGF and insulin, when added simultaneously. Thus, TGF-β may attenuate CT's inhibition on collagen lattice contraction by attenuating CTinduced intracellualr cyclic AMP increse, whereas the attenuation by insulin and aFGF on the inhibition of lattice contraction may be mediated by a cyclic AMPindependent mechannism. © 1993 Wiley-Liss, Inc.     

Nucleotide sequence and organization of full length human U4 RNA pseudogenes

Two loci encoding human U4 RNA, designated U4/7 and U4/14, have been isolated and sequenced. Both are pseudogenes in that their sequences do not match any identified human U4 RNA species perfectly. The U4/7 locus harbours a full-length pseudogene of 144 bp with eight base substitutions in the structural region. This pseudogene might be derived from a hitherto unidentified human U4 RNA gene. The second locus, U4/14, has a complex structure; the structural sequence of a U4 gene has apparently been integrated into an Alu sequence.     

Tip growth in plant cells may be amoeboid and not generated by turgor pressure

Cellular growth in higher plants is generated (powered) by internal turgor pressure. Basic physics shows that the pressure required to deform a plastic tube by elongation is inversely proportional to the tube''s diameter. Accordingly, the turgor required to drive tip growth of very narrow cylindrical plant cells becomes very high, probably too high to be realized in living cells. The non-involvement of turgor in tip growth is demonstrated directly in living diatoms secreting fine tubular spines of silica. In some species, the membrane at the tip of the rigid tube is deformed inwards into its lumen during normal extension, whereas in other species, many cells are partly plasmolysed during normal, active spine (''seta'') extension. Evidence from other cells is consistent with the general conclusion that turgor is not significant in tip growth. We support the alternative hypothesis proposed by M. Harold and colleagues that extension in tip cells can be amoeboid, driven by cycling of the actin cytoskeleton. Actively growing setae display an internal, fibrous, collar-like sleeve, probably of actin at the tip; it is visualized as a molecular treadmill (''nanomachine'') that uses as its support-base the rigid tube that has just been secreted. This scenario can thereby explain how the perfectly even diameter of very long, fine setae is maintained throughout their extension, even when their tips are far distant from the cell body.     

Nuclear ribonucleoprotein complexes containing U1 and U2 RNA.

Nuclear ribonucleoprotein (RNP) complexes that contain the U1 and U2 RNA of chromatin of Novikoff hepatoma cells were extracted with 0.01 M Tris-HCl (pH 8.0) after the nuclei were initially washed with 0.075 M NaCl and 0.025 M EDTA (pH 8.0). These RNP complexes were purified by chromatography on Sepharose 6B columns and centrifugation on sucrose density gradients. The identity of the U1 and U2 RNA in these particles was established by their electrophoretic mobility in polyacrylamide gels and their T1 RNase fingerprints which were identical with those of authentic U1 and U2 RNA (R. Reddy et al. (1974), J. Biol. Chem.249, 6486-6494; H. Shibata et al. (1974), Mol. Cell. Biochem. 4, 3-19). The nuclear riboncleoproteins had a buoyant density of 1.47 g/ml in CsCl gradients. Two-dimensional polyacrylamide gel electrophoresis of their proteins showed these RNP complexes contain 10 polypeptide spots, of which two are phosphorylated in vivo.     

Human sexual dimorphism in size may be triggered by environmental cues

Evolutionary biologists mostly assume that polygyny increases sexual dimorphism in size because, under polygyny, larger males monopolize mating opportunities and pass on their 'large male' genes to their sons. Available data on parent-child correlations in height among humans (Homo sapiens) do not support the crucial assumption that height is transmitted along sex lines. This paper instead suggests that human sexual dimorphism in size emerged, not because men got taller, but because women got shorter by undergoing early menarche in response to polygyny. It further speculates that, rather than genetically transmitted, the sexual dimorphism may emerge anew in each generation in response to the degree of polygyny in society. The analysis of comparative data supports the prediction that polygyny reduces women's height, but has no effect on men's, and is consistent with the speculation that the origin of human sexual dimorphism in size may be cultural, not genetic.     

Isolation of an active gene and of two pseudogenes for mouse U7 small nuclear RNA

Three U7 RNA-related sequences were isolated from mouse genomic DNA libraries. Only one of the sequences completely matches the published mouse U7 RNA sequence, whereas the other two apparently represent pseudogenes. The matching sequence represents a functional gene, as it is expressed after microinjection into Xenopus laevis oocytes. Sequence variations of the conserved cis-acting 5' and 3' elements of U RNA genes may partly explain the low abundance of U7 RNA.     

Carbon dynamics in topsoil and in subsoil may be controlled by different regulatory mechanisms

It is estimated that in excess of 50% of the soil carbon stock is found in the subsoil (below 20–30 cm). Despite this very few studies have paid attention to the subsoil. Although surface and subsurface horizons differ in pedological, environmental and physicochemical features, which are all likely to affect the mechanisms and biological actors involved, models of carbon dynamics tend to assume that the underlying processes are identical in all horizons, but with lower gross fluxes in the subsurface. The aim of this study was to test this assumption by analysing factors governing organic matter decomposition in topsoil (from depths of 5–10 cm) and subsoil (from depths of 80–100 cm). To this end, we established incubations that lasted 51 days, in which factors that were thought to control organic matter mineralization were altered: oxygen concentration, soil structure and the energetic and nutritional status. At the end of the incubation period, the microbial biomass was measured and the community level physiological profiles established. The mineralization per unit organic carbon proved to be as important in the subsoil as it was in surface samples, in spite of lower carbon contents and different catabolic profiles. Differences in the treatment effects indicated that the controls on C dynamics were different in topsoil and subsoil: disrupting the structure of the subsoil caused a 75% increase in mineralization while the surface samples remained unaffected. On the other hand, a significant priming affect was found in the topsoil but not in the subsoil samples. Spatial heterogeneity in carbon content, respiration and microbial communities was greater in subsoil than in topsoil at the field scale. These data suggest greater attention should be paid to the subsoil if global C dynamics is to be fully understood.