Anaerobic Degradation of Hexadecan-2-one by a Microbial Enrichment Culture under Sulfate-Reducing Conditions

A microbial enrichment culture from marine sediment was able to grow on hexadecan-2-one as the sole source of carbon and energy under sulfate-reducing conditions. Oxidation of the ketone involved carboxylation reactions and was coupled to sulfide production. This enrichment culture also grew on 6,10,14-trimethylpentadecan-2-one.     

Primary structure of a chitinase-encoding gene (chi1) from the filamentous fungus Aphanocladium album: similarity to bacterial chitinases

Chitinase 1 (Chil) is the major extracellular chitinase from the hyperparasitic fungus, Aphanocladium album. We determined the complete sequence of the chromosomal and cDNA copies of the structural gene (chi1) coding for Chil. The coding region is interrupted by three short introns (55, 53 and 49 bp long). Chil is 423 aa long and begins with a stretch of 34 aa not found in the mature protein. The Chil sequence presents overall similarities with bacterial chitinases from Serratia marcescens and Bacillus circulans. Compared with other chitinases, A. album Chi1 has only two short similarity regions (12 and 8 aa long), which are also found in bacterial, yeast and some plant chitinases.     

Adjuvant activity of monomeric bacterial cell wall peptidoglycans

We have previously shown that lysozyme solubilized cell walls of Mycobacteria or Nocardiae can replace whole mycobacterial cells or Wax D in Freund's complete adjuvant and it was found quite recently that hydrosoluble peptidoglycans, free of neutral sugars, are also adjuvant active. We show now that the simplest fragment tested — the disaccharide tetrapeptide (I) — increases circulating antibodies to ovalbumin and induces a delayed hypersensitivity toward this antigen. Similar compounds obtained from the basal layer of the cell wall of $\text{E. coli}$ are also active. Thus the immunoadjuvant activity of soluble cell wall peptidoglycans is a property of the monomeric unit and is not restricted to acid fast bacteria.     

Chicken hematopoietic cells transformed by seven strains of defective avian leukemia viruses display three distinct phenotypes of differentiation.

Chicken hematopoietic cells transformed in vitro and in vivo by seven strains of replication-defective avian leukemia viruses were assayed for the expression of six erythroid and five myeloid differentiation parameters, including differentiation-specific surface antigens as detected by newly developed antisera. The transformed cells were found to display three distinct phenotypes of differentiation. First, cells transformed by AEV resemble erythroblasts. They express heme, globin, carbonic anhydrase and erythrocyte cell surface antigen at low levels, and histone H5 and erythroblast cell surface antigen at high levels. Second, cells transformed by MC29, CMII, OK10 and MH2 viruses have macrophage-like properties. They strongly express Fc receptors, phagocytic capacity and macrophage cell surface antigen, but only weakly express myeloblast cell surface antigen and are negative for ATPase activity. Third, cells transformed by AMV and E26 viruses resemble myeloblasts in that they weakly express Fc receptors, phagocytic capacity and macrophage cell surface antigen but strongly express myeloblast cell surface antigen and ATPase activity. No difference was found between in vitro- and in vivo-transformed cells in the parameters tested. In light of recent genetic and biochemical evidence, we believe that these phenotypes reflect the action of three new types of viral-transforming genes, designated erb (erythroblast), mac (macrophage) and myb (myeloblast).     

The evolution of muscular parvalbumins investigated by the maximum parsimony method

Summary Phylogenetic trees requiring the lowest sum of nucleotide replacements and gene duplicative events were constructed from the amino acid sequence data on ten gnathostome parvalbumins (PAR) and two related myofibrillar proteins troponin-C (TNC) and myosin alkali-light-chain (ALC). The origin and differentiation of the structural domains within these proteins were also investigated by the maximum parsimony method and by an alignment statistic for identifying evolutionarily related protein sequences. The results suggest, in agreement with the Weeds-McLachlan model, that tandem duplications in a precursor gene caused a primordial one-domain polypeptide (consisting of two helices with a calcium binding region in between) to double and then quadruple in size. Duplications of the gene coding for this four domain (I–II–III–IV) protein in an early metazoan, pre-gnathostome lineage gave rise to the separate loci for TNC, ALC, and PAR. TNC, which alone retained the Ca-binding function in each of its four domains, evolved much more slowly than either the ALC or PAR lineages. In the PAR lineage the I–II–III–IV structure was degraded, presumably by a partial gene deletion, to the II–III–IV structure during descent to the gnathostome ancestor of parvalbumins. Also during this period the mid region in domain II lost its Ca-binding function and, as it did so, evolved at an accelerated rate over other regions, a pattern indicative of positive selection for a change in function. In turn, from the gnathostome ancestor to the present, the mid regions of domains III and IV, which each retained Ca-bindung function, evolved much more slowly than other regions, a pattern indicative of stabilizing selection for preservation of function. Between the gnathostome and teleost-tetrapod ancestor a gene duplication separated the parvalbumins into an-lineage and a-lineage. During this early vertebrate period PAR genes evolved at the extremely fast rate of 89 nucleotide replacements per 100 codons per 10⁸ years (i.e. 89 NR %), but from the teleost-tetrapod ancestor to the present, both- and-PAR lineages evolved at a much slower rate, about 8 NR %. The use of-parvalbumins as phylogenetic markers was complicated by presumptive evidence that paralogous (i.e. duplication dependent) gene lineages occur within this group. As a final point, in the genealogy of TNC, ALC, and PAR lineages, a non-random pattern of nucleotide replacements was observed between the reconstructed ancestral and descendant mRNA sequences. The pattern was similar to that observed for other protein genealogies and seems to reflect a bias in the genetic code for guanine to adenine and adenine to guanine transitions (especially at the first nucleotide position of the RNA codons) to produce amino acid substitutions which are compatible with the preservation of protein three-dimensional structure.     

Characteristics of a new binding protein distinct from the kinase for guanosine 3′:5′-monophosphate in rat platelets

A new type of cyclic GMP binding protein was recently identified in our laboratory (Hamet, P. and Coquil, J.-F. (1978) J. Cyclic Nucleotide Res. 4, 281–290). The binding, recovered in the supernatant fractions, is highly specific for cyclic GMP and is clearly distinct from the binding to cyclic GMP-dependent protein kinase. Chromatography on DEAE-Sepharose separated the cyclic GMP binding protein from cyclic AMP binding, cyclic AMP-dependent kinase activities, and from guanylate cyclase. The optimal binding occurs at high pH and in the presence of thiol reagents. Several phosphodiesterase inhibitors increase the affinity of binding (K_d was 353 ± 60 nM in the absence and 13.4 ± 1.5 nM in the presence of 1-methyl-3-isobutyl-xanthine). The molecular weight of the binding protein was determined to be about 176 000 and the sedimentation coefficient was 6.4 S. While the binding and phosphodiesterase activities co-migrated on DEAE-Sepharose, gel filtration and sucrose gradients, certain treatments (such as increasing the concentrations of salt and heating) were able to influence one activity while having no effect on the other. Hence, the binding activity may be involved in the regulation of the activity of cyclic GMP phosphodiesterase. Since the binding protein appears to be the only ‘receptor’ for cyclic GMP detectable in platelets, this protein and/or its relation to cyclic GMP phosphodiesterase may play a role in the mechanism of action of cyclic GMP in platelets.     

National forest cover change in Congo Basin: deforestation,reforestation, degradation and regeneration for the years 1990, 2000 and 2005

This research refers to an object‐based automatic method combined with a national expert validation to produce regional and national forest cover change statistics over Congo Basin. A total of 547 sampling sites systematically distributed over the whole humid forest domain are required to cover the six Central African countries containing tropical moist forest. High resolution imagery is used to accurately estimate not only deforestation and reforestation but also degradation and regeneration. The overall method consists of four steps: (i) image automatic preprocessing and preinterpretation, (ii) interpretation by national expert, (iii) statistic computation and (iv) accuracy assessment. The annual rate of net deforestation in Congo Basin is estimated to 0.09% between 1990 and 2000 and of net degradation to 0.05%. Between 2000 and 2005, this unique exercise estimates annual net deforestation to 0.17% and annual net degradation to 0.09%. An accuracy assessment reveals that 92.7% of tree cover (TC) classes agree with independent expert interpretation. In the discussion, we underline the direct causes and the drivers of deforestation. Population density, small‐scale agriculture, fuelwood collection and forest's accessibility are closely linked to deforestation, whereas timber extraction has no major impact on the reduction in the canopy cover. The analysis also shows the efficiency of protected areas to reduce deforestation. These results are expected to contribute to the discussion on the reduction in CO₂ emissions from deforestation and forest degradation (REDD+) and serve as reference for the period.     

Optimal Constrained Stationary Intervention in Gene Regulatory Networks

A key objective of gene network modeling is to develop intervention strategies to alter regulatory dynamics in such a way as to reduce the likelihood of undesirable phenotypes. Optimal stationary intervention policies have been developed for gene regulation in the framework of probabilistic Boolean networks in a number of settings. To mitigate the possibility of detrimental side effects, for instance, in the treatment of cancer, it may be desirable to limit the expected number of treatments beneath some bound. This paper formulates a general constraint approach for optimal therapeutic intervention by suitably adapting the reward function and then applies this formulation to bound the expected number of treatments. A mutated mammalian cell cycle is considered as a case study.