Use of the degeneracy of the genetic code by selective pressure to cut up genes of procaryote genomes

The DNA sequences of three bacteriophages are analysed in order to localise those parts coding for a protein. A weak stability on the DNA molecule allows us to characterize the beginning and the end of genes. A survey of the codons used shows that the cause for this weak stability is the systematic use of A-T bases in third position, which is made possible by the degeneracy of the genetic code.     

What are the drivers of induction? Towards a Material Theory+

John Norton's Material Theory of Induction (Norton, 2003, 2005, 2008, forthcoming) has a two-fold, negative and positive, goal. The negative goal is to establish that formal logics of induction fail if they are understood as universally applicable schemas of induction. The positive goal is to establish that it is material facts that enable and justify inductive inferences. I argue in this paper that Norton is more successful with his negative than with his positive ambition. While I do not deny that facts constitute an important type of enabler and justifier of inductions, they are by no means the only type. This paper suggests that there are no less than six other types of background information scientists need and use to fuel and warrant inductions. The discussion of additional enablers and justifiers of inductions will further show there are practically important and intellectually challenging methodological issues Norton's theory prevents us from seeing because it leaves out this or that type of enabler and justifier.     

Late DNA replication in the sex chromosomes ofDidelphis virginiana

Zusammenfassung Autoradiographisch wurde die späte DNS-Synthese derX- undY-Chromosomen vonDidelphis virginiana (Virginia Opossum) in Knochenmarkzellen untersucht. Die weiblichen Tiere zeigen typische späte Reduplikationsmuster in einemX, die männlichen das späte Reduplikationsmuster inX undY und inY allein.

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This study was supported in part by research grant No. AM-02504 and training grant No. Tl-AM-5277, National Institutes of Health. Dr.Reiss was a predoctoral trainee, National Institute of Arthritis and Metabolic Diseases, U.S. Public Health Service.     

Construction, expression and recognition of an H-2 molecule lacking its carboxyl terminus

A mouse major histocompatibility antigen (H-2) gene, encoding a novel H-2Ld molecule lacking its intracytoplasmic domain, has been constructed and introduced into mouse L-cells. The novel H-2 molecule is found on the surface of the transfected cells at the same level as L-cells transfected with the native H-2Ld gene. Allo- and influenza-specific cytotoxic T lymphocytes can recognize the truncated H-2 gene product nearly as efficiently as the normal H-2Ld gene product. However, vesicular stomatitis virus-specific cytotoxic T lymphocytes recognize the truncated H-2Ld molecule less efficiently than the complete H-2Ld product. The rate of capping of the truncated H-2Ld molecule was investigated and found to be the same as that of the complete H-2Ld gene product.     

E-cadherin plays an essential role in collective directional migration of large epithelial sheets

In wound healing and development, large epithelial sheets migrate collectively, in defined directions, and maintain tight cell-cell adhesion. This type of movement ensures an essential function of epithelia, a barrier, which is lost when cells lose connection and move in isolation. Unless wounded, epithelial sheets in cultures normally do not have overall directional migration. Cell migration is mostly studied when cells are in isolation and in the absence of mature cell-cell adhesion; the mechanisms of the migration of epithelial sheets are less well understood. We used small electric fields (EFs) as a directional cue to instigate and guide migration of epithelial sheets. Significantly, cells in monolayer migrated far more efficiently and directionally than cells in isolation or smaller cell clusters. We demonstrated for the first time the group size-dependent directional migratory response in several types of epithelial cells. Gap junctions made a minimal contribution to the directional collective migration. Breaking down calcium-dependent cell-cell adhesion significantly reduced directional sheet migration. Furthermore, E-cadherin blocking antibodies abolished migration of cell sheets. Traction force analysis revealed an important role of forces that cells in the leading rows exert on the substratum. With EF, the traction forces of the leading edge cells coordinated in directional re-orientation. Our study thus identifies a novel mechanism--E-cadherin dependence and coordinated traction forces of leading cells in collective directional migration of large epithelial sheets.