On thein vitro corticotropin releasing factor (CRF) activity of the heptapeptide: Methionyl-glutaminyl-histidyl-phenylalanyl-arginyl-tryptophyl-glycine

Résumé Au cours d'une série d'expériences décrites en détail nous avons observé le phénomène suivant: l'heptapeptide H-Met-Glu(NH₂)-His-Phe-Arg-Try-Gly-OH est susceptible d'augmenterin vitro, de façon statistiquement significative, la libération de corticotropine par des antéhypophyses de rat isolées.     

Epimutation of the telomeric imprinting center region on chromosome 11p15 in Silver-Russell syndrome

Silver-Russell syndrome (SRS, OMIM 180860) is a congenital disorder characterized by severe intrauterine and postnatal growth retardation, dysmorphic facial features and body asymmetry. SRS is genetically heterogenous with maternal uniparental disomy with respect to chromosome 7 occurring in approximately 10% of affected individuals. Given the crucial role of the 11p15 imprinted region in the control of fetal growth, we hypothesized that dysregulation of genes at 11p15 might be involved in syndromic intrauterine growth retardation. We identified an epimutation (demethylation) in the telomeric imprinting center region ICR1 of the 11p15 region in several individuals with clinically typical SRS. This epigenetic defect is associated with, and probably responsible for, relaxation of imprinting and biallelic expression of H19 and downregulation of IGF2. These findings provide new insight into the pathogenesis of SRS and strongly suggest that the 11p15 imprinted region, in addition to those of 7p11.2-p13 and 7q31-qter, is involved in SRS.     

Inactivation of cystathionase and of cysteine sulfinic acid decarboxylase by proteolytic enzymes: Effect of pyridoxal phosphate

Résumé Les résultats obtenus lors de l'étude de la protéolyse, par la trypsine, l'-chymotrypsine et la pronase, de préparations partiellement purifiées de cystathionase et de décarboxylase de l'acide cysteine sulfinique sont décrits. Il apparait que, pour la cystathionase, la sensibilité à la protéolyse est différente selon que l'on utilise l'apoenzyme ou l'holoenzyme.     

Transposition of an antibiotic resistance element in mycobacteria

Bacterial resistance to antibiotics is often plasmid-mediated and the associated resistance genes encoded by transposable elements. Mycobacteria, including the human pathogens Mycobacterium tuberculosis and M. leprae, are resistant to many antibiotics, and their cell-surface structure is believed to be largely responsible for the wide range of resistance phenotypes. Antibiotic-resistance plasmids have so far not been implicated in resistance of mycobacteria to antibiotics. Nevertheless, antibiotic-modifying activities such as aminoglycoside acetyltransferases and phosphotransferases have been detected in fast-growing species. beta-lactamases have also been found in most fast- and slow-growing mycobacteria. To date no mycobacterial antibiotic-resistance genes have been isolated and characterized. We now report the isolation, cloning and sequencing of a genetic region responsible for resistance to sulphonamides in M. fortuitum. This region also contains an open reading frame homologous to one present in Tn1696 (member of the Tn21 family) which encodes a site-specific integrase. The mycobacterial resistance element is flanked by repeated sequences of 880 base pairs similar to the insertion elements of the IS6 family found in Gram+ and Gram- bacteria. The insertion element is shown to transpose to different sites in the chromosome of a related fast-growing species, M. smegmatis. The characterization of this element should permit transposon mutagenesis in the analysis of mycobacterial virulence and related problems.