PubMed Health⌕ Search

Biomedical subjects

L Paolozzi

Publications and source records attributed to L Paolozzi.

47 records · Page 3Linked to original sources

Restoration of ligase activity in E. coli K12 lig ts7 strain by bacteriophage Mu and cloning of a DNA fragment harbouring the Mu 'lig' gene.

Restoration of ligase activity has been observed in E. coli K12 ligts7 strain lysogenic for Mu, in presence as well in absence of lysogenic immunity. This restoration consist in phenotypic reversal of temperature sensitivity of E. coli ligts7 which also regain the ability to sustain the complete growth cycle of T4 lig-phages. It is possible to put under the control of the gal operon the expression of the viral gene responsible for the restoration effect. This new gene of Mu has been named 'lig'. A 5 kb fragment responsible for the reported effects and localized between genes gam and lys of Mu genome has been cloned in pBR322. This recombinant plasmid used for transforming ligts7 strain restores in it normal behaviour for ligation of Okazaki pieces.

Bacteriophage mu↗

Restoration of DNA synthesis at non-permissive temperature and of UV resistance induced by bacteriophage Mu in Escherichia coli lig ts7 strain.

Infected by Mu, a mutant of E. coli, carrying the mutation lig ts7 shows a UV sensitivity intermediate between that of the uninfected lig-strain and that of the parental lig+ strain. At non-permissive temperature bacterial DNA replication is restored upon infection. These results suggest that DNA-ligase activity is coded for by the phage Mu genome.

Coliphages↗

Mechanism of phage Mu-1 integration: nalidixic acid treatment causes clustering of Mu-1-induced mutations near replication origin.

Frequencies of Mu-1-induced mutants of Escherichia coli have been compared under two different experimental conditions: cells in exponential growth and the same cells treated with nalidixic acid. The average of values obtained from the nalidixic acid-treated culture is 3 times higher than that obtained from the control. Individual ratios of the frequency of mutants in the two cultures yield decreasing values from 6 to 1, starting from the point of origin of DNA replication to the termini of DNA replication. These results are compatible with the idea that Mu-1 integrates at the replication fork.

Coliphages↗

Synchronous division induced in Escherichia coli K12 by phage Mu: analysis of DNA topology and gene expression during the cell cycle.

Bacteriophage Mu mutants in gene gem (Mu gemts2) induce cycles of synchronous divisions after infection of a bacterial population in steady-state conditions. In this paper, two classes of gyrB mutants, synchronizable and non-synchronizable, are described. The existence of the non-synchronizable class suggests that the gyrase B subunit is involved with Gem in the process of synchronization. Cyclical variations in DNA topology of a resident multicopy plasmid occur during synchronous growth and correlate with a modulation of the chromosomal lacZ gene expression. Transcription data for the cell division genes, ftsZ and envA, obtained studying first steps in synchronous growth after infection, show that synthesis of the two mRNA is not constant. The specific mRNA of envA seems to be stimulated soon after infection, whereas the two transcripts initiating upstream from ftsZ apparently decrease to a basal level. In both cases, however, synthesis of the mRNA virtually doubles at the time of cell division.

Bacteriophage mu↗

Mu gem2ts DNA integration is not necessary for induction of synchrony of cell division in Escherichia coli K12.

The gem2ts mutant of bacteriophage Mu induced synchrony of cell division on bacteria surviving infection. Induction of synchronous growth could also be observed as a response to the entire infected bacterial population, as in the case of infection of hic mutants, a peculiar class of gyrB alleles. After Mu wild-type or Mu gem2ts infection of hic mutants, there was a lack of viral DNA integration and replication, while phage gene expression (including that of A gene, coding for the transposase) seemed to be quite normal. These data indicate that the mechanism of bacterial synchronization induced by Mu gem2ts does not require integration nor replication of the phage DNA.

Bacteriophage mu↗

Tiopronine-induced reduction of rheumatoid factor functional affinity and asialylated IgG in patients with rheumatoid arthritis.

Serum and synovial fluid (SF) from 16 rheumatoid arthritis patients were evaluated before and after a 2-month treatment with tiopronine (TP). The levels of rheumatoid factor (RF) declined, as did the functional affinity of the remaining RF (p less than 0.01 in serum and p less than 0.05 in SF). Concomitant restoration of the sialylation of IgG was observed (p less than 0.05 in serum and SF). Following an initial increase, a significant reduction was observed in the level of soluble interleukin-2 receptors in serum (p less than 0.05) and SF (p less than 0.05) after treatment with TP.

Adult↗

A possible linkage of HLA-DRB haplotypes with Tiopronin intolerance in rheumatoid arthritis.

To investigate the relationship between HLA class II genotypes and toxic intolerance during treatment with Tiopronin, a slow-acting drug used in the treatment of rheumatoid arthritis (RA), we studied 40 patients who were divided into two groups: a group of 22 patients without side effects and a group of 18 patients with intolerance to Tiopronin. The PCR-RFLP method was used to determine the HLA-DR, DQ and DP genotypes. The patients in the two groups had similar genetic backgrounds with an expected high frequency of DRI and DR4 alleles. However, DR1/DR4 heterozygosity was significantly increased in patients with intolerance (p = 0.03, Odds Ratio = 10.5). In addition, one intolerant patient had a DR1/DR7 genotype which shared DRw53 (DRB4*0101) with DR1/DR4. Furthermore, two subtypes of DR5, DRB1*1102 and DRB1*1201, were increased among intolerant patients (11.1% vs 0%, p = 0.03, OR = 13.97). In total, DR1/DRw53 heterozygotes, DRB1*1102 and DRB1*1201 represented 61.1% of intolerant patients. Therefore, a detailed HLA class II typing might be useful before RA treatment by Tiopronin to predict and avoid toxic side effects in the patients with increased risk. Further investigation is currently underway.

Adult↗