PubMed Health⌕ Search

Biomedical subjects

E Roulet

Publications and source records attributed to E Roulet.

42 records · Page 3Linked to original sources

Phage Mu transposase: deletion of the carboxy-terminal end does not abolish DNA-binding activity.

We demonstrate that a specific site on the transposase protein, pA, of bacteriophage Mu is highly susceptible to proteolytic cleavage. Cleavage is observed in a minicell system on solubilisation with the non-ionic detergent Triton X-100 or following addition of a solubilised minicell preparation to pA synthesised in a cell-free coupled transcription/translation system. Cleavage occurs at the carboxy-terminal end of the protein and generates a truncated polypeptide of 64 kDa, pA*, which retains some of the DNA-binding properties of pA. These results suggest that pA may be divided into functional domains for DNA binding and for interaction with the proteins involved in phage replication.

Bacteriophage mu↗

Preferential binding of bacteriophage Mu repressor to supercoiled Mu DNA.

It was shown, using a relatively simple assay, that Mu repressor, cI, binds specifically to a region which spans the leftmost HindIII cleavage site on the phage genome. This extends the observations of Kwoh and Zipser [Nature (London) 277, 489-491 (1979)], who were able to define a binding region to the left of this site. These results provide support for the idea that the eight blocks of repeated DNA sequences, which also span the HindIII cleavage site, are involved in repressor binding. These results also indicate that cI repressor has a marked preference for supercoiled DNA.

Bacteriophage mu↗

Tn10 mediated integration of the plasmid R100.1 into the bacterial chromosome: inverse transposition.

Upon integration into the bacterial chromosome the drug resistance plasmid R100.1 often loses its tetracycline resistance character. We have analyzed an Hfr strain formed by such an integration and an R-prime plasmid derived from it. We find that integration took place within the Tn10 transposon, that the two IS10 sequences were retained, but that at least 80% of the transposon segment located between them, and carrying the tetracycline resistance genes, had been lost. We suggest that integration of R100.1 was mediated by an inverse transposition using the IS10 sequences.

Chromosomes, Bacterial↗

Prolonged intermittent drooling and oromotor dyspraxia in benign childhood epilepsy with centrotemporal spikes.

Prolonged isolated sialorrhea of epileptic origin was described by Penfield and Jasper (1954) in a patient with a lesional epilepsy. A child with prolonged but intermittent drooling, lingual dyspraxia, and other clinical and electroencephalographic (EEG) features compatible with benign childhood epilepsy with centrotemporal spikes (BCECS) is described. The fluctuant course of the symptomatology and correlation with the intensity of the paroxysmal discharges on EEG are consistent with an epileptic dysfunction located in the lower rolandic fissure. No lesion was demonstrated by magnetic resonance imaging (MRI). Our case bears analogies with the recently reported status epilepticus of BCECS and the "acquired aphasia-epilepsy syndrome."

Child↗

Acquired aphasia, dementia, and behavior disorder with epilepsy and continuous spike and waves during sleep in a child.

Severe persistent neuropsychological disorders sometimes develop in the course of a focal epilepsy of unknown origin in previously normal children. Very frequent bilateral focal or generalized discharges are often noted on the sleep EEG records of these patients with no evidence of clinical seizures. The relation between these paroxysms and the observed deterioration remains unclear. We report a child with a partial complex epilepsy and severe disturbances of language, cognition, and behavior acquired in the early years of development who was followed for 15 years. A correlation between the evolution of the striking EEG abnormalities during sleep and the neuropsychological disorders could be established retrospectively. The observed sequence of onset and recovery of the aphasia, the dementia, and the "psychotic" behavior makes a direct causal relation between the deficits quite unlikely. Rather it suggests an association of independent symptoms with a specific language disorder becoming manifest in the course of the evolution. This child shows many of the main characteristics of the syndromes of "acquired aphasia with convulsive disorder" (Landau-Kleffner syndrome) and "epilepsy with continuous spike waves during sleep." Both syndromes describe probably different facets of a similar underlying, still unexplained cerebral dysfunction.

Adolescent↗