Allelic association of gene markers on chromosome 11q in Italian families with atopy.

UNLABELLED: In our study, the genetic linkage of the Fcepsilon RIbeta gene with atopy in 77 affected sibling pairs recruited from an Italian panel of 201 subjects has been examined. Atopy was defined by the presence of a positive skin prick test to one or more common aeroallergens, a positive RAST test to one or more common aeroallergens and an elevated circulating total IgE. Genotype analysis was performed by PCR amplification of Fcepsilon RIbeta CA and CI11-319 CA microsatellites. All the family members were also tested for the Ilepsilon 181 mutation with the ARMS method and for Leu181/Leu183 polymorphism. Seventy-two point five percent (72.5%) of the affected sibling pairs shared their maternal allele and 27.5% did not. Therefore, an increased maternal allele sharing was observed: chi2 = 8.10, p < 0.01. Comparing paternal versus maternal allele sharing, a significant difference was observed for the C1II-319 CA marker (chi2 = 4.32, p < 0.05). Atopy phenotype with positive skin prick test, RASTs, and high total serum IgE also showed greater sharing of maternal than paternal alleles in affected sibling pairs. Of the 201 subjects studied, 17 (8.4%) were positive for Leu181. Ten of these were children and seven (70%) had inherited the variant maternally. The seven children had maternally inherited Leu181/Leu183 and were atopic. Within this sample the maternal inheritance of Fcepsilon RIbeta Leu181/Leu183 was associated with an increased risk of IgE responses to common allergens, raised eosinophil counts and increased skin prick test reactions. Therefore, the variant identified a genetic risk factor for atopy. CONCLUSION: The central role of Fcepsilon RIbeta in atopy and the linkage data presented here point to the possibility that genetic variation in Fcepsilon RIbeta or its controlling element may cause differences in the extent of IgE responses between atopic and non-atopic subjects. A search for such mutations or polymorphisms will need to take into account some carriers of atopy among the normal population and genetic heterogeneity among atopic individuals.

Arginine-specific repression in Saccharomyces cerevisiae: kinetic data on ARG1 and ARG3 mRNA transcription and stability support a transcriptional control mechanism.

A specific repression mechanism regulates arginine biosynthesis in Saccharomyces cerevisiae. The involvement of regulatory proteins displaying DNA-binding features and the location of an operator region between the TATA box and the transcription start of the structural gene ARG3 suggest that this mechanism operates at the level of transcription. A posttranscriptional mechanism has, however, been proposed to account for the conspicuous lack of proportionality between ARG3 mRNA steady-state levels (as determined by Northern [RNA] assays; F. Messenguy and E. Dubois, Mol. Gen. Genet. 189:148-156, 1983) and the cognate enzyme activities. In this work, we have analyzed the time course of the incorporation of radioactive precursors into ARG1 and ARG3 mRNAs and the kinetics of their decay under different regulatory statuses. The results (expressed in terms of relative mRNA levels, relative transcription rates, and mRNA half-lives) give the picture expected from a purely transcriptional control. A similar analysis of expression of the gene CPA1, for which a translational regulation by arginine has been clearly demonstrated (M. Werner, A. Feller, F. Messenguy, and A. Piérard, Cell 49:805-813, 1987), indicates that this gene is also partly regulated at the transcriptional level by the ARGR repressor system. Moreover, the half-life of CPA1 mRNA is reduced twofold in the presence of excess arginine; we suggest that this could be inherent in the mechanism of translational regulation of CPA1.

[Original survey and analysis method of the vestibulo-ocular transfer using the microcomputer. Contribution to the diagnosis of vestibular pathology]. / Méthode originale de relevé et d'analyse par micro-ordinateur de la fonction de transfert vestibulo-oculaire. Contribultion à la détection de la pathologie vestibulaire.

This report presents a new and well-tolerated technique that quickly tests the labyrinthic system by moving the head, via a helmet mounted on a servo controlled torque motor, with a sinusoidal stimulus small enough (10 to 15 degrees of amplitude) to avoid the triggering of quick phases. A personal PC (Olivetti M24) digitizes the amplified and filtered eye and head movement data for storage and analysis. Compared to the low frequency patterns of stimulation by the sinusoidal acceleration test (SHA), our procedure, because of the reduced mass of inertia, investigates the bandwidth of frequencies corresponding to those normally incurred during natural movements. For each of 14 normal persons, 1 patient with Ménière's disease and 2 with a history of labyrinthic trauma, the phase difference of the eye position relative to the head and the gain are computed. The mean phase lag of 180 degrees, from 0.1 Hz to 2.5 Hz, in the normal group maintains steady gaze during head rotation in significant opposition to the phase lag, varying at 1 Hz from 264 to 354 degrees, of the patients with vestibular disorders. The phase lag is the most reliable parameter in detecting vestibular dysfunction and its correct determination can be made in a few minutes, at physiological frequencies, by our low-cost simplified method.

Genetics of the relB locus in Escherichia coli.

A mutant of Escherichia coli with a delayed relaxed phenotype very similar to that of a previously described relB mutant has been obtained using a new selection procedure. The mutation giving rise to this phenotype has been shown to map at 34.5 min and to be 12% cotransducible with man. It is recessive, revertible, and most likely an allele of the relB gene.