The GNAS1 gene encodes the ␣ subunit of the G protein G s , which couples receptor binding by several hormones to activation of adenylate cyclase. Null mutations of GNAS1 cause pseudohypoparathyroidism (PHP) type Ia, in which hormone resistance occurs in association with a characteristic osteodystrophy. The observation that PHP Ia almost always is inherited maternally has led to the suggestion that GNAS1 may be an imprinted gene. Here, we show that, although G s ␣ expression (directed by the promoter upstream of exon 1) is biallelic, GNAS1 is indeed imprinted in a promoter-specific fashion. We used parthenogenetic lymphocyte DNA to screen by restriction landmark genomic scanning for loci showing differential methylation between paternal and maternal alleles. This screen identified a region that was found to be methylated exclusively on a maternal allele and was located Ϸ35 kb upstream of GNAS1 exon 1. This region contains three novel exons that are spliced into alternative GNAS1 mRNA species, including one exon that encodes the human homologue of the large G protein XL␣s. Transcription of these novel mRNAs is exclusively from the paternal allele in all tissues examined. The differential imprinting of separate protein products of GNAS1 therefore may contribute to the anomalous inheritance of PHP Ia.

We describe a set of face processing tests suitable for use with children aged from 4 to 10 years, which include tests of expression, lipreading and gaze processing as well as identification. The tests can be administered on paper or using a computer, and comparisons between the performance on computer- and paper-based versions suggest that format of administration makes little difference. We present results obtained from small samples of children at four different age groups (Study 1, computer-based tests), and larger samples at three age groups (Study 2, paper-based tests) from preschool to 10 years of age. The tests were found to be developmentally sensitive. There were quite strong correlations between performance on different tests of the same face processing ability (e.g. gaze processing), and generally rather weaker correlations between tests of different abilities

The book describes the biological ways in which diseases of plants, caused by pathogenic microbes, can be controlled without the use of chemical pesticides. The basis of biocontrol (in microbiology, ecology and plant pathology) is described and many examples of control measures in commercial use or development are given. There is increasing interest in biocontrol from the general public, environmentalists and the major world agrochemical companies, and this easily read text presents recent developments in the subject. The book provides enough references and literature citations to allow a more detailed investigation of particular diseases or control systems to be made. This textbook is suitable for graduate and undergraduate students in botany, biology, microbiology, plant pathology, agriculture, horticulture, crop science, microbial ecology, crop protection and related courses.

A screening programme was used to search for biocontrol agents against Gaeumannomyces graminis causing take-all disease of wheat. Of the 1800 rhizosphere microorganisms tested, 10% controlled the disease in a secondary screen. The 30 most effective isolates were further investigated for mode of action. Although 72% of the sites sampled for antagonistic microbes were planted to continuous cereals, they yielded only 23% of the most effective isolates. Of all the isolates selected. 63% belonged to the genera Bacillus. Pseudomonas and Penicillium, Beauveria and Rhodococcus were also antagonistic. Fluorescent pseudomonads. all producing siderophores in low-iron medium, accounted for 23"., of the isolates. Over 50% of strains produced ^-glucanases and chitinases. Less than 50% of the strains selected by the in vivo screen inhibited G. graminis in agar plate tests. In the gnotobiotic system used, the Pseudomonas strains were faster in colonizing the wheat roots than the majority of the Bacillus and fungal strains.

Variation in the phenotypic expression of Albright's hereditary osteodystrophy (AHO) determined by the parent of transmission, suggests that the human Gsa gene (GNAS1), in which mutations occur in AHO, may be under imprinted control. GNAS1 is also known to map to a chromosomal region (20q13.11) showing syntenic homology with the imprinted mouse region 2E1-2H3. To establish if GNAS1 is indeed imprinted, we have examined the parental origin of GNAS1 transcription in human fetal tissues. Of 75 fetuses genotyped, at gestational ages ranging from 6 to 13 weeks, 13 heterozygous for a FokI polymorphism in exon 5 of GNAS1 were identified whose mothers were homozygous for one or other allele. RNA from up to 10 different tissues from each fetus was analysed by RT-PCR. In all cases expression from both parental alleles was shown by FokI digestion of RT-PCR products and quantification of the resulting fragments. No tissue specific pattern of expression was discerned in these experiments.If genomic imprinting regulates the expression of the human GNAS1 gene, our data suggest that the effect must either be subtle and quantitative, or be confined to a small subset of specialised hormone responsive cells within the target tissues.

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