Chemical investigation ofAbroma august a Linn. identity of abromine with betaine

Zusammenfassung Isolierung und Charakterisierung verschiedener Stoffe aus der indischen PflanzeAbroma augusta Linn.     

The occurrence of 12, 13-epoxytrichothecenes in seeds of safflower infected with Fusarium oxysporum f. sp. carthami

Summary From the seeds of safflower (Carthamus tinctorius Linn.), infected with Fusarium oxysporum f. sp. carthami, 3 toxic compounds have been isolated in quatities sufficient to cause mycotoxicosis on prolonged ingestion. 2 of these have been identified as diacetoxyscirpenol and T-2 toxin, while the third one has also been partially characterized as a 12, 13-epoxytrichothecene. Additionally, the incidence of secondary fusarial infection of healthy seeds due to contamination with the infected ones has been reported for the first time.     

Mutagenic effect of UV-light and X-rays onStreptomyces nigrifaciens and yield of the antifungal substance

Résumé Changement de capacité de production antibiotique chez mutants nouveaux deStreptomyces nigrifaciens.

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Thanks are due to PrincipalS. Sinha of Agra College, Agra, for providing all facilities and to C.S.I.R., New Delhi, for award of research followship to S.G.     

The AID antibody diversification enzyme is regulated by protein kinase A phosphorylation

Antibodies, which are produced by B-lineage cells, consist of immunoglobulin heavy (IgH) and light (IgL) chains that have amino-terminal variable regions and carboxy-terminal constant regions. In response to antigens, B cells undergo two types of genomic alterations to increase antibody diversity. Affinity for antigen can be increased by introduction of point mutations into IgH and IgL variable regions by somatic hypermutation. In addition, antibody effector functions can be altered by changing the expressed IgH constant region exons through IgH class switch recombination (CSR). Somatic hypermutation and CSR both require the B-cell-specific activation-induced cytidine deaminase protein (AID), which initiates these reactions through its single-stranded (ss)DNA-specific cytidine deaminase activity. In biochemical assays, replication protein A (RPA), a ssDNA-binding protein, associates with phosphorylated AID from activated B cells and enhances AID activity on transcribed double-stranded (ds)DNA containing somatic hypermutation or CSR target sequences. This AID-RPA association, which requires phosphorylation, may provide a mechanism for allowing AID to access dsDNA targets in activated B cells. Here we show that AID from B cells is phosphorylated on a consensus protein kinase A (PKA) site and that PKA is the physiological AID kinase. Thus, AID from non-lymphoid cells can be functionally phosphorylated by recombinant PKA to allow interaction with RPA and promote deamination of transcribed dsDNA substrates. Moreover, mutation of the major PKA phosphorylation site of AID preserves ssDNA deamination activity, but markedly reduces RPA-dependent dsDNA deamination activity and severely impairs the ability of AID to effect CSR in vivo. We conclude that PKA has a critical role in post-translational regulation of AID activity in B cells.     

Aberrant regulation of ras proteins in malignant tumour cells from type 1 neurofibromatosis patients.

Defects in the NF1 gene have been implicated in the inherited disorder neurofibromatosis type 1, which is characterized by several developmental abnormalities including an increased frequency of benign and malignant tumours of neural crest origin (neurofibromas and neurofibrosarcomas respectively). The NF1 gene encodes a ubiquitous protein homologous to p120GAP, the GTPase-activating protein (GAP) for the products of the ras protooncogenes. When expressed in non-mammalian systems, the region of the NF1 gene homologous to p120GAP produces a protein with GAP-like activity. Here we present evidence that the ras proteins in malignant tumour cell lines from patients with type 1 neurofibromatosis are in a constitutively activated state, as judged by the guanine nucleotide bound to them, and are necessary for cellular proliferation. These cells contain p21ras and p120GAP that are both functionally wild type, but barely any functional NF1 protein. Our results show that the NF1 protein is normally essential for correct negative regulation of ras proteins in the cell, even in the presence of normal p120GAP, and they support the hypothesis that NF1 is a tumour-suppressor gene whose product acts upstream of ras.