Nature of RNA synthesis on embikhin-damaged templates

Embichin, a bifunctional alkylating mutagenic agent, inhibits RNA-synthesizing capacity of DNA and chromatin. The template capacity for decreasing the embichin-injured chromatin is caused by substantial reduction in the number of RNA molecules synthesized by this template. When DNA extracted from embichin-injured chromatin is used as a template, its template restriction is accounted for by an approximately 5-fold decrease in the RNA average molecular weight. The deoxyribonucleoprotein complexes reconstituted from embichin-injured DNA and control chromatic proteins had a lower template capacity compared with that of DNP reconstituted from control DNA. It is concluded that both links between DNA and proteins and DNA injuries are responsible for the inhibition of genome template capacity.     

Relaxation of DNA-protein interactions in mouse lymphoblastic leukemic cells exposed to antineoplastic agents

It has been demonstrated by nucleoproteid-celite chromatography that 1-nitroso-1-methylurea, potassium cyanate and prospidin reduce DNA-protein interactions in chromatin of cell cultures from LL mice with lymphoblastic leukemia.     

Inactivation of cyclic GMP-dependent protein kinase by N alpha-tosyl-L-lysine chloromethylketone

Cyclic GMP-dependent protein kinase from bovine lung and cyclic AMP-dependent protein kinase from bovine heart are inactivated by N^α-tosyl-L-lysine chloromethylketone (TLCK) in the presence of cyclic GMP and cyclic AMP, respectively. The inactivation of both protein kinases is pseudo-first order, suggesting the rate limiting step is beyond the binding of TLCK. Cyclic GMP-dependent protein kinase is inactivated less than $\text{1}\text{4}$ as rapidly as cyclic AMP-dependent protein kinase, although it shows a higher apparent affinity for TLCK. Cyclic AMP stimulated the rate of inactivation of cyclic AMP-dependent protein kinase 10-fold but cyclic GMP stimulated the rate of inactivation of cyclic GMP-dependent protein kinase only 1.5-fold. The rate of inactivation of cyclic GMP-dependent protein kinase by TLCK is sufficiently rapid (half-time of about 30 min at 37°C with 2 mM TLCK) to account for the effects of TLCK on cell growth observed by others.     

Membrane filter staining method: bacterial plate counts in 24 H

We describe a technique to stain bacterial colonies on membrane filters. The procedure yielded reliable and reproducible bacterial plate counts in 24 h. The procedure can be applied to treated and untreated water samples requiring prompt analysis.     

Changes in sensitivity of human tumour cells to growth inhibition by proteinase inhibitors.

Inhibition of a cell-surface proteinase can inhibit the growth of many normal human cell types in culture. Some tumour cells are also sensitive to proteinase inhibitors, but others are resistant, and continue to grow in the presence of these inhibitors. Here we describe two human tumour cell lines which convert from the sensitive to the resistant state. In one case, the conversion occurs during routine passaging, but, in the other, it is determined by growth conditions, and is reversible.