LOSS OF VIABILITY AND /cap beta/-GALACTOSIDASE-FORMING ABILITY AS A CONSEQUENCE OF TRITIUM DECAY IN ESCHERICHIA COLI
Decay of tritium incorporated into Escherichia coli prevented the bacteria from growing into colonies or from forming BETA -galactosidase. The rate of viability loss was similar when the H/sup 3/ was incorporated into DNA or into total nucleic acids. The somewhat slower rate of inactivation by H/sup 3/ incorporated into proteins was attributed to a geometrical factor. Ionizations caused by the emitted 3-particles are thought to be primarily responsible for viability loss. Decays of H/sup 3/ in DNA were much more effective in preventing BETA -galactosidase formation than were decays in RNA or protein. Loss of enzyme-forming ability was attributed to recoil damage in the DNA. The similar sensitivities of viability and enzyme formation appear coincidental, since they were caused by different consequences of H/sup 3/ decay. Mated bacteria were prepared, radioactive in all parts except the genetic material carrying specificity for BETA galactosidase formation. Viability but not enzyme formation was sensitive to H/sup 3/ decay. This suggests that only H/sup 3/ decays in the specificity-carrying chromosome inactive enzyme-forming ability. (auth)
- Research Organization:
- Univ. of California, Berkeley
- NSA Number:
- NSA-17-014005
- OSTI ID:
- 4734830
- Journal Information:
- Biochimica et Biophysica Acta (Netherlands), Vol. Vol: 68; Other Information: Orig. Receipt Date: 31-DEC-63
- Country of Publication:
- Country unknown/Code not available
- Language:
- English
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