LOSS OF VIABILITY AND /cap beta/-GALACTOSIDASE-FORMING ABILITY AS A CONSEQUENCE OF TRITIUM DECAY IN ESCHERICHIA COLI

Journal Article · Tue Jan 29 04:00:00 EST 1963 · Biochimica et Biophysica Acta (Netherlands)

DOI:https://doi.org/10.1016/0006-3002(63)90111-2· OSTI ID:4734830

Rachmeler, M; Pardee, A B

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), Journal Name: Biochimica et Biophysica Acta (Netherlands) Vol. Vol: 68; ISSN BBACA
• Country of Publication: Country unknown/Code not available
• Language: English

Related Subjects

BACTERIA
BIOCHEMISTRY
BIOLOGY AND MEDICINE
CHROMOSOMES
DECAY
ENZYMES
ESCHERICHIA COLI
GALACTOSIDASE
GENETICS
IONIZATION
NUCLEIC ACIDS
PROTEINS
RADIATION EFFECTS
RADIOACTIVITY
RIBONUCLEIC ACID
SUGARS
TRITIUM