Reference

Effect of anisomycin on the cellular level of native ribosomal subunits

Effect of anisomycin on the cellular level of native ribosomal subunits. Van Venrooij, Walther J.; Van Eenbergen, Jet; Janssen, Albert P. M. (Dep. Biochem., Univ. Nijmegen, Nijmegen, Neth.). Biochemistry, 16(11), 2343-8 (English) 1977. CODEN: BICHAW. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Interactions) Section cross-reference(s): 6, 1 Treatment of Ehrlich ascites cells with anisomycin (I) [22862-76-6] (an inhibitor of protein synthesis in mammalian cells but not in bacteria) induced an almost 3-fold increase in the level of native 60S ribosomal subunits. This increase was caused by a defect in the joining of the 60S subunit to the smaller initiation complex to form an 80S complex. Such a blocking of the joining reaction was indicated by the formation of the so-called "half-mer"-type oligosomes and by the release of extra 40S subunits when these oligosomes were treated with ribonuclease. The increase of 60S subunits induced by I may be helpful in estg. the amt. of initiating mRNA in the cell.

Adaptation to trichodermin and anisomycin in Physarum polycephalum

Adaptation to trichodermin and anisomycin in Physarum polycephalum. Gorman, Jessica A. (McArdle Lab., Univ. Wisconsin, Madison, Wis., USA). J. Cell. Physiol., 92(3), 447-56 (English) 1977. CODEN: JCLLAX. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Interactions) Addn. of trichodermin (I) [4682-50-2] or anisomycin (II) [22862-76-6] to growing cultures of the eucaryotic myxomycete P. polycephalum halted cell division, but growth resumed on continued incubation. The renewed growth was not due to external inactivation of the drugs or to the selection of stable drug-resistant mutants, but apparently involved an adaptation to the inhibitors. The mechanism for the development of drug resistance is not known, although growth inhibition presumably resulted from an inhibition of protein synthesis. Cross adaptation between I and II (which both act at the ribosomal level) suggested an overlapping of the ribosomal sites affected by the antibiotics.