MOLECULAR-BASIS OF EMETINE RESISTANCE IN CHINESE-HAMSTER OVARY CELLS - ALTERATION IN 40S RIBOSOMAL-SUBUNIT
MOLECULAR-BASIS OF EMETINE RESISTANCE IN CHINESE-HAMSTER OVARY CELLS - ALTERATION IN 40S RIBOSOMAL-SUBUNIT
复制标题
DOI:
10.1016/0092-8674(77)90140-4
复制
发表时间:
1977-01-01
期刊:
影响因子:
64.5
通讯作者:
SIMINOVITCH, L
中科院分区:
文献类型:
--
作者:
GUPTA, RS;SIMINOVITCH, L
The molecular basis of resistance to the protein synthesis inhibitor emetine was examined in cell-free, protein-synthesizing extracts derived from normal and emetine-resistant (EmtR) [Chinese hamster ovary, CHO] mutants. Protein synthesis in extracts of the mutant cells is resistant to the inhibitory action of the emetin. When extracts from a wild-type and mutant cell line were fractionated into supernatant (S-100) and polyribosome fractions and mixed in different combinations, resistance to emetine was associated with the mutant polyribosome fraction. Further fractionation of wild-type and mutant polyribosomes into 40S and 60S ribosomal subunits and mixing them in various combinations with an S-100 fraction from the wild-type cell indicates that resistance of mutant cells to emetine involves an alteration in the 40S ribosomal subunit. The behavior of EmtR was also examined in somatic cell hybrids. Studies of EmtR .times. EmtS hybrid cell lines in vivo and in vitro show that EmtR is phenotypically recessive to EmtS, which is consistent with the ribosomal location of the genetic change.