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The 2 chloroplast ribosome deficient mutants of Chlamydomonas reinhardi , ac-20 and cr-I form low levels of 66-s and 70-s chloroplast ribosome monomers compared to wild type, but differ in that cr-I also accumulates substantial amounts of the large (54-S) chloroplast subunit. Unlike wild type, ac-20 , cr-I and the double mutant ac-20 cr-I make little or none of the CO 2 - fixing enzyme ribulose diphosphate carboxylase (RuDPCase) when grown in the light with acetate and CO 2 as carbon sources ( mixotrophic growth ) whereas all 3 mutant genotypes form at least some enzyme when grown photosynthetically with CO 2 as the sole carbon source ( phototrophic growth ). All 3 mutant genotypes also show a characteristic defect in the organization of their chloroplast lamellar system when grown mixotrophically, but their chloroplast membrane organization approaches that of wild type when grown phototrophically. No change in the level of chloroplast ribosomes accompanies these changes in chloroplast organization and RuDPCase formation. We propose that the pleiotropic effects on chloroplast structure and function in mixotrophically grown cells of the mutants result because their chloroplast ribosomes synthesize certain specific chloroplast components with low efficiency, whereas they perform this function with greater efficiency when the cells are grown phototrophically.

Three clones of morphologically altered cells (L − MC29) of singular properties were isolated from MC29 (subgroup A) leukosis virus-infected chick embryo cells. Supernatant fluids from cultures of the cloned cells produced no transforming or interfering activity on chick embryo cells susceptible to known avian leukosis-sarcoma viruses. No virus associated with the cells was demonstrable by fluorescent-antibody staining or by electron microscopy. All L − MC29 clone cells were activated, however, by four strains of Rous-associated viruses (RAV) representative of A, B, C, and D subgroup avian leukosis viruses and by two strains of MC29 virus. Virus L − MC29 cells activated by superinfection with RAV-1 and RAV-2 was characterized by helper-dependent and helper-independent properties. These findings suggest that the strain MC29 leukosis virus, or a component thereof, possesses properties of defectiveness similar to those of the Bryan high-titer Rous sarcoma virus.