Section 12 — Plasmatic Inheritance 



12.4. Interactions between a Cytoplasmic Factor and 

 Nuclear Genes in Neurospora crassa. Selma 

 Silagi (New York, U.S.A.). 



Mitchell and Mitchell showed that the slow- 

 growing aspect of the phenotype of poky, a 

 maternally inherited condition, could be sup- 

 pressed by a nuclear gene, f. 



As a result of crosses between poky and several 

 other strains of Neurospora it has been found 

 that the f locus is closely linked to inositol on 

 linkage group V, with a centromere distance of 

 approximately 35 units. It has also been observed 

 that the f gene manifests itself in the poky strain 

 not only by increasing the growth rate but also by 

 shortening the lag period associated with ascos- 

 pore germination. 



Additional attempts have been made to see if 

 other genes might modify the growth rate of 

 poky strains, including crosses with pe m fl. 

 Poky strains containing fluffy, and therefore 

 aconidial, were found to have a relatively short 

 lag phase, resembling in this respect the behavior 

 of hyphal fragments of "cured" growing 

 mycelium. From this and other evidence which 

 will be presented it appears that the formation 

 and/or germination of conidia or ascospores are 

 a prerequisite for the full expression of the poky 

 phenotype. 



12.5. A Gene-induced Cytoplasmic Mutation in Yeast. 



M. Grenson (Brussels, Belgium). 



Following the application of X-rays, a mutant 

 of Saccharomyces cerevisiae was isolated (D77) 

 which simultaneously requires glutamic acid 

 and is respiratory deficient. 



When crossed with normal strains, D77 give 

 a mixture of normal and respiratory deficient 

 diploid clones, all glutamic-acid-sufficient. It 

 behaves thus as a suppressive petite. Tetrad 

 analysis of normal diploids show a 2 : 2 segre- 

 gation of both deficiencies, which are linked with- 

 out exception. 



However, the respiratory deficiency behaves, 

 at the same time, as an extrachromosomal 

 character, since it does not complement a 

 neutral cytoplasmic petite. 



Two nuclear petites, N2 and N4, were shown 

 to be complemented by D77. 



A hundred glutamic-acid-sufficient revertants 

 isolated from D77 remained respiratory deficient 

 without exception. 



The above may be understood if we assume 

 that the glutamic deficiency block is responsible 

 for the induction of a cytoplasmic petite mu- 

 tation. 



This is further supported by the observation 

 that the cytoplasmic petite mutation can be 

 avoided in the ascospores carrying the glutamic 

 acid deficiency when germination takes place on 

 glycerol, lactate or acetate, instead of on 

 glucose, as the carbon source. Under these con- 

 ditions, the clones arising from the two glutamic- 

 acid-less spores exhibit normal respiration as do 

 the two glutamic-acid-sufficient clones. 



12.6. The Inheritance of a Killer Character in Yeast 

 (Saccharomyces cereviseae). M. Makower 

 and E. A. Bevan (Oxford, Great Britain). 



In certain strains of yeast three phenotypes 

 have been observed: "killer", "sensitive", and 

 "neutral". When killer and sensitive cells are 

 grown together in the same broth or agar medium 

 a high proportion of the latter are killed. No 

 killing takes place when neutral are grown with 

 either killer or sensitive cells. 



Crosses between different killer and neutral 

 strains followed by Ascus analyses of over 800 

 tetrads reveal that the difference between killer 

 and neutral cells is controlled by two loci N/n and 

 K/k, showing 36 per cent recombination. The 

 presence of N determines the neutral phenotype; 

 its recessive n, the killer phenotype. K is epistatic 

 to N. Thus, all neutral strains are Nk, but either 

 of three genotypes, NK, nK or nk, may determine 

 the killer phenotype. 



Sensitive cultures are never recovered follow- 

 ing crosses of sensitive by killer or neutral. But 

 the results of such crosses show that sensitive 

 cells may possess any of the above four 

 possible nuclear genotypes all lacking a cyto- 

 plasmic component which is present in both 

 killer and neutral cells. 



Mutant sensitive strains have been recovered 

 at a frequency of 0.26 per cent following treat- 

 ment of killers with ethyl-methane-sulphonate. 

 These mutants retain the nuclear genotype of the 

 original strain. No mutation of sensitive to either 

 killer or neutral has yet been observed. These 

 observations provide evidence for the conclusion 

 that sensitives differ from killers and neutrals in 

 lacking a cytoplasmic component. 



12.7. The Physiological Basis of the Killer Character 

 in Yeast. E. A. Bevan and M. Makower 

 (Oxford, Great Britain). 



A high percentage of sensitive cells are killed 

 when incubated in cell-free filtrates of buffered 



202 



