REGULATION 147 



When the capacity of making respiratory enzymes or chloroplasts is lost 

 permanently, it is not possible so far to decide whether this is due to the 

 eventual loss of some structural information or to the permanent jamming 

 of the mechanism of its expression, but the latter possibility looks very 

 probable in view of the facts just mentioned. 



In the case of the 'poky' mutant of Neurospora crassa, there is clear 

 evidence that no structural information is lost: young cultures of this 

 maternally inherited mutant are devoid of 'succinoxidase' and cytochrome 

 oxidase, but older organisms actually make these enzyme systems in 

 amounts which exceed 50 per cent of the titre of the normal wild strain 

 (Haskins et al., 1953). Therefore, the complete structural information for 

 these proteins is contained in 'poky' ; the abnormality is that, in spite of the 

 presence of the structural information, the synthesis of the enzymes failed 

 to occur before the fifth or sixth day of growth. This strongly suggests that 

 the extrachromosomal factor in 'poky' in some way regulates or conditions 

 the biochemical process of synthesis of the respiratory enzymes. 



If this is so, the extrachromosomal hereditary factor need not be regarded 

 any more as a wandering gene-like particle or plasmagene or self-duplicat- 

 ing entity; it should rather be considered as a piece of a controlling mechan- 

 ism. One may even wonder whether the experimental facts could not be 

 explained by the existence of alternative and mutually exclusive steady 

 states maintained by some kind of feed back system; the non-chromosomal 

 mutation might be an irreversible switch from one of these states to the 

 other. It has indeed been long realized that alternative stable steady states 

 could mimic heredity (Wright, 1945; Delbruck, 1949; Pollock, 1953; De 

 Deken-Grenson, 1957; Beale, 1958). 



In the case of Euglena, the rate of cytoplasmic mutation depends entirely 

 on the physiological state of the cell at the time the mutagenic agent is 

 applied (De Deken-Grenson, 1960). A steady state system would account 

 for these observations more easily than a plasmagene model. 



In recent discussions on cytoplasmic inheritance (Ephrussi, 1958; 

 Lederberg, 1958; Nanney, 1958; Catcheside, 1958; De Deken-Grenson, 

 1960) the respective merits of the plasmagene versus steady states were 

 compared; efforts were made in most cases to advocate one of the models 

 or to decide into which picture a given phenomenon can best be fitted. 

 But it is more and more clearly apparent from these discussions that each 

 type of explanation has valuable features, although none accounts satis- 

 factorily for all the aspects of cytoplasmic heredity. In the author's opinion, 

 a satisfactory model should have the sharpness of the plasmagene theory 

 and the flexibility of the steady state principle. 



A unifying theory could possibly be derived from the concept of 'auto- 

 catal)rtic particle' which was proposed (Campbell, 1960) as an interpreta- 

 tion of long term adaptation of yeast to galactose (Winge and Roberts, 



