138 TEMPORAL ORGANIZATION IN CELLS 



Karakashian and Hastings (1962) has shown the effectivenes of actinomycin 

 in completely suppressing the luminescence rhythm in Gonyaulax, presum- 

 ably by interfering with mRNA synthesis. The main feature of the experi- 

 ments suggested here, and which puts them in contrast with previous work, 

 is the attempt to produce periodic transients which would tend to either excite 

 the oscillatory system or to damp it, without involving a radical change of 

 microscopic state such as occurs when cells are permanently exposed to 

 a new chemical environment. 



If treatment with puromycin or actinomycin is effective in decreasing 6 

 then continuation of the treatment should eventually produce a state where the 

 talandic temperature is so small that the non-linearities of the oscillations are 

 greatly reduced and the circadian organization of the cell begins to decay. 

 Clearly this can occur without causing the death of the cell. In fact such a state 

 has been produced in Gonyaulax by Karakashian and Hastings both with 

 actinomycin and with puromycin. At a concentration of 0-02 ^g/ml actino- 

 mycin suppresses the luminescence rhythm, but growth is only partially in- 

 hibited. There are at least two possible interpretations of this in terms of the 

 present study as we have seen in Chapter 7, only one of which involves the idea 

 that 6 is reduced to the point where non-linear interaction becomes too weak to 

 generate temporal organization. However, it remains to be seen if the pulsing 

 treatment suggested with the antibiotics can produce a state of good viability 

 but no circadian time structure such as resulted from permanent exposure to 

 actinomycin at a certain concentration. 



The importance of physical temperature as an experimental parameter for 

 the study of cell behaviour in general, and circadian organization in particular 

 suggests that we might have chosen it rather than the supply of nutrients or 

 inhibitors as the means of trying to alter G-levels in cells. The difficulty is 

 that the cell is normally subjected to variations in temperature, and so it has 

 built into its time-keeping machinery a fairly successful temperature-com- 

 pensating device. Just how this works is the subject of considerable research, 

 because in general, biochemical reactions are quite sensitive to changes in 

 temperature and one would normally have thought that a biochemical clock 

 would show a similar sensitivity. However, even the simple result of equation 

 (57) shows us that the mean frequency of oscillation of a biochemical feed-back 

 control system bears a relatively complicated relation to the elementary 

 biochemical events involved in its operation and we can begin to see even from 

 this simplest model how temperature compensation might occur. We have, 

 for large d, 



■^^ " "'Me) 



From equation (33) we have B = CiXiiXj-pj), so that the above relation can be 

 written as 



^/[27TXi(Xi-pi)] 



