Three bacteriophages (S-13, C-36 and S taph-K ) were irrad ia ted by y-rays, X -rays and a-rays. The survival curves were exponential, and the effect of a given dose was independent of the exposure tim e. F or any given phage the inactivation doses of the three radiations increased in the order y-rays, X -rays, a-rays, while for any given rad iation the inactivation doses of the three phages dim inished in the order S-13, C-36, S taph-K , which is the order of in ­ creasing size. These observations lead to the conclusion th a t a single ionization suffices to inactivate a phage particle. In the case of the sm allest phage investigated (S-13) th is ionization is effective w herever in the particle it is produced, and reasons are given for concluding from th is fact th a t S-13 is a m acrom olecular type of virus analogous to the erystallizable p lan t viruses. In the case of the larger phages (C-36 and Staph-K ), while a single ionization can in ­ ac tiva te a phage particle it is no t sufficient for it to be produced anyw here in the phage partic le ; to be effective it m ust be produced in a more restric ted region. I t is suggested th a t th is radiosensitive region constitu tes the genetical m ateria l of the phage, and on the basis of th is differentiation into genetic and non-genetic m ateria l these phages are regarded as p rim itive single-celled organism s ra th e r th an macromolecules.

Statistical calculations are made of the distribution numbers of mutants in a culture of bacteria in which the number of mutants increases on account both of new mutations and of division of old mutants. In this way the largely qualitative conclusions of Luria and Delbruck are extended and placed on a firm quantitative basis. The results of these calculations, which enable the mutation rate to be inferred from experiments with parallel cultures, are presented in the form of tables. Statistically efficient methods of using these tables are discussed.

A theory is given of the process of chromosomal structural rearrangement following irradiation. The theory applies to nuclei in which the union of breakage ends is at random, and assumes that the number of breaks primarily produced is proportional to the dose.

Three bacteriophages (S-13, C-36 and Staph-K) were irradiated by γ -rays, X -rays and α -rays. The survival curves were exponential, and the effect of a given dose was independent of the exposure time. For any given phage the inactivation doses of the three radiations increased in the order γ -rays, X -rays, α -rays, while for any given radiation the inactivation doses of the three phages diminished in the order S-13, C-36, Staph-K, which is the order of increasing size. These observations lead to the conclusion that a single ionization suffices to inactivate a phage particle. In the case of the smallest phage investigated (S-13) this ionization is effective wherever in the particle it is produced, and reasons are given for concluding from this fact that S-13 is a macromolecular type of virus analogous to the crystallizable plant viruses. In the case of the larger phages (C-36 and Staph-K ), while a single ionization can in­ activate a phage particle it is not sufficient for it to be produced anywhere in the phage particle; to be effective it must be produced in a more restricted region. It is suggested that this radiosensitive region constitutes the genetical material of the phage, and on the basis of this differentiation into genetic and non-genetic material these phages are regarded as primitive single-celled organisms rather than macromolecules.

Recent experiments on the inactivation of plant, animal, and bacterial viruses by γ rays, X rays, and α rays are reviewed. In sufficiently dilute aqueous solutions the inactivation is mainly indirect, i.e., is due to the production of ionization in the water rather than in the virus itself. If the virus is irradiated dry, however, or in an aqueous solution of sufficiently high solid content, larger doses are required and the inactivation is mainly direct, i.e., the inactivation of a virus particle is due to the production of ionization in the virus particle itself. There is evidence that a single ionization suffices to inactivate a virus particle. A correlation exists between the inactivation dose for the direct effect and the size of the virus, in the direction of the inactivation dose being greatest for the smallest viruses. The experimental relation between inactivation dose and virus size is compared with the relation calculated on the hypothesis that a single ionization anywhere in the virus particle...

1. Experiments are described on the transmission of mottle and vein-distorting viruses by aphides. 2. A quantitative analysis is made of Watson's experiments on the aphis transmission of persistent and non-persistent viruses. The principal features of the experimental results can be explained in terms of different rates of inactivation of the virus in the insect. 3. It is shown that these considerations explain why non-persistent viruses are more commonly sap-transmissible than persistent viruses.

Many experiments have been described in which a batch of animals are painted or injected with a carcinogen, and the dates recorded when warts or malignant growths are detected. The object of such experiments is usually to compare the potency of different carcinogens, or of different doses or methods of application, or else to compare the sensitivity of different batches of animals to a given carcinogen. It is convenient to have some means of summarizing the results of each experiment in a single number, together with an indication of its precision. The purpose of the present paper is to describe suitable procedures for arriving at such a number. The methods described are not essentially new; in particular the procedures advocated by C. I. Bliss (4) in a paper on the calculation of the time-mortality curve are in the main applicable to the present problem, and the method given below for dealing with experiments in which some animals die prematurely without tumor is an adaptation of a method described by W. L. Stevens (17) in an appendix to the Bliss paper.

The suggestion is put forward that radiation-induced recessive lethals, or a large proportion of them, are due to chromosome breaks. About one-third of all the chromosome breaks primarily induced by the radiation are lethals. If the break restitutes, a lethal unaccompanied by chromosomal aberration (type A lethal) results. If the break takes part in chromosome interchange a type C lethal, which is associated with chromosomal structural change, results. Arguments are given against the alternative position-effect explanation of type C lethals.

The rate of X-ray induction of dominant lethals in the sperm of the Oregon-R stock ofDrosophila melanogaster is, at low doses, 12% per 1000 r. for death in the embryo stage, and 20% per 1000 r. for death at any stage between the zygote and the adult. At higher doses of X-rays both rates increase. Over the whole dose range, therefore, the doseaction curve does not fit a single-hit type of action, though this is approximated at low doses.

At various times it has been proposed that the size of the gene can be estimated from experiments on the yield of mutations obtained with known doses of X-rays. The assumptions involved in calculations of this sort are discussed, and some of the objections which have been raised against them answered. It is pointed out that similar assumptions, applied to experiments on the inactivation of enzymes and viruses, lead to estimates of the sizes of these bodies correct to a factor of two in diameter. The estimate arrived at for the size of the gene inDrosophila is 4–8 mμ diameter. The length of the euchromatic region of theX-chromosome thread in the sperm is deduced to be 10–20 μ.

When tissue is irradiated by X rays, neutrons or radioactive radiations, energy is dissipated mainly by ionization and excitation. Ionization means the removal from atoms of electrons, leaving the atom electrically charged. It is possible that this seperation of charge sometimes has a biological significance, but it is more probable that the biological effect follows the chemical change associated with ionization. For, when an atom is ionized, the molecule of which it is a part usually undergoes chemical change. Dr. Allsopp will describe chemical evidence for this statement. The excitation of a molecule is a less drastic process than ionization, and it is not certain how far excitation is of importance in comparison with ionization. I shall not speak of excitation further, but what I have to say will not need serious modification should it turn out that excitation is of comparable importance to ionization. If ionization is the cause of the biological effect, it is clearly necessary to understand two things: (a) the amount of ionization produced in tissue by one röntgen of any radiation; (b) the manner in which this ionization is distributed. Slides were shown as follows:— (1) A table showing the energy dissipation and ionization per cubic micron produced per röntgen by various radiations in tissues of various composition. As a rough working rule, one röntgen corresponds to the production of two ionizations per cubic micron in tissue, the exact figure varying a little with different radiations and different tissue compositions.

1. The coefficients of chromatid breakage (compare Table 4) are highest with AgL-radiation (λ=4·1 A.) and fall off through CuK-radiation (λ=1·5 A.) to medium X-rays (λ=0·15 A.) and to AlK-radiation (λ=8·3 A.) where they are least.