A significant positive correlation was observed between multiplicity of infection and burst size of mycobacteriophage 13. During multiple infections, the average contribution of each infecting phage to the burst size was inversely correlated with multiplicity of infection even when bacterial resources were not limiting. We conclude that the efficiency of phage-coded functions rather than the extent of bacterial resources determines the burst size.

The growth patterns ofMycobacterium smegmatis SN2 in a minimal medium and in nutrient broth have been compared. The growth was monitored by absorbancy (Klett readings), colony forming units, wet weight and content of DNA, RNA and protein. During the early part of the growth cycle, the bacteria had higher wet weight and macromolecular content in nutrient broth than in minimal media. During the latter half of the growth cycle however, biosynthesis stopped much earlier in nutrient broth and the bacteria had a much lower content of macromolecules than in the minimal medium. In both the media, a general pattern of completing biosynthesis rapidly in the initial phase and a certain amount of cell division at a later time involving the distribution of preformed macromolecules was seen. The possible adaptive significance of this observation has been discussed.

We propose a molecular mechanism for the intra-cellular measurement of the ratio of the number of X chromosomes to the number of sets of autosomes, a process central to both sex determination and dosage compensation inDrosophila melanogaster. In addition to the two loci,da andSxl, which have been shown by Cline(Genetics, 90, 683, 1978)and others to be involved in these processes, we postulate two other loci, one autosomal (Ω) and the other, X-linked (π). The product of the autosomal locusda stimulates Ω and initiates synthesis of a limited quantity of repressor.Sxl and π ,both of which are X-linked, compete for this repressor as well as for RNA polymerase. It is assumed thatSxl has lower affinity than π for repressor as well as polymerase and that the binding of polymerase to one of these sites modulates the binding affinity of the other site for the enzyme. It can be shown that as a result of these postulated interactions transcription from theSxl site is proportional to the X/A ratio such that the levels ofSxl⁺ product are low in males, high in females and intermediate in the intersexes. If, as proposed by Cline, theSxl^- product is an inhibitor of X chromosome activity, this would result in dosage compensation. The model leads to the conclusion that high levels ofSxl⁺ product promote a female phenotype and low levels, a male phenotype. One interesting consequence of the assumptions on which the model is based is that the level ofSxl⁺ product in the cell, when examined as a function of increasing repressor concentration, first goes up and then decreases, yielding a bell-shaped curve. This feature of the model provides an explanation for some of the remarkable interactions among mutants at theSxl, da andmle loci and leads to several predictions. The proposed mechanism may also have relevance to certain other problems, such as size regulation during development, which seem to involve measurement of ratios at the cellular level.

The evolution of social groupings in insects, especially wasps, is compared to that of social amoebae (cellular slime moulds). They both show a gamut of colony sizes, from solitary forms to complex colonies with a division of labour. The various ideas as to how there might have been an evolution of complexity within insect societies, such as the role of genetic relatedness, the role of mutualism, the origin of sterility, the manipulation and exploitation of some individuals by others within a colony, are discussed, and then applied to social amoebae. The result is both interesting and instructive: despite some differences, there are many striking parallels, which suggests that there are some common denominators in the formation and evolution of a social existence among organisms.