Charles Galperin

In this two-part study, I shall first examine the initial foundations of developmental genetics in the works of Edward B. Lewis. The earliest models based on the relation one gene–one function gave us the idea of functioning, that is, the linking of functions in a chain leading to the final observable phenotype. The second part shows that the conception of models was to be completely modified with the multifunctionality of genes and proteins. I will then indicate three consequences. The first echoes François Jacob’s lesson (Science 196:1161–1166, 1977): “The hierarchy in the complexity of objects is thus accompanied by a series of restrictions and limitations. At each level, new properties may appear which impose new constraints on the system.” In evolutionary perspectives this translates as the “successive recruitment of a gene to produce increasing multifunctionality.” The second consequence is the necessity of new models and thereby for new analytical tools, such as, as Joram Piatigorsky (Gene sharing and evolution: the diversity of protein functions. Harvard University Press, Cambridge, MA, 2007) illustrates, a “network analysis” that “concerns simultaneous changes in the expression of many genes and can predict new functional associations.” The third consequence is that evolutionary diversification is based on a strongly preserved molecular cluster that allows to produce the most varied forms in organisms. The multifunctionality of genes and proteins offers new models that will shed light on this paradox and allow to penetrate more deeply into the relations between, on the one hand, the complexity of genes and their regulation and, on the other, the complexity of development and evolution.

One of the bases of developmental genetics resides in the alliance of clonal analysis and genetic analysis. But the study of cell lineage — cells which have their genealogical relationship — and the study of the cellular labelled progeny, have their own history. We have tried to follow it since its foundation with C.O. Whitman (1878) and E.B. Wilson (1892). A.H. Sturtevant (1929) and C. Stern (1936) the first tools to study the 'cell lineage' in Drosophila. We stress the contribution of the pioneer work realised around 1940. In the following period we witness the emergence of developmental genetics in Drosophila mainly with E. Hadorn (1949-1966), C. Stern (1954-1968) and E.B. Lewis (1963-1964). We conclude with A. Garcia-Bellido's view of compartments: supra-cellular units of development (1973). A postcript presents the most recent publications and some critical focuses

'Lysogeny is the hereditary power to produce bacteriophage'. This definition, coined by André Lwoff in 1953, seems simple enough. However, it summarizes a very complex history, which began with the discovery of bacteriophages. How was the novel relationship between a virus and a bacterial cell conceived? In what way did this relationship renew the question of the nature of viruses? How did it generate a theory of hereditary factors? It was soon shown that bacteria can produce a lysogenic agent without exogenic phages. That was in 1925 with the discovery of lysogeny. In an attempt to throw light on the history of lysogeny, I have traced the work of Eugène Wollman from 1919 to 1943, and have examined the work of J. Bordet, O. Bail and F.M. Burnet. The second part of this paper is devoted to the experiments that led to the elucidation of lysogeny. Of particular importance was the shaping of the concept of 'prophage'. Lysogeny was studied anew and clarified at the Institut Pasteur in Paris under the guidance of André Lwoff. How was genetic determinism of lysogeny brought to light? What new models and new concepts then formed the basis of genetic analysis of the relationship between the virus and its bacterial host? These aspects are seen in the light of the work of André Lwoff, François Jacob, Joshua Lederberg and Elie Wollman