When normal quiescent (G0) cells are stimulated by mitogens to enter the cell cycle, the metabolic derepression which occurs is similar in a variety of cells. The mechanisms initiating these responses and their relationship to subsequent progression through G1 to DNA synthesis in S phase, however, are generally undefined. The clearest evidence has been obtained in sea urchin eggs, where fertilization by sperm causes a rapid, transient increase in the concentration of free cytoplasmic Ca2+ [(Ca]i), followed by a sustained increase in cytoplasmic pH (pHi). It has been demonstrated clearly that these ionic responses are obligatory for progression to DNA synthesis by the normal pathway after fertilization, although the Ca2+ signal can be bypassed by parthenogenetic agents which elevate directly pHi (for example, NH+4 ions). These observations raise the questions of whether other eukaryotic cells show the same sequence of ionic responses when stimulated by mitogens and whether such signals are an obligatory component of their mitogenic pathways. We show here that a common sequence of [Ca]i and pHi responses occurs in both quiescent mouse thymocytes and Swiss 3T3 fibroblasts stimulated by appropriate mitogens. Furthermore, 'opportunistic' mitogens (those that do not act on the cells in vivo, such as concanavalin A (Con A), the Ca2+ ionophore A23187 and 12-o-tetradecanoyl phorbol 13-acetate CTPA] that are mitogenic for both mouse thymocytes and 3T3 fibroblast, each produce characteristic ionic responses that are the same in both types of cell.

Aggregation and fusion of myoblasts to form myotubes is essential for myogenesis in many organisms. In Drosophila the formation of syncytial myotubes is seeded by founder myoblasts. Founders fuse with clusters of fusion-competent myoblasts. Here we identify the gene dumbfounded (duf) and show that it is required for myoblast aggregation and fusion. duf encodes a member of the immunoglobulin superfamily of proteins that is an attractant for fusion-competent myoblasts. It is expressed by founder cells and serves to attract clusters of myoblasts from which myotubes form by fusion.

Mef2 is a conserved and significant transcription factor in the control of muscle gene expression. In cell culture Mef2 synergises with MyoD-family members in the activation of gene expression and in the conversion of fibroblasts into myoblasts. Amongst its in vivo roles, Mef2 is required for both Drosophila muscle development and mammalian muscle regeneration. Mef2 has functions in other cell-types too, but this review focuses on skeletal muscle and surveys key findings on Mef2 from its discovery, shortly after that of MyoD, up to the present day. In particular, in vivo functions, underpinning mechanisms and areas of uncertainty are highlighted. We describe how Mef2 sits at a nexus in the gene expression network that controls the muscle differentiation program, and how Mef2 activity must be regulated in time and space to orchestrate specific outputs within the different aspects of muscle development. A theme that emerges is that there is much to be learnt about the different Mef2 proteins (from different paralogous genes, spliced transcripts and species) and how the activity of these proteins is controlled.

Promoter sequences required for activation of the Xenopus cardiac actin gene in embryonic muscle were analysed by micro‐injecting chimeric actin/beta‐globin genes into the two‐cell Xenopus embryo. Transcription was monitored during subsequent differentiation of embryonic muscle and non‐muscle tissues. The effect of a variety of mutations including internal deletions and linker scan mutations between −64 and −396 within the cardiac actin promoter were tested. This region contains four copies of a conserved motif, the CArG box, common to vertebrate striated muscle acting gene promoters. In the Xenopus cardiac actin gene, the most proximal of these motifs (CArG box 1) located at −80, was essential for muscle‐specific transcription. Other CArG motifs could functionally substitute for CArG box 1 when placed in this position. CArG boxes 3 and 4 bound the same activity in a neurula embryo nuclear extract as CArG box 1 and the amount of this binding activity was constant through early development.

This book originates from graduate courses given in Cambridge and London. It provides a brisk, thorough treatment of the foundations of algebraic number theory, and builds on that to introduce more advanced ideas. Throughout, the authors emphasise the systematic development of techniques for the explicit calculation of the basic invariants, such as rings of integers, class groups, and units. Moreover they combine, at each stage of development, theory with explicit computations and applications, and provide motivation in terms of classical number-theoretic problems. A number of special topics are included that can be treated at this level but can usually only be found in research monographs or original papers, for instance: module theory of Dedekind domains; tame and wild ramifications; Gauss series and Gauss periods; binary quadratic forms; and Brauer relations. This is the only textbook at this level which combines clean, modern algebraic techniques together with a substantial arithmetic content. It will be indispensable for all practising and would-be algebraic number theorists.