Who pulls the string to pattern cell division in Drosophila?

• Published in: Trends in genetics 1998-09, Vol.14 (9), p.337-339
• Main Author: Skaer, Helen
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Body Patterning; Cell Cycle; Cell Division; Classical genetics, quantitative genetics, hybrids; development; Drosophila - cytology; Drosophila - embryology; Drosophila - genetics; Drosophila melanogaster; Fundamental and applied biological sciences. Psychology; Genes, Insect; Genetics of eukaryotes. Biological and molecular evolution; Invertebrata; pattern formation; wing; Wings, Animal - cytology; Wings, Animal - embryology
• ISSN: 0168-9525
• DOI: 10.1016/S0168-9525(98)01544-3

One of the most exquisite specimens in a medical museum I once visited was a diminutive foetus, stained to reveal the cartilaginous placodes of the skeleton; minute structures laid down quite separate from each other, but instantly recognizable by their positions and proportions as precursors of the adult structures. From these tiny beginnings, the bones grow with a precision that allows the skeleton to become a coordinated structure. We are familiar with the concept that cell fate and differentiation are patterned in space, but the growth of these tiny bone precursors also involves the intricate patterning of cell proliferation and this, in turn, means the activation of cell division in some regions and the imposition of cell-cycle arrest in others. Our understanding of the cell cycle, its control points and the molecular machinery that regulates the passage of cells through them, has reached a high level of sophistication, thanks to extensive analysis of organisms as widely diverse as yeasts, clams, flies, frogs, moulds and humans. We know that two of these control points act at the G1-S and G2-M transitions, and that crossing them depends on the activity of cyclin-dependent kinases (CDKs). CDK activity is controlled at three levels: (1) they form complexes with cyclins, so called because they appear and are broken down at specific phases of the cell cycle; (2) the complex must be phosphorylated at an activation site; and (3) in the case of the G2-M transition, the complex must be dephosphorylated at an inhibitory site. Progress through the cycle can, therefore, be regulated by cyclin production or by phosphorylation/dephosphorylation at either of these sites.