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First published online May 5, 2004
doi: 10.1242/10.1242/dev.01180

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Cell cycling through development

Department of Ophthalmology and Visual Sciences, Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, UT 84112, USA

View larger version (22K): [in a new window]   Fig. 1. Cell cycles discussed at the meeting. Cell cycle phases can be modified to meet the demands of a cell at specific developmental stages. The first three cycles shown increase cell number by incorporating mitosis (M), but their coupling to external influences, such as growth, vary. In the fourth cycle shown, M is repressed, and the primary result of this is polyploidy, which is associated with growth and differentiation in many plant cell types and in some animal cell types.

View larger version (101K): [in a new window]   Fig. 2. Examples of negative regulators of proliferation. (A) In the Drosophila eye, Shar-pei (Salvador) controls cell number by inhibiting cell proliferation and promoting cell death. This is indicated by the increase of interommatidial cells in the sharpei/salvador mutant compared with wild type. (B) In the mouse cochlea, hair cells (brackets) re-enter the cell cycle in the absence of p19Ink4d. Myosin VIIa is a marker of postmitotic, differentiated hair cells, and BrdU incorporation is shown in a p19Ink4d-/- hair cell (arrow). In this experiment, BrdU was given to animals after the period when hair cells are generated. (C) In the mouse retina, differentiated amacrine cells [Glycine Transporter 1 (GlyT1) immunoreactive] and horizontal cells (Calbindin immunoreactive) reenter the cell cycle as a result of the combined absence of p19Ink4d and p27Kip1, as indicated by BrdU incorporation (arrows). Similar to the experiment shown in B, BrdU was given to animals after the period when amacrine and horizontal cells are generated. Panels modified with permission from Kango-Singh et al., Chen et al. and Cunningham et al. (Kango-Singh et al., 2002; Chen et al., 2003; Cunningham et al., 2002).

View larger version (20K): [in a new window]   Fig. 3. How changes in regulation can modify cell cycle types. (A) In the Drosophila oocyte cyst, there is a transition from somatic cell cycles to endocycles during oocyte maturation in the nurse and follicle cells, whereas the oocyte is maintained in prophase arrest during Meiosis I. As nurse cells and the oocyte are coupled cytoplasmically, an important question is how these cells maintain different cell cycle states. Lilly described (see main text) how this appears to be regulated by the local modulation of Dacapo levels, which regulate CycE/Cdk2 activity. The pathways mediating this mechanism are not yet known. Ruholla-Baker described how the transition to endocycles in the follicle cells is mediated by activation of the Notch pathway through Delta ligand expressed by the oocyte and nurse cells (see main text). Notch signaling may regulate the cell cycle in at least three ways: repression of CycB/Cdk1 activity by downregulation of Stringcdc25; upregulation of Fzr/Cdh1-dependent APC activity; and activation of CycE/Cdk2 activity by downregulation of Dacapo. (B) In Arabidopsis and Medicago trunculata, the transition from a somatic cell cycle to an endocycle during differentiation appears to depend on the activity of the CDK CdkB1;1. This may involve Fzr/Cdh1-dependent APC activity and downregulation of CycD3;1, although the specific nature of the interactions of these proteins with CdkB1;1 is not yet known.