Asymmetric Cell Divisions: Zygotes of Fucoid Algae as a Model System

The generation and orientation of cellular and organismic polarity are fundamental aspects of development. Mutations in the gene lin-44 of the nematode Caenorhabditis elegans reverse both the relative positions of specific sister cells and the apparent polarities of these cells. Thus, lin-44 mutants appear to generate polar cells but to misorient these cells along the body axis of the animal. We postulate that lin-44 acts to specify the orientation of polar cells.

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discordia mutations specifically misorient asymmetric cell divisions during development of the maize leaf epidermis

Development ◽

10.1242/dev.126.20.4623 ◽

1999 ◽

Vol 126 (20) ◽

pp. 4623-4633 ◽

Cited By ~ 2

Author(s):

K. Gallagher ◽

L.G. Smith

Keyword(s):

Cell Division ◽

Preprophase Band ◽

Cytochalasin D ◽

Leaf Epidermis ◽

Asymmetric Cell Divisions ◽

Maize Leaf ◽

Cell Divisions ◽

Cytoskeletal Structure ◽

Dividing Cells ◽

Preprophase Bands

In plant cells, cytokinesis depends on a cytoskeletal structure called a phragmoplast, which directs the formation of a new cell wall between daughter nuclei after mitosis. The orientation of cell division depends on guidance of the phragmoplast during cytokinesis to a cortical site marked throughout prophase by another cytoskeletal structure called a preprophase band. Asymmetrically dividing cells become polarized and form asymmetric preprophase bands prior to mitosis; phragmoplasts are subsequently guided to these asymmetric cortical sites to form daughter cells of different shapes and/or sizes. Here we describe two new recessive mutations, discordia1 (dcd1) and discordia2 (dcd2), which disrupt the spatial regulation of cytokinesis during asymmetric cell divisions. Both mutations disrupt four classes of asymmetric cell divisions during the development of the maize leaf epidermis, without affecting the symmetric divisions through which most epidermal cells arise. The effects of dcd mutations on asymmetric cell division can be mimicked by cytochalasin D treatment, and divisions affected by dcd1 are hypersensitive to the effects of cytochalasin D. Analysis of actin and microtubule organization in these mutants showed no effect of either mutation on cell polarity, or on formation and localization of preprophase bands and spindles. In mutant cells, phragmoplasts in asymmetrically dividing cells are structurally normal and are initiated in the correct location, but often fail to move to the position formerly occupied by the preprophase band. We propose that dcd mutations disrupt an actin-dependent process necessary for the guidance of phragmoplasts during cytokinesis in asymmetrically dividing cells.

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