scholarly journals The Tangled1 Gene Is Required for Spatial Control of Cytoskeletal Arrays Associated with Cell Division during Maize Leaf Development

1998 ◽  
Vol 10 (11) ◽  
pp. 1875
Author(s):  
Ann L. Cleary ◽  
Laurie G. Smith
2012 ◽  
Vol 22 (13) ◽  
pp. 1183-1187 ◽  
Author(s):  
Hilde Nelissen ◽  
Bart Rymen ◽  
Yusuke Jikumaru ◽  
Kirin Demuynck ◽  
Mieke Van Lijsebettens ◽  
...  

2012 ◽  
Vol 22 (13) ◽  
pp. 1266 ◽  
Author(s):  
Hilde Nelissen ◽  
Bart Rymen ◽  
Yusuke Jikumaru ◽  
Kirin Demuynck ◽  
Mieke Van Lijsebettens ◽  
...  

Development ◽  
1996 ◽  
Vol 122 (2) ◽  
pp. 481-489 ◽  
Author(s):  
L.G. Smith ◽  
S. Hake ◽  
A.W. Sylvester

It is often assumed that in plants, where the relative positions of cells are fixed by cell walls, division orientations are critical for the generation of organ shapes. However, an alternative perspective is that the generation of shape may be controlled at a regional level independently from the initial orientations of new cell walls. In support of this latter view, we describe here a recessive mutation of maize, tangled-1 (tan-1), that causes cells to divide in abnormal orientations throughout leaf development without altering overall leaf shape. In normal plants, leaf cells divide either transversely or longitudinally relative to the mother cell axis; transverse division are associated with leaf elongation and longitudinal divisions with leaf widening. In tan-l mutant leaves, cells in all tissue layers at a wide range of developmental stages divide transversely at normal frequencies, but longitudinal divisions are largely substituted by a variety of aberrantly oriented divisions in which the new cell wall is crooked or curved. Mutant leaves grow more slowly than normal, but their overall shapes are normal at all stages of their growth. These observations demonstrate that the generation of maize leaf shape does not depend on the precise spatial control of cell division, and support the general view that mechanisms independent from the control of cell division orientations are involved in the generation of shape during plant development.


2001 ◽  
Vol 152 (1) ◽  
pp. 231-236 ◽  
Author(s):  
Laurie G. Smith ◽  
Suzanne M. Gerttula ◽  
Shengcheng Han ◽  
Joshua Levy

Spatial control of cytokinesis in plant cells depends on guidance of the cytokinetic apparatus, the phragmoplast, to a cortical “division site” established before mitosis. Previously, we showed that the Tangled1 (Tan1) gene of maize is required for this process during maize leaf development (Cleary, A.L., and L.G. Smith. 1998. Plant Cell. 10:1875–1888.). Here, we show that the Tan1 gene is expressed in dividing cells and encodes a highly basic protein that can directly bind to microtubules (MTs). Moreover, proteins recognized by anti-TAN1 antibodies are preferentially associated with the MT-containing cytoskeletal structures that are misoriented in dividing cells of tan1 mutants. These results suggest that TAN1 protein participates in the orientation of cytoskeletal structures in dividing cells through an association with MTs.


Development ◽  
1999 ◽  
Vol 126 (20) ◽  
pp. 4623-4633 ◽  
Author(s):  
K. Gallagher ◽  
L.G. Smith

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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