A cytokinesis-defective mutant of Arabidopsis (cyt1) characterized by embryonic lethality, incomplete cell walls, and excessive callose accumulation.
The genetic control of cell division in eukaryotes has been addressed in part through the analysis of cytokinesis-defective mutants. Two allelic mutants of Arabidopsis (cyt1-1 and cyt1-2) altered in cytokinesis and cell-wall architecture during embryogenesis are described in this report. Mutant embryos appear slightly abnormal at the heart stage and then expand to form a somewhat disorganized mass of enlarged cells with occasional incomplete walls. In contrast to the keule and knolle mutants of Arabidopsis and the cyd mutant of pea, which also exhibit defects in cytokinesis during embryogenesis, cyt1 embryos cannot be rescued in culture, are desiccation-intolerant at maturity, and produce cell walls with excessive callose as revealed through staining with the aniline blue fluorochrome, Sirofluor. Some cyt1 defects can be partially phenocopied by treatment with the herbicide dichlobenil, which is thought to interfere with cellulose biosynthesis. The distribution of unesterified pectins in cyt1 cell walls is also disrupted as revealed through immunocytochemical localization of JIM 5 antibodies. These features indicate that CYT1 plays an essential and unique role in plant growth and development and the establishment of normal cell-wall architecture.[1]References
- A cytokinesis-defective mutant of Arabidopsis (cyt1) characterized by embryonic lethality, incomplete cell walls, and excessive callose accumulation. Nickle, T.C., Meinke, D.W. Plant J. (1998) [Pubmed]
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