A cytokinesis‐defective mutant of Arabidopsis ( cyt1 ) characterized by embryonic lethality, incomplete cell walls, and excessive callose accumulation
Summary 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. M...
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Published in | The Plant journal : for cell and molecular biology Vol. 15; no. 3; pp. 321 - 332 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Science Ltd
01.08.1998
Blackwell Science |
Subjects | |
Online Access | Get full text |
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Summary: | Summary
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. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0960-7412 1365-313X |
DOI: | 10.1046/j.1365-313X.1998.00212.x |