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Arabidopsis COPPER MODIFIED RESISTANCE 1/ PATRONUS 1 is essential for growth adaptation to stress and required for mitotic onset control
Author(s) -
Juraniec Michal,
Heyman Jefri,
Schubert Veit,
Salis Pietrino,
De Veylder Lieven,
Verbruggen Nathalie
Publication year - 2016
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.13589
Subject(s) - arabidopsis , adaptation (eye) , biology , chemistry , biochemistry , mutant , gene , neuroscience
Summary The mitotic checkpoint ( MC ) guards faithful sister chromatid segregation by monitoring the attachment of spindle microtubules to the kinetochores. When chromosome attachment errors are detected, MC delays the metaphase‐to‐anaphase transition through the inhibition of the anaphase‐promoting complex/cyclosome ( APC /C) ubiquitin ligase. In contrast to yeast and mammals, our knowledge on the proteins involved in MC in plants is scarce. Transient synchronization of root tips as well as promoter–reporter gene fusions were performed to analyze temporal and spatial expression of COPPER MODIFIED RESISTANCE 1/ PATRONUS 1 ( CMR 1/ PANS 1 ) in developing Arabidopsis thaliana seedlings. Functional analysis of the gene was carried out, including CYCB 1;2 stability in CMR 1/ PANS 1 knockout and overexpressor background as well as metaphase–anaphase chromosome status. CMR 1/ PANS 1 is transcriptionally active during M phase. Its deficiency provokes premature cell cycle exit and in consequence a rapid consumption of the number of meristematic cells in particular under stress conditions that are known to affect spindle microtubules. Root growth impairment is correlated with a failure to delay the onset of anaphase, resulting in anaphase bridges and chromosome missegregation. CMR 1/ PANS 1 overexpression stabilizes the mitotic CYCB 1;2 protein. Likely, CMR 1/ PANS 1 coordinates mitotic cell cycle progression by acting as an APC /C inhibitor and plays a key role in growth adaptation to stress.