Cross-talk between cell-cycle control and the environment
type: Dataset
contact point: Organization
  fn: CCSD
keyword: cdkds
keyword: infoeu-reposemanticsdoctoralthesis
keyword: cercle-circadien
keyword: cell-cycle
keyword: dommages-a-ladn
keyword: cycle-cellulaire
keyword: sdvsalife-sciences-q-bioagricultural-sciences
keyword: circadian-clock
keyword: arabidopsis
keyword: phosphorylation
keyword: dna-damage
keyword: cdka-1
keyword: theses
landing page: https://theses.hal.science/tel-00998938
description: Even though the understanding of cell-cycle regulators in plants has tremendously increased over the last years, still little is known about cell-cycle regulation in response to environmental signals like DNA damage. A ubiquitous stress for any organism is DNA stress that can either be caused by exogenous sources or internal processes like chromatid separation or DNA strands separation during replication. The posttranslational regulation of Cdk1-type kinases through inhibitory phosphorylation through Wee1-type kinases in the so-called P-loop at the residue Tyr15 or the analogous positions has been found to be of pivotal importance for the arrest of the cell cycle after DNA damage in yeast and animals. But this mechanism is apparently not conserved in plants, as suggested by the hypersensitivity analysis of CDKA;1 dephospho-mutants. The first half of this study focus on possible regulation of CDKA;1 through T-loop phosphorylation upon replication stress in Arabidopsis. The positively acting phosphorylation on T161 and analogous residues in the so-called T-loop of the kinase that is required for full CDK activity and serves in substrate recognition. Remarkably, a T-loop phospho-mimicry mutant of CDKA;1, was almost 100% resistant to hydroxyurea (HU) and can partially rescue the hypersensitivity of wee1 to HU. T-loop phosphorylation is catalyzed by CDK activating kinases (CAKs) that are themselves CDKs with typical P- and T-loop regions. Evidence is obtained that WEE1 might inhibit CDKDs (Cdk-activating kinases) that would subsequently result in reduced CDKA;1 activity, and thus, cell-cycle arrest upon DNA damage. It is revealed that dephospho-mimicry mutants of CDKD;2 and 3, which can not be inhibited through WEE1 showed hypersensitivity to HU and not to bleomycin, suggesting their involvement in cell-cycle arrest specifically upon replication stress. Hypersensitivity of cdkd;2cdkd;3 to replication stress suggested possible activation of CDKA;1 through CDKD;1 independe…
identifier: NNT: 2013STRAJ031
issued: 2026-05-05T09:50:55.560637
language: en
modified: 2026-05-05T09:50:55.560642

test_moissonnage_selune
type: Agent

Cross-talk between cell-cycle control and the environment
type: Distribution
access URL: https://theses.hal.science/tel-00998938
format: HTML
issued: 2026-05-05T09:50:55.564963
modified: 2026-05-05T09:50:55.535880