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Transcriptome Profiles of Differentiated arabidopsis Leaf Cells and Dedifferentiating Protoplasts of Ler and kyp mutant

ABSTRACT: Dedifferentiation signifies the capacity of somatic cells to acquire stem cell-likeproperties. This process characterizes the transition of differentiated plant cells toprotoplasts (plant cells devoid of cell walls), a transition accompanied by widespreadchromatin decondensation. Transcriptome profiling of dedifferentiating cells revealedstriking similarities with senescing cells; both display a large increase in the expressionof genes of specific transcription factor (TF) families including ANAC, WRKY, bZIPand C2H2. We further showed that leaves induced to senesce by exposure to dark displaycharacteristic features of dedifferentiating cells including widespread chromatindecondensation, disruption of the nucleolus and condensation of rRNA genes.Considering that premature senescence can be induced by various stress conditions, ourresults suggest that plant cells response to certain stresses converges on cellulardedifferentiation whereby cells first acquire stem cell-like state prior to acquisition of anew cell fate (e.g., reentry into the cell cycle, or death).

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE15515 | GEO | 2009/04/02

SECONDARY ACCESSION(S): PRJNA115681

REPOSITORIES: GEO

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Project description:Kollarovic2016 - Cell fate decision at G1-S transition This model is described in the article: To senesce or not to senesce: how primary human fibroblasts decide their cell fate after DNA damage. Kollarovic G, Studencka M, Ivanova L, Lauenstein C, Heinze K, Lapytsko A, Talemi SR, Figueiredo AS, Schaber J. Aging (Albany NY) 2016 Jan; Abstract: Excessive DNA damage can induce an irreversible cell cycle arrest, called senescence, which is generally perceived as an important tumour-suppressor mechanism. However, it is unclear how cells decide whether to senesce or not after DNA damage. By combining experimental data with a parameterized mathematical model we elucidate this cell fate decision at the G1-S transition. Our model provides a quantitative and conceptually new understanding of how human fibroblasts decide whether DNA damage is beyond repair and senesce. Model and data imply that the G1-S transition is regulated by a bistable hysteresis switch with respect to Cdk2 activity, which in turn is controlled by the Cdk2/p21 ratio rather than cyclin abundance. We experimentally confirm the resulting predictions that to induce senescence i) in healthy cells both high initial and elevated background DNA damage are necessary and sufficient, and ii) in already damaged cells much lower additional DNA damage is sufficient. Our study provides a mechanistic explanation of a) how noise in protein abundances allows cells to overcome the G1-S arrest even with substantial DNA damage, potentially leading to neoplasia, and b) how accumulating DNA damage with age increasingly sensitizes cells for senescence. This model is hosted on BioModels Database and identified by: BIOMD0000000632. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Transcriptome Profiles of Differentiated arabidopsis Leaf Cells and Dedifferentiating Protoplasts of Ler and kyp mutant

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