Expression data from root segments of barley (Hordeum vulgare) during a transient water deficit repressing lateral root formation
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ABSTRACT:
ORGANISM(S): Hordeum vulgare
PROVIDER: GSE67367 | GEO | 2016/12/31
SECONDARY ACCESSION(S): PRJNA279593
REPOSITORIES: GEO
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Project description:Lateral root initiation was used as a model system to study the mechanisms behind auxin-induced cell division. Genome-wide transcriptional changes were monitored during the early steps of lateral root initiation. Inclusion of the dominant auxin signaling mutant solitary root1 (slr1) identified genes involved in lateral root initiation that act downstream of the AUX/IAA signaling pathway. Interestingly, key components of the cell cycle machinery were strongly defective in slr1, suggesting a direct link between AUX/IAA signaling and core cell cycle regulation. However, induction of the cell cycle in the mutant background by overexpression of the D-type cyclin (CYCD3;1) was able to trigger complete rounds of cell division in the pericycle that did not result in lateral root formation. Therefore, lateral root initiation can only take place when cell cycle activation is accompanied by cell fate respecification of pericycle cells. The microarray data also yielded evidence for the existence of both negative and positive feedback mechanisms that regulate auxin homeostasis and signal transduction in the pericycle, thereby fine-tuning the process of lateral root initiation. Keywords: time-course wild type vs mutant comparison
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Project description:Lateral root initiation was used as a model system to study the mechanisms behind auxin-induced cell division. Genome-wide transcriptional changes were monitored during the early steps of lateral root initiation. Inclusion of the dominant auxin signaling mutant solitary root1 (slr1) identified genes involved in lateral root initiation that act downstream of the AUX/IAA signaling pathway. Interestingly, key components of the cell cycle machinery were strongly defective in slr1, suggesting a direct link between AUX/IAA signaling and core cell cycle regulation. However, induction of the cell cycle in the mutant background by overexpression of the D-type cyclin (CYCD3;1) was able to trigger complete rounds of cell division in the pericycle that did not result in lateral root formation. Therefore, lateral root initiation can only take place when cell cycle activation is accompanied by cell fate respecification of pericycle cells. The microarray data also yielded evidence for the existence of both negative and positive feedback mechanisms that regulate auxin homeostasis and signal transduction in the pericycle, thereby fine-tuning the process of lateral root initiation. Experiment Overall Design: Seedlings of both wild type (Col-0) and the lateral root defective mutant (slr-1) were germinated on MS medium supplemented with 10μM NPA (=auxin transport inhibitor). Three days after germination, such seedlings were transferred to MS supplemented with 10μM NAA for 0h, 2h and 6h respectively. The segment between root meristem and root-hypocotyl junction was harvested from about 1500 seedling per time point. All treatments were repeated biologically. 5.8 μg total RNA was used for the preparation of biotinylated cRNA. Labeled RNA was hybridised to ATH1 Affymetrix chips. The resulting data was MAS5.0 normalised.
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Project description:Control of the dimensions of organ primordia is crucial for proper organogenesis in the development of multicellular organisms. Lateral root formation is a major type of plant organogenesis important for postembryonic development of the root system. Lateral root formation begins with a few rounds of asymmetric, anticlinal cell division (formative cell division) in the pericycle, which determines the basal dimensions of root primordia. Here we show, based on molecular genetic analysis of temperature-dependent fasciation (TDF) mutants of Arabidopsis thaliana, that mitochondria play an unexpected role in the restriction of formative cell division and thus in the control of the basal dimensions of lateral root primordia. Three TDF mutants, root redifferentiation defective 1 (rrd1), rrd2, and root initiation defective 4 (rid4), exhibit lateral root fasciation from excess formative cell division under high-temperature conditions. We identify RRD1 as encoding a poly(A)-specific ribonuclease (PARN)-like protein and RRD2 and RID4 as encoding pentatricopeptide repeat (PPR) proteins. Subcellular localization and predicted functions of these proteins implicate them in poly(A)-dependent RNA degradation in mitochondria. This characterization is supported by the finding that mitochondrial RNAs with poly(A) tails, most of which are mRNAs of respiratory chain components, accumulate at an unusually high level in these TDF mutants. Explants of three mutants (rrd1, rrd2, rid4) and wild type were cultured on B5 medium supplemented with 0.5 mg/L IBA for the induction of lateral root formation. After 12 hours of culture at 28C, explants were collected and used for microarray analysis. Analysis was performed in three biological replicates.
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Project description:Control of the dimensions of organ primordia is crucial for proper organogenesis in the development of multicellular organisms. Lateral root formation is a major type of plant organogenesis important for postembryonic development of the root system. Lateral root formation begins with a few rounds of asymmetric, anticlinal cell division (formative cell division) in the pericycle, which determines the basal dimensions of root primordia. Here we show, based on molecular genetic analysis of temperature-dependent fasciation (TDF) mutants of Arabidopsis thaliana, that mitochondria play an unexpected role in the restriction of formative cell division and thus in the control of the basal dimensions of lateral root primordia. Three TDF mutants, root redifferentiation defective 1 (rrd1), rrd2, and root initiation defective 4 (rid4), exhibit lateral root fasciation from excess formative cell division under high-temperature conditions. We identify RRD1 as encoding a poly(A)-specific ribonuclease (PARN)-like protein and RRD2 and RID4 as encoding pentatricopeptide repeat (PPR) proteins. Subcellular localization and predicted functions of these proteins implicate them in poly(A)-dependent RNA degradation in mitochondria. This characterization is supported by the finding that mitochondrial RNAs with poly(A) tails, most of which are mRNAs of respiratory chain components, accumulate at an unusually high level in these TDF mutants.
2012-02-10 | GSE34595 | GEO