Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of Arabidopsis klu-2 mutants vs. wild type

ABSTRACT: The Arabidopsis cytochrome P450 KLUH (KLU)/CYP78A5 promotes organ growth in a non-cell autonomous manner. To identify genes regulated by KLU activity, homozygous klu-2 mutants carrying constructs for EtOH-inducible overexpression of wild-type KLU (35S::AlcR-AlcA::KLU) or of enzymatically inactive KLU protein (35S::AlcR-AlcA::KLUmut) were induced with EtOH and sampled at 90 min and 240 min after induction for gene expression changes. Experiment Overall Design: For both constructs (i.e. overexpression of wild-type and of mutant KLU protein as a control), two independently transformed lines were used, serving as biological replicates. These were sampled at 90 min and 240 min after induction. In addition, plants with the wild-type construct were also sampled immediately before induction as a control, together resulting in ten hybridizations.

ORGANISM(S): Arabidopsis thaliana

SUBMITTER: Michael Lenhard

PROVIDER: E-GEOD-9201 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Control of plant organ size by KLUH/CYP78A5-dependent intercellular signaling.

Anastasiou Elena E Kenz Sabine S Gerstung Moritz M MacLean Daniel D Timmer Jens J Fleck Christian C Lenhard Michael M

Developmental cell 20071201 6

Plant organs grow to characteristic sizes that are genetically controlled. In animals, signaling by mobile growth factors is thought to be an effective mechanism for measuring primordium size, yet how plants gauge organ size is unclear. Here, we identify the Arabidopsis cytochrome P450 KLUH (KLU)/CYP78A5 as a stimulator of plant organ growth. While klu loss-of-function mutants form smaller organs because of a premature arrest of cell proliferation, KLU overexpression leads to larger organs with ...[more]

PMID: 18061566

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Dataset Information

Transcription profiling of Arabidopsis klu-2 mutants vs. wild type

Publications

Control of plant organ size by KLUH/CYP78A5-dependent intercellular signaling.

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